Strain Name:

STOCK Cav1tm1Mls/J

Stock Number:

004585

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These Caveolin 1 knock-out mice show hyperproliferative and vascular abnormalities. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Young mutant mice exhibit characteristics of Alzheimer's disease. This mutant mouse strain may be useful in studies of vesicular and cholesterol trafficking, signal transduction, neurodegeneration and tumorigenesis.

Note that this allele is also available on a C57BL/6J congenic background (Stock No. 007083).

Description

Strain Information

Former Names STOCK Cavtm1Mls/J    (Changed: 21-DEC-04 )
Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
Generation?+F24 (05-MAR-13)
Generation Definitions
 
Donating Investigator Michael P. Lisanti,   The Albert Einstein College of Medicine

Description
Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction response to the alpha-1-adrenergic receptor agonist, phenylephrine, and an enhanced vasorelaxation response to acetylcholine. Histological examination of lung tissue from mutant mice shows thickened alveolar septa, hypercellularity, reduced alveolar spaces and increased density of basement membranes and reticulin fibers. Further immunohistochemical examination of lung tissue shows an increased number of endothelial cells. Mutant derived MEF cells proliferate two times faster and are denser at confluence as indicated by growth curves and cell cycle analysis. Electron microscopy analysis reveals a complete absence of caveolae (plasmalemmal vesicles) in endothelial cells. In vitro studies measuring uptake of fluorescently-labeled albumin and in vivo studies following uptake of gold-conjugated albumin demonstrate caveolar endocytosis impairment.

Young (3-6 month old) mutant mice exhibit multiple characteristics of Alzheimer's disease pathologies including increased amyloid beta and tau deposits, neurodegeneration, astrogliosis and decreased cerebrovascular volume. The neuronal aging found in the hippocampi of young mutant mice resembles that found in aged (> 18 months of age) wild-type mice. The donating investigator noted diminished reproductive performance as the backcross to C57BL/6J background progressed.

Development
A targeting vector containing a neomycin resistance gene was used to disrupt 2.2 Kb of sequence containing exons 1 and 2. The construct was electroporated into WW6 embryonic stem (ES) cells(75% 129/Sv, 20% C57BL/6J, 5% SJL). Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6J mice for approximately 5 generations. The donating investigator noted diminished reproductive performance as the backcross to C57BL/6J background progressed and backcrossed to a 129S6/SvEv background for 1 generation. The mice are now maintained as homozygotes and are primarily a mix of 129 and C57BL/6, but a minor contribution from the SJL background (contributed from the originating ES cell line) should not be discounted.

Control Information

  Control
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Cav1tm1Mls allele
007083   B6.Cg-Cav1tm1Mls/J
View Strains carrying   Cav1tm1Mls     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Alzheimer Disease; AD
Breast Cancer
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Lipodystrophy, Congenital Generalized, Type 3; CGL3   (CAV1)
Partial Lipodystrophy, Congenital Cataracts, and Neurodegeneration Syndrome; LCCNS   (CAV1)
Pulmonary Hypertension, Primary, 3; PPH3   (CAV1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cav1tm1Mls/Cav1tm1Mls

        involves: 129/Sv * C57BL/6 * SJL
  • mortality/aging
  • increased susceptibility to bacterial infection induced morbidity/mortality
    • mutants exhibit a decrease in survival (7 days vs. 13 days in wild-type) when challenged with Salmonella enterica serovar Typhimurium   (MGI Ref ID J:115914)
  • premature death
    • 50% reduction in life span, with viability declining between 27 and 65 weeks of age   (MGI Ref ID J:87282)
    • mice that die within this time frame, die suddenly, without any visible signs of disease   (MGI Ref ID J:87282)
  • respiratory system phenotype
  • abnormal pulmonary alveolar parenchyma morphology
    • parenchymal hypercellularity   (MGI Ref ID J:75193)
  • abnormal pulmonary endothelial cell surface
    • reactive endothelial cell proliferation   (MGI Ref ID J:87282)
  • lung inflammation
    • increase in inflammatory infiltrates in the lung   (MGI Ref ID J:87282)
  • pulmonary hyperemia
    • hyperemic lungs   (MGI Ref ID J:87282)
    • alveolar spaces are filled with extravasated red blood cells   (MGI Ref ID J:87282)
  • thick pulmonary interalveolar septum   (MGI Ref ID J:75193)
  • cardiovascular system phenotype
  • abnormal myocardium layer morphology
    • myocardium is thickened in both the left and right ventricles at 12 months of age   (MGI Ref ID J:87282)
    • abnormal myocardial fiber morphology
      • myocyte hypertrophy and disorganization   (MGI Ref ID J:87282)
  • abnormal pulmonary endothelial cell surface
    • reactive endothelial cell proliferation   (MGI Ref ID J:87282)
  • abnormal vasoconstriction
    • impaired response to phenylephrine (PE) due to increased Nos3 activity   (MGI Ref ID J:75193)
  • abnormal vasodilation
    • impaired acetylcholine induced relaxation of the aortic rings   (MGI Ref ID J:75193)
  • cardiac fibrosis
    • increase in fibrosis at 12 months of age   (MGI Ref ID J:87282)
  • congestive heart failure
    • severe right-sided heart failure   (MGI Ref ID J:87282)
  • decreased cardiac muscle contractility
    • 29% decrease in fractional shortening at 12 months of age, indicating reduction in left ventricular systolic fraction   (MGI Ref ID J:87282)
  • dilated heart right ventricle
    • the right ventricular chamber is about 70% and 25% larger than in wild-type at 4 and 12 months of age, respectively   (MGI Ref ID J:87282)
  • heart left ventricle hypertrophy
    • 12 month old mutants exhibit concentric left ventricular hypertrophy   (MGI Ref ID J:87282)
  • pulmonary hyperemia
    • hyperemic lungs   (MGI Ref ID J:87282)
    • alveolar spaces are filled with extravasated red blood cells   (MGI Ref ID J:87282)
  • pulmonary hypertension   (MGI Ref ID J:87282)
  • thick interventricular septum
    • increase in intraventricular septal thickness during diastole   (MGI Ref ID J:87282)
  • thick ventricular wall
    • about 18% and 36% increase in left ventricular wall thickness at 4 and 12 months of age, respectively   (MGI Ref ID J:87282)
  • cellular phenotype
  • abnormal vesicle-mediated transport
    • uptake and transport of albumin from the blood to the interstitium by endothelial cells is defective due to absence of caveolae   (MGI Ref ID J:73489)
  • absent caveolae   (MGI Ref ID J:116286)
    • endothelial cells lack caveolae membranes   (MGI Ref ID J:75193)
    • adipocytes from peri-gonadal white adipose tissue show barren membrane architecture indicating a loss of caveolae   (MGI Ref ID J:75192)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • plasma glucose, insulin, and cholesterol levels were similar to wild-type in both fasting and post-prandial states at 12 weeks of age, standard chow diet   (MGI Ref ID J:75192)
    • mutants do not exhibit significant changes in paremeters of energy expenditure such as VO2, VCO2, respiratory quotient, heat release, or movement, indicating that leanness is not due to increased energy expenditure   (MGI Ref ID J:75192)
    • abnormal homeostasis
      • transvascular protein transport is increased, with mutants showing higher albumin and IgM clearance from the plasma to peritoneium, and increased clearance of high molecular weight Ficoll   (MGI Ref ID J:116286)
      • abnormal blood homeostasis
        • plasma ACRP30 (an adipoctye secreted factor) levels are reduced by 8-10 fold   (MGI Ref ID J:75192)
        • abnormal circulating free fatty acids level
          • free fatty acids levels fail to undergo the expected post-eating reduction seen in wild-type   (MGI Ref ID J:75192)
        • decreased circulating leptin level
          • plasma leptin levels are reduced more than 2-fold   (MGI Ref ID J:75192)
        • increased circulating interferon-gamma level
          • increased production of interferon-gamma at 3 days post Salmonella infection   (MGI Ref ID J:115914)
        • increased circulating interleukin-6 level
          • increased production of IL-6 at 3 days post Salmonella infection   (MGI Ref ID J:115914)
        • increased circulating triglyceride level
          • triglyceride levels are elevated in the fasted state and increased even more post-prandially, due to perturbed lipoprotein lipase activity   (MGI Ref ID J:75192)
          • increased circulating VLDL triglyceride level
            • the chylomicron/VLDL fraction of triglycerides is increased during fasting and increases dramatically above wild-type mice in the post-prandial state   (MGI Ref ID J:75192)
        • increased circulating tumor necrosis factor level
          • increased production of TNF-alpha at 3 days post Salmonella infection   (MGI Ref ID J:115914)
      • abnormal cytokine level   (MGI Ref ID J:115914)
        • abnormal chemokine level
          • increased production of the chemokines CCL3, CXCL10 and CXCL10 at 3 days post Salmonella infection   (MGI Ref ID J:115914)
        • increased circulating interferon-gamma level
          • increased production of interferon-gamma at 3 days post Salmonella infection   (MGI Ref ID J:115914)
        • increased circulating interleukin-6 level
          • increased production of IL-6 at 3 days post Salmonella infection   (MGI Ref ID J:115914)
        • increased circulating tumor necrosis factor level
          • increased production of TNF-alpha at 3 days post Salmonella infection   (MGI Ref ID J:115914)
      • abnormal lipid homeostasis
        • mutants show kinetically delayed clearance of triglycerides in an oral fat tolerance test   (MGI Ref ID J:75192)
        • abnormal circulating free fatty acids level
          • free fatty acids levels fail to undergo the expected post-eating reduction seen in wild-type   (MGI Ref ID J:75192)
        • increased circulating triglyceride level
          • triglyceride levels are elevated in the fasted state and increased even more post-prandially, due to perturbed lipoprotein lipase activity   (MGI Ref ID J:75192)
          • increased circulating VLDL triglyceride level
            • the chylomicron/VLDL fraction of triglycerides is increased during fasting and increases dramatically above wild-type mice in the post-prandial state   (MGI Ref ID J:75192)
      • abnormal nitric oxide homeostasis
        • lungs exhibit increased NOS3 (eNOS)-derived nitric oxide production and impaired NOS2 (iNOS)-derived nitric oxide production after LPS challenge   (MGI Ref ID J:139304)
      • decreased susceptibility to diet-induced obesity
        • mutants are resistant to obesity when challenged with a high fat diet for 36 weeks   (MGI Ref ID J:75192)
    • cardiac fibrosis
      • increase in fibrosis at 12 months of age   (MGI Ref ID J:87282)
    • impaired exercise endurance
      • exercise intolerance when compared to wild-type in a swimming test   (MGI Ref ID J:75193)
    • increased cerebral infarction size
      • mutants exhibit an increase of cerebral volume of infarction compared to wild-type, with fewer numbers of proliferating endothelial cells and increased numbers of cells undergoing apoptotic cell death in ischemic brains   (MGI Ref ID J:133702)
    • increased incidence of tumors by chemical induction
      • mutants are more susceptible to DMBA (7,12-dimethylbenzanthracene)-induced skin carcinogenesis   (MGI Ref ID J:83485)
      • 100% of mice develop tumors at 12 weeks of age compared to 10% of wild-type mice   (MGI Ref ID J:83485)
      • tumor multiplicity is greatly increased   (MGI Ref ID J:83485)
  • muscle phenotype
  • abnormal myocardial fiber morphology
    • myocyte hypertrophy and disorganization   (MGI Ref ID J:87282)
  • abnormal skeletal muscle fiber morphology
    • skeletal muscle fibers of males exhibit and increase in tubular aggregate formation with age   (MGI Ref ID J:117199)
    • sarcoplasmic reticulum is dilated in skeletal muscle of males   (MGI Ref ID J:117199)
  • abnormal vasoconstriction
    • impaired response to phenylephrine (PE) due to increased Nos3 activity   (MGI Ref ID J:75193)
  • abnormal vasodilation
    • impaired acetylcholine induced relaxation of the aortic rings   (MGI Ref ID J:75193)
  • decreased cardiac muscle contractility
    • 29% decrease in fractional shortening at 12 months of age, indicating reduction in left ventricular systolic fraction   (MGI Ref ID J:87282)
  • endocrine/exocrine gland phenotype
  • abnormal mammary gland morphology
    • size of mammary glands is reduced, however overall architecture is intact   (MGI Ref ID J:75192)
    • abnormal mammary gland duct morphology
      • the number of mammary ducts per field is increased   (MGI Ref ID J:75192)
      • the mammary ductal epithelia exhibits hyperproliferation   (MGI Ref ID J:75192)
      • mammary gland duct hyperplasia
        • intraductal hyperplasia, with the epithelial cell layer 3-4 cells thick   (MGI Ref ID J:109251)
    • abnormal mammary gland epithelium morphology
      • mammary epithelial cell hyperplasia, even in 6 week old virgin mice   (MGI Ref ID J:109251)
    • mammary gland hyperplasia
      • mammary epithelial cell hyperplasia, even in 6 week old virgin mice   (MGI Ref ID J:109251)
  • tumorigenesis
  • *normal* tumorigenesis
    • mice fail to spontaneously develop mammary tumors, even at up to 9 months of age, although mammary glands at this age show pronounced lobular development with numerous acini per terminal ductal lobular unit, hyperplasia of the mammary epithelial lining, and fibrosis   (MGI Ref ID J:109251)
    • increased incidence of tumors by chemical induction
      • mutants are more susceptible to DMBA (7,12-dimethylbenzanthracene)-induced skin carcinogenesis   (MGI Ref ID J:83485)
      • 100% of mice develop tumors at 12 weeks of age compared to 10% of wild-type mice   (MGI Ref ID J:83485)
      • tumor multiplicity is greatly increased   (MGI Ref ID J:83485)
  • immune system phenotype
  • abnormal cytokine level   (MGI Ref ID J:115914)
    • abnormal chemokine level
      • increased production of the chemokines CCL3, CXCL10 and CXCL10 at 3 days post Salmonella infection   (MGI Ref ID J:115914)
    • increased circulating interferon-gamma level
      • increased production of interferon-gamma at 3 days post Salmonella infection   (MGI Ref ID J:115914)
    • increased circulating interleukin-6 level
      • increased production of IL-6 at 3 days post Salmonella infection   (MGI Ref ID J:115914)
    • increased circulating tumor necrosis factor level
      • increased production of TNF-alpha at 3 days post Salmonella infection   (MGI Ref ID J:115914)
  • abnormal macrophage physiology
    • macrophages exhibit increased inflammatory responses and increased nitric oxide production in vitro in response to Salmonella LPS   (MGI Ref ID J:115914)
    • macrophages show no differences in the uptake of opsonized bacteria from wild-type   (MGI Ref ID J:115914)
  • abnormal neutrophil physiology
    • polymorphonuclear neutrophil (PMN) sequestration in lungs is reduced in mutants compared to wild-type after LPS challenge   (MGI Ref ID J:139304)
    • impaired neutrophil recruitment
      • mutants lack infiltration of white pulp by neutrophils when infected with Salmonella   (MGI Ref ID J:115914)
  • abnormal osteoclast morphology
    • marrow cultures from mutants generate about 20% more osteoclasts than wild-type cultures   (MGI Ref ID J:141361)
  • decreased susceptibility to endotoxin shock
    • mutants show reduced mortality compared to wild-type mice following LPS challenge due to elevated nitric oxide as mutants treated with an NOS3 inhibitor show 100% mortality   (MGI Ref ID J:139304)
    • lungs are protected from LPS-induced lung injury, showing no increase in lung microvascular permeability or edema formation as in wild-type mice   (MGI Ref ID J:139304)
    • adhesion of wild-type PMN to mutant endothelial cells is reduced after LPS challenge   (MGI Ref ID J:139304)
  • increased susceptibility to bacterial infection
    • mutants exhibit increased production of inflammatory cytokines, chemokines, and nitric oxide in response to Salmonella infection but are unable to control the systemic infection and have higher bacterial burden in spleen and liver   (MGI Ref ID J:115914)
    • increased susceptibility to bacterial infection induced morbidity/mortality
      • mutants exhibit a decrease in survival (7 days vs. 13 days in wild-type) when challenged with Salmonella enterica serovar Typhimurium   (MGI Ref ID J:115914)
  • lung inflammation
    • increase in inflammatory infiltrates in the lung   (MGI Ref ID J:87282)
  • nervous system phenotype
  • increased cerebral infarction size
    • mutants exhibit an increase of cerebral volume of infarction compared to wild-type, with fewer numbers of proliferating endothelial cells and increased numbers of cells undergoing apoptotic cell death in ischemic brains   (MGI Ref ID J:133702)
  • hematopoietic system phenotype
  • abnormal macrophage physiology
    • macrophages exhibit increased inflammatory responses and increased nitric oxide production in vitro in response to Salmonella LPS   (MGI Ref ID J:115914)
    • macrophages show no differences in the uptake of opsonized bacteria from wild-type   (MGI Ref ID J:115914)
  • abnormal neutrophil physiology
    • polymorphonuclear neutrophil (PMN) sequestration in lungs is reduced in mutants compared to wild-type after LPS challenge   (MGI Ref ID J:139304)
    • impaired neutrophil recruitment
      • mutants lack infiltration of white pulp by neutrophils when infected with Salmonella   (MGI Ref ID J:115914)
  • abnormal osteoclast morphology
    • marrow cultures from mutants generate about 20% more osteoclasts than wild-type cultures   (MGI Ref ID J:141361)
  • skeleton phenotype
  • abnormal bone mineralization
    • mineral apposition rate is increased at both metaphyseal and cortical sites at 5 weeks of age and regresses by 8 weeks of age   (MGI Ref ID J:141361)
  • abnormal bone trabecula morphology
    • metaphyseal trabeculae are greater in number and show reduced spacing, however trabecular thickness is not different from wild-typ   (MGI Ref ID J:141361)
    • increased bone trabecula number
      • increase in trabecular number in the distal femoral epiphysis   (MGI Ref ID J:141361)
  • abnormal compact bone morphology
    • 33% increase in stiffness and 33% decrease in postyield deflection of cortical bone   (MGI Ref ID J:141361)
    • increased compact bone area
      • at the femoral mid-diaphysis, the total cortical area is increased by 19.7% and 13.8%, at 5 and 8 weeks of age, respectively, with expanded periosteal and endocortical surfaces at 8 weeks   (MGI Ref ID J:141361)
  • abnormal long bone epiphysis morphology
    • 58.4% increase in ephiphyseal bone volume at 5 weeks   (MGI Ref ID J:141361)
  • abnormal long bone metaphysis morphology
    • 77.4 % increase in metaphyseal bone volume at 8 weeks but not at 5 weeks of age   (MGI Ref ID J:141361)
  • abnormal osteoclast morphology
    • marrow cultures from mutants generate about 20% more osteoclasts than wild-type cultures   (MGI Ref ID J:141361)
  • increased bone strength
    • stiffer bone capable of bearing a greater load before failure   (MGI Ref ID J:141361)
    • 25% increase in maximum force   (MGI Ref ID J:141361)
  • increased trabecular bone thickness
    • increase in thickness of the distal femoral epiphysis   (MGI Ref ID J:141361)
  • premature bone ossification
    • increase in bone formation rate at the trabecular and cortical sites at 5 weeks of age   (MGI Ref ID J:141361)
  • adipose tissue phenotype
  • abnormal fat cell morphology
    • at 12 weeks of age, female mammary gland 4/subcutaneous adipocytes contain reduced lipid droplets   (MGI Ref ID J:75192)
    • lipid droplet size in adipoctyes is about 2-3-fold smaller than in wild-type   (MGI Ref ID J:75192)
    • decreased white fat cell lipid droplet size
      • lipid droplet size in adipoctyes is about 2-3-fold smaller than in wild-type   (MGI Ref ID J:75192)
  • abnormal gonadal fat pad morphology
    • underdeveloped peri-gonadal fat pads   (MGI Ref ID J:75192)
  • abnormal mammary fat pad morphology
    • at 36 weeks of age on a high fat diet, mammary gland 4 fat is severely perturbed in females, with reduced numbers of adipoctyes that are heterogeneous in size and marked interstitial fibrosis and hypercellularity   (MGI Ref ID J:75192)
  • absent subcutaneous adipose tissue
    • the hypodermal fat layer is absent in both males and females at 12 weeks of age   (MGI Ref ID J:75192)
  • decreased subcutaneous adipose tissue amount
    • underdeveloped subcutaneous fat pads   (MGI Ref ID J:75192)
    • at 36 weeks of age on a high fat diet, subcutaneous fat is severely perturbed in females, with reduced numbers of adipoctyes that are heterogeneous in size and marked interstitial fibrosis and hypercellularity   (MGI Ref ID J:75192)
  • decreased total body fat amount
    • 2-fold reduction in the fat-to-water ratio   (MGI Ref ID J:75192)
    • at 35 weeks of age on a high fat diet, mutants only show minor gains in fat mass compared to wild-type and have dramatically reduced adiposity in all fat pads compared to wild-type   (MGI Ref ID J:75192)
  • decreased white adipose tissue amount
    • at 12 weeks of age on a high fat diet, mutants exhibit a 2-fold reduction in female mammary gland/subcutaneous WAT   (MGI Ref ID J:75192)
  • increased brown adipose tissue amount
    • mutants on a high fat diet exhibit hyperplastic brown adipose tissue, putatively secondary to elevated triglyceride levels   (MGI Ref ID J:75192)
  • behavior/neurological phenotype
  • impaired exercise endurance
    • exercise intolerance when compared to wild-type in a swimming test   (MGI Ref ID J:75193)
  • increased food intake
    • daily food intake is higher in females   (MGI Ref ID J:75192)
  • growth/size/body phenotype
  • decreased body weight
    • mice are leaner than wild-type mice on a chow diet   (MGI Ref ID J:75192)
    • relative decrease in weight is exacerbated on a high fat diet   (MGI Ref ID J:75192)
    • resistance to diet-induced obesity due to an inability to convert lipoprotein triglycerides into the fat droplet storage form   (MGI Ref ID J:75192)
    • slow postnatal weight gain
      • lack of weight gain   (MGI Ref ID J:75192)
  • decreased susceptibility to diet-induced obesity
    • mutants are resistant to obesity when challenged with a high fat diet for 36 weeks   (MGI Ref ID J:75192)
  • decreased total body fat amount
    • 2-fold reduction in the fat-to-water ratio   (MGI Ref ID J:75192)
    • at 35 weeks of age on a high fat diet, mutants only show minor gains in fat mass compared to wild-type and have dramatically reduced adiposity in all fat pads compared to wild-type   (MGI Ref ID J:75192)
  • liver/biliary system phenotype
  • *normal* liver/biliary system phenotype
    • livers show no increase in weight or steatosis   (MGI Ref ID J:75192)
  • integument phenotype
  • abnormal mammary gland morphology
    • size of mammary glands is reduced, however overall architecture is intact   (MGI Ref ID J:75192)
    • abnormal mammary gland duct morphology
      • the number of mammary ducts per field is increased   (MGI Ref ID J:75192)
      • the mammary ductal epithelia exhibits hyperproliferation   (MGI Ref ID J:75192)
      • mammary gland duct hyperplasia
        • intraductal hyperplasia, with the epithelial cell layer 3-4 cells thick   (MGI Ref ID J:109251)
    • abnormal mammary gland epithelium morphology
      • mammary epithelial cell hyperplasia, even in 6 week old virgin mice   (MGI Ref ID J:109251)
    • mammary gland hyperplasia
      • mammary epithelial cell hyperplasia, even in 6 week old virgin mice   (MGI Ref ID J:109251)
  • absent subcutaneous adipose tissue
    • the hypodermal fat layer is absent in both males and females at 12 weeks of age   (MGI Ref ID J:75192)
  • decreased subcutaneous adipose tissue amount
    • underdeveloped subcutaneous fat pads   (MGI Ref ID J:75192)
    • at 36 weeks of age on a high fat diet, subcutaneous fat is severely perturbed in females, with reduced numbers of adipoctyes that are heterogeneous in size and marked interstitial fibrosis and hypercellularity   (MGI Ref ID J:75192)
  • epidermal hyperplasia
    • mutants develop extensive epidermal hyperplasia in response to DMBA treatment before tumor formation   (MGI Ref ID J:83485)

Cav1tm1Mls/Cav1tm1Mls

        STOCK Cav1tm1Mls/J
  • endocrine/exocrine gland phenotype
  • abnormal thyroid follicular cell morphology
    • more than a 4-fold increase in thyrocyte proliferation, however mice do not develop a goiter because there is an increase in thyrocyte apoptosis   (MGI Ref ID J:119709)
  • cardiovascular system phenotype
  • decreased vasoconstriction
    • phenylephrine causes vascular contraction that is significantly reduced compared to wild-type on a high salt diet, however when the phenylephrine contraction is presented as a percentage of maximum and the ED50 is calculated, there is no significant difference   (MGI Ref ID J:132392)
    • vascular contraction in response to membrane depolarization by high KCl is reduced in mutants compared to wild-type mice on a high salt diet   (MGI Ref ID J:132392)
  • increased systemic arterial blood pressure
    • mice on a high salt diet treated with N-G-nitro-L-arginine methyl ester (L-NAME) exhibit a more elevated blood pressure than similarly treated wild-type mice, however no differences are seen on a low salt diet   (MGI Ref ID J:132392)
  • increased vasodilation
    • acetylcholine causes enhanced aortic relaxation compared to wild-type on a high salt and low salt diet   (MGI Ref ID J:132392)
  • growth/size/body phenotype
  • decreased body weight
    • total body weight is reduced in mutants compared to wild-type on both high salt and low salt diets   (MGI Ref ID J:132392)
  • muscle phenotype
  • decreased vasoconstriction
    • phenylephrine causes vascular contraction that is significantly reduced compared to wild-type on a high salt diet, however when the phenylephrine contraction is presented as a percentage of maximum and the ED50 is calculated, there is no significant difference   (MGI Ref ID J:132392)
    • vascular contraction in response to membrane depolarization by high KCl is reduced in mutants compared to wild-type mice on a high salt diet   (MGI Ref ID J:132392)
  • increased vasodilation
    • acetylcholine causes enhanced aortic relaxation compared to wild-type on a high salt and low salt diet   (MGI Ref ID J:132392)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Cav1tm1Mls/Cav1tm1Mls

        involves: 129/Sv * C57BL/6J * SJL
  • growth/size/body phenotype
  • decreased body weight
    • a defect in insulin-regulated lipogenesis contributes to the lean phenotype   (MGI Ref ID J:84260)
  • homeostasis/metabolism phenotype
  • abnormal cellular cholesterol metabolism
    • mouse embryonic fibroblasts (MEFs) and macrophages under normal conditions or loaded with cholesterol contain reduced free cholesterol but increased esterified-cholesterol content   (MGI Ref ID J:116292)
    • however, when cholesterol loaded, macrophages show an increase in total cellular cholesterol content   (MGI Ref ID J:116292)
    • cellular cholesterol efflux not affected although ABCA1-mediated cholesterol efflux is more sensitive to the inhibitory effects of glyburide in macrophages   (MGI Ref ID J:116292)
  • abnormal nitric oxide homeostasis
    • interstitial cells of Cajal and smooth muscles of the intestine (longitudinal muscles) show reduced responsiveness to endogenous and exogenous nitric oxide   (MGI Ref ID J:114334)
    • N-omega-nitro-L-arginine is ineffective to inhibit intestinal relaxation and exogenous nitric oxide donor sodium nitroprusside relaxes longitudinal muscle less than in controls   (MGI Ref ID J:114334)
    • apamin significantly reduces small intestinal tissue relaxation to electrical field stimulation in nonadrenergic noncholinergic conditions in mutants but not controls indicating that the normal spontaneous contraction of intestinal muscle is probably maintained by increased activity of apamin-sensitive mediators   (MGI Ref ID J:114334)
  • abnormal vascular wound healing
    • ligation of the common carotid artery causes a significant increase in neointimal lesion formation compared to wild-type mice   (MGI Ref ID J:115492)
  • impaired lipolysis
    • serum nonesterified fatty acid levels fail to rise in mutants in response to prolonged fasting   (MGI Ref ID J:89326)
    • mutants exhibit a 5-fold reduction in their lipolytic response to a beta3-specific adrenergic receptor agonist   (MGI Ref ID J:89326)
  • impaired wound healing
    • mutants show a slower wound healing rate when circular punch biopsies are done on the back skin compared to wild-type   (MGI Ref ID J:134719)
  • increased circulating insulin level
    • post-prandial serum levels of insulin were increased in mice that had been on a high fat diet for 9 months   (MGI Ref ID J:84260)
  • insulin resistance
    • mutants show a blunted decline in glucose levels upon insulin injection   (MGI Ref ID J:84260)
  • cardiovascular system phenotype
  • abnormal vascular endothelial cell morphology
    • lung capillaries exhibit smaller tight junctions and abnormalities in capillary endothelial cell adhesion to the basement membrane   (MGI Ref ID J:79595)
  • abnormal vascular wound healing
    • ligation of the common carotid artery causes a significant increase in neointimal lesion formation compared to wild-type mice   (MGI Ref ID J:115492)
  • decreased vasoconstriction
    • at pressures between 30 and 70 mmHg, cerebral arteries develop less myogenic tone than wild-type, indicating attenuated pressure-induced constriction   (MGI Ref ID J:120603)
    • pressure induces a smaller depolarization and smaller arterial wall intracellular calcium elevation in mutant cerebral arteries than in wild-type, resulting in reduced myogenic constriction   (MGI Ref ID J:120603)
    • membrane depolarization induced by 60 mM potassium results in attenuated arterial wall intracellular calcium elevation and constriction in cerebral arteries   (MGI Ref ID J:120603)
    • N-omega-nitro-L-arginine, a nitric oxide synthase inhibitor, does not restore myogenic tone in cerebral arteries, indicating that NOS activation and nitric oxide generation do not significantly contribute to the attenuated myogenic response   (MGI Ref ID J:120603)
  • increased vascular permeability
    • large increase in microvascular permeability as indicated by an increased rate of clearance for iodinated serum albumin from the circulatory system and lower levels of endogenous serum albumin   (MGI Ref ID J:79595)
    • paracellular movement of Ruthenium Red is increased in lung endothelial cells indicating hyperpermeable tight junctions/capillaries   (MGI Ref ID J:79595)
    • treatment with L-NAME, a nitric-oxide synthasae inhibitor, restores normal microvascular permeability   (MGI Ref ID J:79595)
  • adipose tissue phenotype
  • abnormal fat cell morphology
    • perigonadal adipocytes completely lack an electron-dense thick band of material that surrounds the normal lipid droplet   (MGI Ref ID J:89326)
  • cellular phenotype
  • abnormal cell chemotaxis
    • MEFs plated on fibronectin move faster and exhibit impaired directional migration compared to wild-type MEFs   (MGI Ref ID J:134719)
    • wound closure and chemotactic response of MEFs in a transwell assay are impaired   (MGI Ref ID J:134719)
  • abnormal cell morphology
    • mouse embryonic fibroblasts (MEFs) lose polarity when plated on fibronectin, exhibiting a round shape with aberrant actin cytoskeleton architecture   (MGI Ref ID J:134719)
    • microtubule organizing center reorientation toward the leading edge of a wound is reduced in MEFs   (MGI Ref ID J:134719)
    • protrusive and retractile activities at cell edges are higher in MEFs and protrusions and retractions occurs throughout the cell perimeter instead of protrusions in the direction of movement and retractions in the rear end as in wild-type MEFs   (MGI Ref ID J:134719)
    • absent caveolae
      • absence of caveolae in vascular smooth muscle cells   (MGI Ref ID J:115492)
      • chondrocytes lack caveolae   (MGI Ref ID J:128103)
      • caveolae are absent in the longitudinal muscles of the intestine   (MGI Ref ID J:114334)
  • abnormal cellular cholesterol metabolism
    • mouse embryonic fibroblasts (MEFs) and macrophages under normal conditions or loaded with cholesterol contain reduced free cholesterol but increased esterified-cholesterol content   (MGI Ref ID J:116292)
    • however, when cholesterol loaded, macrophages show an increase in total cellular cholesterol content   (MGI Ref ID J:116292)
    • cellular cholesterol efflux not affected although ABCA1-mediated cholesterol efflux is more sensitive to the inhibitory effects of glyburide in macrophages   (MGI Ref ID J:116292)
  • skeleton phenotype
  • abnormal cartilage morphology
    • cartilage of the costochondral junction is more cellular   (MGI Ref ID J:128103)
    • abnormal hyaline cartilage morphology
      • hyaline cartilage is more cellular, extending distally from the rib   (MGI Ref ID J:128103)
    • abnormal long bone epiphyseal plate morphology
      • at 8 weeks of age, cartilage extends into the epiphyseal bone and metaphyseal marrow   (MGI Ref ID J:128103)
      • abnormal long bone epiphyseal plate proliferative zone
        • increase in the number of columns of cells in the proliferating cell zone   (MGI Ref ID J:128103)
      • abnormal long bone hypertrophic chondrocyte zone
        • increase in the number of columns of cells in the hypertrophic cell zone of growth plates   (MGI Ref ID J:128103)
        • number of hypertrophic cells is increased for each column of cells   (MGI Ref ID J:128103)
      • increased long bone epiphyseal plate size
        • tibial growth plates are 12.3% longer than in wild-type   (MGI Ref ID J:128103)
        • costochondral growth plates are longer   (MGI Ref ID J:128103)
        • growth plates of femoral chondyles are extended, both vertically and in cross-section   (MGI Ref ID J:128103)
  • abnormal chondrocyte physiology
    • growth zone chondrocytes fail to exhibit a response to 1,25-dihydroxyvitaminD3   (MGI Ref ID J:128103)
  • abnormal long bone metaphysis morphology
    • metaphyseal bone volume is greater   (MGI Ref ID J:128103)
    • increase in number of trabeculae in metaphyseal bone   (MGI Ref ID J:128103)
    • at 8 weeks of age, in the metaphysis the trabeculae are coated with a thin layer of bone   (MGI Ref ID J:128103)
  • abnormal trabecular bone morphology
    • increase in number of trabeculae in metaphyseal bone   (MGI Ref ID J:128103)
    • at 8 weeks of age, in the metaphysis the trabeculae are coated with a thin layer of bone   (MGI Ref ID J:128103)
  • behavior/neurological phenotype
  • abnormal involuntary movement
    • mutants exhibit spinning upon tail suspension; frequency and intensity of spinning increases progressively with age such that by 50 weeks, it is seen in 50% of mutants and in all mutants by 80-90 weeks of age   (MGI Ref ID J:110712)
    • limb grasping
      • exhibit clasping as early as 20 weeks of age and the number of mutants that clasp increases with age   (MGI Ref ID J:110712)
  • abnormal locomotor behavior
    • mutants tend to stop and/or change direction of movement while traversing a tunnel more often than controls   (MGI Ref ID J:110712)
    • abnormal gait
      • wider overlap (distance between superimposed hindpaw and forepaw) that coincides with stride abnormalities   (MGI Ref ID J:110712)
      • short stride length
        • evident by 10 weeks of age   (MGI Ref ID J:110712)
    • hypoactivity
      • mutants are less active than their wild-type littermates   (MGI Ref ID J:110712)
  • decreased exploration in new environment
    • exploratory behavior in a new environment is reduced as early as 13 weeks of age   (MGI Ref ID J:110712)
  • decreased grip strength
    • mutants exhibit impaired ability to hold and maneuver on a bar   (MGI Ref ID J:110712)
  • nervous system phenotype
  • abnormal brain internal capsule morphology
    • the internal capsule fiber bundles are smaller in size in the striatum   (MGI Ref ID J:110712)
  • decreased brain size
    • brains are smaller at 60 weeks of age but not at 11 weeks of age   (MGI Ref ID J:110712)
    • decreased brain weight   (MGI Ref ID J:110712)
  • digestive/alimentary phenotype
  • abnormal digestive system physiology
    • mutants exhibit impaired small intestinal nitric oxide function   (MGI Ref ID J:114334)
  • muscle phenotype
  • decreased vasoconstriction
    • at pressures between 30 and 70 mmHg, cerebral arteries develop less myogenic tone than wild-type, indicating attenuated pressure-induced constriction   (MGI Ref ID J:120603)
    • pressure induces a smaller depolarization and smaller arterial wall intracellular calcium elevation in mutant cerebral arteries than in wild-type, resulting in reduced myogenic constriction   (MGI Ref ID J:120603)
    • membrane depolarization induced by 60 mM potassium results in attenuated arterial wall intracellular calcium elevation and constriction in cerebral arteries   (MGI Ref ID J:120603)
    • N-omega-nitro-L-arginine, a nitric oxide synthase inhibitor, does not restore myogenic tone in cerebral arteries, indicating that NOS activation and nitric oxide generation do not significantly contribute to the attenuated myogenic response   (MGI Ref ID J:120603)

Cav1tm1Mls/Cav1tm1Mls

        involves: 129/Sv * C57BL/6 * FVB/N * SJL
  • endocrine/exocrine gland phenotype
  • abnormal mammary gland morphology
    • ovariectomized female mice exposed to estrogen exhibit a 2-fold increase in ductal thickening and extensive side-branching compared to similarly treated wild-type mice   (MGI Ref ID J:147439)
    • estrogen-induced secondary branching is 3- to 4-fold greater and tertiary branching 5- to 7-fold greater than in similarly treated wild-type mice   (MGI Ref ID J:147439)
    • female mice exposed to high levels of estrogen develop abnormal mammary lesions or focal dysplasia unlike similarly treated wild-type mice with a 4-fold increase in lesion frequency and a 2.5-fold increase in lesion diameter   (MGI Ref ID J:147439)
  • tumorigenesis
  • increased mammary gland tumor incidence
    • estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice   (MGI Ref ID J:147439)
    • estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels   (MGI Ref ID J:147439)
    • ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells   (MGI Ref ID J:147439)
    • ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis   (MGI Ref ID J:147439)
  • integument phenotype
  • abnormal mammary gland morphology
    • ovariectomized female mice exposed to estrogen exhibit a 2-fold increase in ductal thickening and extensive side-branching compared to similarly treated wild-type mice   (MGI Ref ID J:147439)
    • estrogen-induced secondary branching is 3- to 4-fold greater and tertiary branching 5- to 7-fold greater than in similarly treated wild-type mice   (MGI Ref ID J:147439)
    • female mice exposed to high levels of estrogen develop abnormal mammary lesions or focal dysplasia unlike similarly treated wild-type mice with a 4-fold increase in lesion frequency and a 2.5-fold increase in lesion diameter   (MGI Ref ID J:147439)

Cav1tm1Mls/Cav1tm1Mls

        B6.Cg-Cav1tm1Mls
  • endocrine/exocrine gland phenotype
  • abnormal lactation
    • premature lactation; at day 18 of pregnancy, mammary glands of mutants are engorged with milk whereas wild-type glands are just beginning milk production and exhibit accelerated milk protein production   (MGI Ref ID J:120010)
  • abnormal mammary gland growth during pregnancy
    • premature development of the lobuloalveolar compartment of the mammary gland during pregnancy   (MGI Ref ID J:120010)
    • however, serum prolactin levels are normal   (MGI Ref ID J:120010)
  • reproductive system phenotype
  • abnormal mammary gland growth during pregnancy
    • premature development of the lobuloalveolar compartment of the mammary gland during pregnancy   (MGI Ref ID J:120010)
    • however, serum prolactin levels are normal   (MGI Ref ID J:120010)
  • adipose tissue phenotype
  • abnormal fat cell morphology
    • adipocytes lack caveolae   (MGI Ref ID J:205741)
    • abnormal brown fat cell morphology
      • mitochodria of brown adipocytes are larger and dilated and much less electron dense than mitochondria of wild-type mice   (MGI Ref ID J:105133)
      • increased brown fat cell lipid droplet size
        • adipocytes of brown adipose tissue contain larger lipid droplets than in wild-type mice   (MGI Ref ID J:105133)
  • homeostasis/metabolism phenotype
  • abnormal triglyceride level
    • the reduction of triglyceride content of brown adipose tissue (BAT) induced after fasting/cold treatment is much lower than in controls (3-fold reduction in mutants vs. 10-fold reduction in controls), indicating defective release of stored triglycerides in BAT   (MGI Ref ID J:105133)
  • decreased core body temperature
    • mild, but significant, decrease in resting core body temperature   (MGI Ref ID J:105133)
  • decreased fatty acid level
    • mutants fail to exhibit the normal increase in serum nonesterifited fatty acids induced by fasting or fasting/cold treatment   (MGI Ref ID J:105133)
  • impaired adaptive thermogenesis
    • mutants show a decrease in body temperature in response to fasting or fasting/cold treatment, however cold treatment alone has no further effect on temperature   (MGI Ref ID J:105133)
  • impaired lipolysis
    • lipolysis fails to occur when mice are fasted or fasted/cold treated   (MGI Ref ID J:105133)
    • after fasting/cold treatments, BAT adipocytes of wild-type mice are devoid of lipid droplets while those of mutants still contain lipid droplets, indicating decreased lipid utilization after fasting/cold treatment   (MGI Ref ID J:105133)
  • integument phenotype
  • abnormal lactation
    • premature lactation; at day 18 of pregnancy, mammary glands of mutants are engorged with milk whereas wild-type glands are just beginning milk production and exhibit accelerated milk protein production   (MGI Ref ID J:120010)
  • abnormal mammary gland growth during pregnancy
    • premature development of the lobuloalveolar compartment of the mammary gland during pregnancy   (MGI Ref ID J:120010)
    • however, serum prolactin levels are normal   (MGI Ref ID J:120010)
  • cardiovascular system phenotype
  • abnormal lung vasculature morphology
    • gaps in the lung capillary   (MGI Ref ID J:205741)
  • abnormal vascular endothelial cell morphology
    • absence of caveolae in microvascular endothelia (lung, heart and fat)   (MGI Ref ID J:205741)
  • cellular phenotype
  • absent caveolae
    • absence of caveolae in microvascular endothelia (lung, heart and fat) and fat adipocyte   (MGI Ref ID J:205741)
  • respiratory system phenotype
  • abnormal lung vasculature morphology
    • gaps in the lung capillary   (MGI Ref ID J:205741)

Cav1tm1Mls/Cav1tm1Mls

        B6.Cg-Cav1tm1Mls/J
  • cellular phenotype
  • absent caveolae   (MGI Ref ID J:143600)
  • reproductive system phenotype
  • reduced fertility
    • decrease in fertility on a C57BL/6J background   (MGI Ref ID J:143600)
  • respiratory system phenotype
  • abnormal lung morphology
    • increase in collagen deposition in the lung parenchyma and the periphery of airways   (MGI Ref ID J:143600)
    • 60% increase in elastic fiber deposits in the lungs, with thicker layers of elastic fibers primarily around airways and arteries   (MGI Ref ID J:143600)
    • however, mutants do not exhibit emphysema   (MGI Ref ID J:143600)
    • abnormal pulmonary elastic fiber morphology
      • 60% increase in elastic fiber deposits in the lungs, with thicker layers of elastic fibers primarily around airways and arteries   (MGI Ref ID J:143600)
  • abnormal respiratory mechanics
    • from 3 months on, mutants exhibit altered respiratory mechanics, suggesting stiffening of the lung tissue   (MGI Ref ID J:143600)
    • decreased lung compliance
      • from 3 months on, mutants exhibit a decrease in lung compliance   (MGI Ref ID J:143600)
    • increased airway resistance
      • from 3 months on, mutants exhibit an increase in airway resistance   (MGI Ref ID J:143600)
  • increased lung elastance
    • from 3 months on, mutants exhibit a a sustained increase in lung elastance   (MGI Ref ID J:143600)
  • pulmonary edema
    • presence of vascular-derived fluid in pulmonary tissues   (MGI Ref ID J:143600)
  • homeostasis/metabolism phenotype
  • pulmonary edema
    • presence of vascular-derived fluid in pulmonary tissues   (MGI Ref ID J:143600)
  • cardiovascular system phenotype
  • increased vascular permeability
    • increase in permeability of the pulmonary endothelial barrier to plasma proteins as indicated by an accumulation of proteins, especially albumin, in bronchoalveolar lavage from 1-9 months of age and leakage of Evans blue in pulmonary tissues   (MGI Ref ID J:143600)

Cav1tm1Mls/Cav1tm1Mls

        Background Not Specified
  • nervous system phenotype
  • CNS ischemia
    • young mice subjected to ischemic preconditioning prior to lethal ischemia lack the ability to protect CA1 neurons, a phenomenon observed in aged wild-type mice   (MGI Ref ID J:168335)
  • abnormal CNS glial cell morphology
    • increase in glia and glial scar formation within the dentate gyrus   (MGI Ref ID J:168335)
    • abnormal astrocyte morphology
      • astrocytes in young mice are disorganized as compared to young wild-type mice   (MGI Ref ID J:168335)
  • abnormal brain vasculature morphology
    • 20-25% reduction in cerebrovascular volume is observed in the hippocampi from young mice   (MGI Ref ID J:168335)
  • abnormal dendrite morphology
    • cytoskeletal architecture within dendrites is unorganized   (MGI Ref ID J:168335)
  • abnormal dentate gyrus morphology
    • young (3-6 months) mice exhibit a reduction in the number of neurons within the dentate gyrus   (MGI Ref ID J:168335)
    • increase in glia and glial scar formation within the dentate gyrus   (MGI Ref ID J:168335)
  • abnormal hippocampus CA1 region morphology
    • young (3-6 months) mice exhibit a reduction in the number of neurons in the CA1 region   (MGI Ref ID J:168335)
    • young mice exhibit areas of potential plaque development and disorganized astrocytes   (MGI Ref ID J:168335)
    • Fluoro-Jade B and Nissl staining of the CA1 region from 12 month old mice indicates increased neuronal degeneration as compared to age-matched controls   (MGI Ref ID J:168335)
  • amyloid beta deposits
    • amyloid beta production is increased in the hippocampus of young mice   (MGI Ref ID J:168335)
  • decreased CNS synapse formation
    • young mice exhibit a significant reduction in hippocampal synapses in comparison to age-matched wild-type mice, but similar to aged wild-type mice   (MGI Ref ID J:168335)
  • hippocampal neuron degeneration
    • Fluoro-Jade B and Nissl staining of the CA1 region from 12 month old mice indicates increased neuronal degeneration as compared to age-matched controls   (MGI Ref ID J:168335)
  • tau protein deposits
    • tau deposits are elevated in hippocampal homogenates from young mice   (MGI Ref ID J:168335)
  • cardiovascular system phenotype
  • abnormal brain vasculature morphology
    • 20-25% reduction in cerebrovascular volume is observed in the hippocampi from young mice   (MGI Ref ID J:168335)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • amyloid beta production is increased in the hippocampus of young mice   (MGI Ref ID J:168335)

Cav1tm1Mls/Cav1tm1Mls

        FVB.Cg-Cav1tm1Mls
  • homeostasis/metabolism phenotype
  • abnormal homeostasis
    • increase in lactate levels following 3-mercaptopicolinic acid treatment   (MGI Ref ID J:182288)
    • elevated circulating peroxide levels and a small decrease in circulating pyruvate levels   (MGI Ref ID J:182288)
    • abnormal circulating amino acid level
      • elevated circulating branched-chain amino acid levels   (MGI Ref ID J:182288)
    • abnormal free fatty acids level
      • delay in suppression of free fatty acid levels following refeeding   (MGI Ref ID J:182288)
      • impaired beta3-AR agonist induced release of free fatty acids   (MGI Ref ID J:182288)
    • abnormal glucose homeostasis
      • maintain glucose levels better in the fasted state better than wild-type controls   (MGI Ref ID J:182288)
      • exposure to 3-mercaptopicolinic acid causes a larger drop in glucose levels compared to wild-type mice   (MGI Ref ID J:182288)
      • abnormal gluconeogenesis
        • enhanced hepatic gluconeogenesis   (MGI Ref ID J:182288)
        • treatment with enoximone, a phospodiesterase inhibitor, potently increases glucose levels   (MGI Ref ID J:182288)
        • following a glycerol bolus, glycerol induced glucose production is enhanced but glycerol clearance is delayed   (MGI Ref ID J:182288)
      • decreased liver glycogen level
        • in the fed state   (MGI Ref ID J:182288)
      • hyperglycemia
        • upon refeeding display fairly severe hyperglycemia   (MGI Ref ID J:182288)
      • increased circulating insulin level   (MGI Ref ID J:182288)
      • increased liver glycogen level
        • in moderately fasted mice   (MGI Ref ID J:182288)
      • insulin resistance   (MGI Ref ID J:182288)
    • abnormal respiratory quotient
      • variability in the respiratory exchange ratio over a 24 hour period is reduced   (MGI Ref ID J:182288)
      • increased respiratory quotient   (MGI Ref ID J:182288)
    • decreased adiponectin level
      • reduced total circulating levels and a decrease in the proportion of the HMW form   (MGI Ref ID J:182288)
    • decreased susceptibility to diet-induced obesity
      • when placed on a high fat diet   (MGI Ref ID J:182288)
    • enhanced lipolysis   (MGI Ref ID J:182288)
    • increased blood urea nitrogen level   (MGI Ref ID J:182288)
    • increased circulating glycerol level
      • following 3-mercaptopicolinic acid treatment   (MGI Ref ID J:182288)
    • increased oxygen consumption   (MGI Ref ID J:182288)
    • increased triglyceride level
      • in fed and fasted mice   (MGI Ref ID J:182288)
  • cellular phenotype
  • abnormal cellular respiration
    • MEFs display a preference for glycolysis in glucose-deprived media   (MGI Ref ID J:182288)
    • abnormal respiratory electron transport chain
      • expression analysis indicates altered mitochondrial function   (MGI Ref ID J:182288)
      • mitochondria in MEFs display dramatically increased membrane potential   (MGI Ref ID J:182288)
      • however, mitochondria isolated from liver and lung tissue display similar function compared to wild-type controls   (MGI Ref ID J:182288)
  • adipose tissue phenotype
  • abnormal adipose tissue physiology
    • enhanced uptake of leucine in mildly fasted mice   (MGI Ref ID J:182288)
  • decreased total body fat amount
    • reduced fat mass   (MGI Ref ID J:182288)
  • growth/size/body phenotype
  • decreased susceptibility to diet-induced obesity
    • when placed on a high fat diet   (MGI Ref ID J:182288)
  • decreased total body fat amount
    • reduced fat mass   (MGI Ref ID J:182288)
  • weight loss
    • lose more weight when fasted   (MGI Ref ID J:182288)
  • behavior/neurological phenotype
  • increased food intake   (MGI Ref ID J:182288)
  • muscle phenotype
  • abnormal skeletal muscle morphology
    • skeletal muscle tissue has a darker appearance indicating an increased mitochondrial content   (MGI Ref ID J:182288)
  • liver/biliary system phenotype
  • abnormal liver physiology
    • alternate day fasting has no effect of hepatic lipid content unlike in wild-type mice   (MGI Ref ID J:182288)
    • hepatic triglyceride synthesis appears to be reduced   (MGI Ref ID J:182288)
  • decreased liver glycogen level
    • in the fed state   (MGI Ref ID J:182288)
  • decreased susceptibility to hepatic steatosis
    • fasting induced and high fat diet induced hepatic steatosis are reduced   (MGI Ref ID J:182288)
  • increased liver glycogen level
    • in moderately fasted mice   (MGI Ref ID J:182288)
  • increased liver weight
    • under all conditions tested   (MGI Ref ID J:182288)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Neurobiology Research
Alzheimer's Disease

Cav1tm1Mls related

Cardiovascular Research
Hypertriglyceridemia
Vascular Defects

Developmental Biology Research
Growth Defects

Diabetes and Obesity Research
Obesity Without Diabetes
      diet-induced, resistant

Internal/Organ Research
Adipose Defects

Metabolism Research
Lipid Metabolism

Neurobiology Research
Alzheimer's Disease

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Cav1tm1Mls
Allele Name targeted mutation 1, Michael P Lisanti
Allele Type Targeted (Null/Knockout)
Common Name(s) Cav-1 KO; Cav-1-; Cavtm1Mls; Caveolin-1 KO; cav-;
Mutation Made By Michael Lisanti,   The Albert Einstein College of Medicine
Strain of OriginSTOCK 129/Sv and C57BL/6J and SJL
ES Cell Line NameWW6
ES Cell Line StrainSTOCK 129/Sv and C57BL/6J and SJL
Gene Symbol and Name Cav1, caveolin 1, caveolae protein
Chromosome 6
Gene Common Name(s) BSCL3; CGL3; Cav; Cav-1; LCCNS; MSTP085; PPH3; VIP21; caveolin-1;
Molecular Note A 2.2 kb region of the gene including exons 1 and 2 and part of the promoter region was replaced with a neo resistance cassette via homologous recombination. Absence of gene expression in homozygous mutant animals was verified by Western blot analysis ofheart, adipose, and lung tissue, and also of mouse embryonic fibroblasts cultured from E13.5 homozygous mutant embryos. [MGI Ref ID J:75193]

Genotyping

Genotyping Information

Genotyping Protocols

NntC57BL/6J,

Separated MCA


Cav1tm1Mls, Melt Curve Analysis
Cav1tm1Mls, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Razani B; Engelman JA; Wang XB; Schubert W; Zhang XL; Marks CB; Macaluso F; Russell RG; Li M; Pestell RG; Di Vizio D; Hou H Jr; Kneitz B; Lagaud G; Christ GJ; Edelmann W; Lisanti MP. 2001. Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities. J Biol Chem 276(41):38121-38. [PubMed: 11457855]  [MGI Ref ID J:75193]

Additional References

Capozza F; Williams TM; Schubert W; McClain S; Bouzahzah B; Sotgia F; Lisanti MP. 2003. Absence of caveolin-1 sensitizes mouse skin to carcinogen-induced epidermal hyperplasia and tumor formation. Am J Pathol 162(6):2029-39. [PubMed: 12759258]  [MGI Ref ID J:83485]

Cohen AW; Razani B; Schubert W; Williams TM; Wang XB; Iyengar P; Brasaemle DL; Scherer PE; Lisanti MP. 2004. Role of caveolin-1 in the modulation of lipolysis and lipid droplet formation. Diabetes 53(5):1261-70. [PubMed: 15111495]  [MGI Ref ID J:89326]

Cohen AW; Razani B; Wang XB; Combs TP; Williams TM; Scherer PE; Lisanti MP. 2003. Caveolin-1-deficient mice show insulin resistance and defective insulin receptor protein expression in adipose tissue. Am J Physiol Cell Physiol 285(1):C222-35. [PubMed: 12660144]  [MGI Ref ID J:84260]

Park DS; Woodman SE; Schubert W; Cohen AW; Frank PG; Chandra M; Shirani J; Razani B; Tang B; Jelicks LA; Factor SM; Weiss LM; Tanowitz HB; Lisanti MP. 2002. Caveolin-1/3 double-knockout mice are viable, but lack both muscle and non-muscle caveolae, and develop a severe cardiomyopathic phenotype. Am J Pathol 160(6):2207-17. [PubMed: 12057923]  [MGI Ref ID J:77372]

Razani B; Combs TP; Wang XB; Frank PG; Park DS; Russell RG; Li M; Tang B; Jelicks LA; Scherer PE; Lisanti MP. 2002. Caveolin-1-deficient Mice Are Lean, Resistant to Diet-induced Obesity, and Show Hypertriglyceridemia with Adipocyte Abnormalities. J Biol Chem 277(10):8635-47. [PubMed: 11739396]  [MGI Ref ID J:75192]

Schubert W; Frank PG; Woodman SE; Hyogo H; Cohen DE; Chow CW; Lisanti MP. 2002. Microvascular hyperpermeability in caveolin-1 (-/-) knock-out mice. Treatment with a specific nitric-oxide synthase inhibitor, L-name, restores normal microvascular permeability in Cav-1 null mice. J Biol Chem 277(42):40091-8. [PubMed: 12167625]  [MGI Ref ID J:79595]

Cav1tm1Mls related

Adebiyi A; Zhao G; Cheranov SY; Ahmed A; Jaggar JH. 2007. Caveolin-1 abolishment attenuates the myogenic response in murine cerebral arteries. Am J Physiol Heart Circ Physiol 292(3):H1584-92. [PubMed: 17098833]  [MGI Ref ID J:120603]

Ahmad F; Lindh R; Tang Y; Ruishalme I; Ost A; Sahachartsiri B; Stralfors P; Degerman E; Manganiello VC. 2009. Differential regulation of adipocyte PDE3B in distinct membrane compartments by insulin and the beta3-adrenergic receptor agonist CL316243: effects of caveolin-1 knockdown on formation/maintenance of macromolecular signalling complexes. Biochem J 424(3):399-410. [PubMed: 19747167]  [MGI Ref ID J:159971]

Albinsson S; Nordstrom I; Sward K; Hellstrand P. 2008. Differential dependence of stretch and shear stress signaling on caveolin-1 in the vascular wall. Am J Physiol Cell Physiol 294(1):C271-9. [PubMed: 17989209]  [MGI Ref ID J:130507]

Albinsson S; Shakirova Y; Rippe A; Baumgarten M; Rosengren BI; Rippe C; Hallmann R; Hellstrand P; Rippe B; Sward K. 2007. Arterial remodeling and plasma volume expansion in caveolin-1-deficient mice. Am J Physiol Regul Integr Comp Physiol 293(3):R1222-31. [PubMed: 17626133]  [MGI Ref ID J:143002]

Alves-Filho JC; Freitas A; Souto FO; Spiller F; Paula-Neto H; Silva JS; Gazzinelli RT; Teixeira MM; Ferreira SH; Cunha FQ. 2009. Regulation of chemokine receptor by Toll-like receptor 2 is critical to neutrophil migration and resistance to polymicrobial sepsis. Proc Natl Acad Sci U S A 106(10):4018-23. [PubMed: 19234125]  [MGI Ref ID J:146272]

Aravamudan B; VanOosten SK; Meuchel LW; Vohra P; Thompson M; Sieck GC; Prakash YS; Pabelick CM. 2012. Caveolin-1 knockout mice exhibit airway hyperreactivity. Am J Physiol Lung Cell Mol Physiol 303(8):L669-81. [PubMed: 22923642]  [MGI Ref ID J:193436]

Asterholm IW; Mundy DI; Weng J; Anderson RG; Scherer PE. 2012. Altered mitochondrial function and metabolic inflexibility associated with loss of caveolin-1. Cell Metab 15(2):171-85. [PubMed: 22326219]  [MGI Ref ID J:182288]

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Berger K; Lindh R; Wierup N; Zmuda-Trzebiatowska E; Lindqvist A; Manganiello VC; Degerman E. 2009. Phosphodiesterase 3B is localized in caveolae and smooth ER in mouse hepatocytes and is important in the regulation of glucose and lipid metabolism. PLoS ONE 4(3):e4671. [PubMed: 19262749]  [MGI Ref ID J:147378]

Bhattacharya S; Mahavadi S; Al-Shboul O; Rajagopal S; Grider JR; Murthy KS. 2013. Differential regulation of muscarinic M2 and M3 receptor signaling in gastrointestinal smooth muscle by caveolin-1. Am J Physiol Cell Physiol 305(3):C334-47. [PubMed: 23784544]  [MGI Ref ID J:205074]

Bianco C; Strizzi L; Mancino M; Watanabe K; Gonzales M; Hamada S; Raafat A; Sahlah L; Chang C; Sotgia F; Normanno N; Lisanti M; Salomon DS. 2008. Regulation of Cripto-1 signaling and biological activity by caveolin-1 in mammary epithelial cells. Am J Pathol 172(2):345-57. [PubMed: 18202186]  [MGI Ref ID J:131372]

Boyan BD; Wong KL; Wang L; Yao H; Guldberg RE; Drab M; Jo H; Schwartz Z. 2006. Regulation of growth plate chondrocytes by 1,25-dihydroxyvitamin D3 requires caveolae and caveolin-1. J Bone Miner Res 21(10):1637-47. [PubMed: 16995819]  [MGI Ref ID J:128103]

Cai L; Yi F; Dai Z; Huang X; Zhao YD; Mirza MK; Xu J; Vogel SM; Zhao YY. 2014. Loss of caveolin-1 and adiponectin induces severe inflammatory lung injury following LPS challenge through excessive oxidative/nitrative stress. Am J Physiol Lung Cell Mol Physiol 306(6):L566-73. [PubMed: 24441873]  [MGI Ref ID J:210894]

Capozza F; Trimmer C; Castello-Cros R; Katiyar S; Whitaker-Menezes D; Follenzi A; Crosariol M; Llaverias G; Sotgia F; Pestell RG; Lisanti MP. 2012. Genetic ablation of Cav1 differentially affects melanoma tumor growth and metastasis in mice: role of Cav1 in Shh heterotypic signaling and transendothelial migration. Cancer Res 72(9):2262-74. [PubMed: 22396494]  [MGI Ref ID J:185751]

Capozza F; Williams TM; Schubert W; McClain S; Bouzahzah B; Sotgia F; Lisanti MP. 2003. Absence of caveolin-1 sensitizes mouse skin to carcinogen-induced epidermal hyperplasia and tumor formation. Am J Pathol 162(6):2029-39. [PubMed: 12759258]  [MGI Ref ID J:83485]

Cerezo A; Guadamillas MC; Goetz JG; Sanchez-Perales S; Klein E; Assoian RK; del Pozo MA. 2009. The absence of caveolin-1 increases proliferation and anchorage- independent growth by a Rac-dependent, Erk-independent mechanism. Mol Cell Biol 29(18):5046-59. [PubMed: 19620284]  [MGI Ref ID J:152600]

Chang CF; Chen SF; Lee TS; Lee HF; Chen SF; Shyue SK. 2011. Caveolin-1 deletion reduces early brain injury after experimental intracerebral hemorrhage. Am J Pathol 178(4):1749-61. [PubMed: 21435456]  [MGI Ref ID J:169846]

Chang SH; Feng D; Nagy JA; Sciuto TE; Dvorak AM; Dvorak HF. 2009. Vascular permeability and pathological angiogenesis in caveolin-1-null mice. Am J Pathol 175(4):1768-76. [PubMed: 19729487]  [MGI Ref ID J:153053]

Chen W; Gassner B; Borner S; Nikolaev VO; Schlegel N; Waschke J; Steinbronn N; Strasser R; Kuhn M. 2012. Atrial natriuretic peptide enhances microvascular albumin permeability by the caveolae-mediated transcellular pathway. Cardiovasc Res 93(1):141-51. [PubMed: 22025581]  [MGI Ref ID J:194877]

Chen ZH; Lam HC; Jin Y; Kim HP; Cao J; Lee SJ; Ifedigbo E; Parameswaran H; Ryter SW; Choi AM. 2010. Autophagy protein microtubule-associated protein 1 light chain-3B (LC3B) activates extrinsic apoptosis during cigarette smoke-induced emphysema. Proc Natl Acad Sci U S A 107(44):18880-5. [PubMed: 20956295]  [MGI Ref ID J:166237]

Chow AK; Cena J; El-Yazbi AF; Crawford BD; Holt A; Cho WJ; Daniel EE; Schulz R. 2007. Caveolin-1 inhibits matrix metalloproteinase-2 activity in the heart. J Mol Cell Cardiol 42(4):896-901. [PubMed: 17349656]  [MGI Ref ID J:120811]

Chow AK; Daniel EE; Schulz R. 2010. Cardiac function is not significantly diminished in hearts isolated from young caveolin-1 knockout mice. Am J Physiol Heart Circ Physiol :. [PubMed: 20693397]  [MGI Ref ID J:163844]

Chung JJ; Shim SH; Everley RA; Gygi SP; Zhuang X; Clapham DE. 2014. Structurally distinct Ca(2+) signaling domains of sperm flagella orchestrate tyrosine phosphorylation and motility. Cell 157(4):808-22. [PubMed: 24813608]  [MGI Ref ID J:214399]

Cohen AW; Park DS; Woodman SE; Williams TM; Chandra M; Shirani J; Pereira de Souza A; Kitsis RN; Russell RG; Weiss LM; Tang B; Jelicks LA; Factor SM; Shtutin V; Tanowitz HB; Lisanti MP. 2003. Caveolin-1 null mice develop cardiac hypertrophy with hyperactivation of p42/44 MAP kinase in cardiac fibroblasts. Am J Physiol Cell Physiol 284(2):C457-74. [PubMed: 12388077]  [MGI Ref ID J:82042]

Cohen AW; Razani B; Schubert W; Williams TM; Wang XB; Iyengar P; Brasaemle DL; Scherer PE; Lisanti MP. 2004. Role of caveolin-1 in the modulation of lipolysis and lipid droplet formation. Diabetes 53(5):1261-70. [PubMed: 15111495]  [MGI Ref ID J:89326]

Cohen AW; Razani B; Wang XB; Combs TP; Williams TM; Scherer PE; Lisanti MP. 2003. Caveolin-1-deficient mice show insulin resistance and defective insulin receptor protein expression in adipose tissue. Am J Physiol Cell Physiol 285(1):C222-35. [PubMed: 12660144]  [MGI Ref ID J:84260]

Cohen AW; Schubert W; Brasaemle DL; Scherer PE; Lisanti MP. 2005. Caveolin-1 expression is essential for proper nonshivering thermogenesis in brown adipose tissue. Diabetes 54(3):679-86. [PubMed: 15734843]  [MGI Ref ID J:105133]

Costa MJ; Senou M; Van Rode F; Ruf J; Capello M; Dequanter D; Lothaire P; Dessy C; Dumont JE; Many MC; Van Sande J. 2007. Reciprocal negative regulation between thyrotropin/3',5'-cyclic adenosine monophosphate-mediated proliferation and caveolin-1 expression in human and murine thyrocytes. Mol Endocrinol 21(4):921-32. [PubMed: 17202321]  [MGI Ref ID J:119709]

Crist RC; Roth JJ; Lisanti MP; Siracusa LD; Buchberg AM. 2011. Identification of Mom12 and Mom13, two novel modifier loci of Apc (Min) -mediated intestinal tumorigenesis. Cell Cycle 10(7):1092-9. [PubMed: 21386660]  [MGI Ref ID J:201191]

Davies BS; Goulbourne CN; Barnes RH 2nd; Turlo KA; Gin P; Vaughan S; Vaux DJ; Bensadoun A; Beigneux AP; Fong LG; Young SG. 2012. Assessing mechanisms of GPIHBP1 and lipoprotein lipase movement across endothelial cells. J Lipid Res 53(12):2690-7. [PubMed: 23008484]  [MGI Ref ID J:190731]

Diehl SA; McElvany B; Noubade R; Seeberger N; Harding B; Spach K; Teuscher C. 2014. G proteins Galphai1/3 are critical targets for Bordetella pertussis toxin-induced vasoactive amine sensitization. Infect Immun 82(2):773-82. [PubMed: 24478091]  [MGI Ref ID J:209809]

El-Yazbi AF; Cho WJ; Boddy G; Daniel EE. 2005. Caveolin-1 gene knockout impairs nitrergic function in mouse small intestine. Br J Pharmacol 145(8):1017-26. [PubMed: 15937515]  [MGI Ref ID J:114334]

El-Yazbi AF; Cho WJ; Boddy G; Schulz R; Daniel EE. 2006. Impact of caveolin-1 knockout on NANC relaxation in circular muscles of the mouse small intestine compared with longitudinal muscles. Am J Physiol Gastrointest Liver Physiol 290(2):G394-403. [PubMed: 16166342]  [MGI Ref ID J:106049]

El-Yazbi AF; Cho WJ; Schulz R; Daniel EE. 2006. Caveolin-1 knockout alters beta-adrenoceptors function in mouse small intestine. Am J Physiol Gastrointest Liver Physiol 291(6):G1020-30. [PubMed: 16782699]  [MGI Ref ID J:116899]

Feher A; Rutkai I; Beleznai T; Ungvari Z; Csiszar A; Edes I; Bagi Z. 2010. Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity. Cardiovasc Res 87(4):732-9. [PubMed: 20299334]  [MGI Ref ID J:176099]

Feng H; Guo L; Song Z; Gao H; Wang D; Fu W; Han J; Li Z; Huang B; Li XA. 2010. Caveolin-1 protects against sepsis by modulating inflammatory response, alleviating bacterial burden, and suppressing thymocyte apoptosis. J Biol Chem 285(33):25154-60. [PubMed: 20534584]  [MGI Ref ID J:165996]

Fernandez-Rojo MA; Gongora M; Fitzsimmons RL; Martel N; Martin SD; Nixon SJ; Brooks AJ; Ikonomopoulou MP; Martin S; Lo HP; Myers SA; Restall C; Ferguson C; Pilch PF; McGee SL; Anderson RL; Waters MJ; Hancock JF; Grimmond SM; Muscat GE; Parton RG. 2013. Caveolin-1 is necessary for hepatic oxidative lipid metabolism: evidence for crosstalk between caveolin-1 and bile acid signaling. Cell Rep 4(2):238-47. [PubMed: 23850288]  [MGI Ref ID J:202109]

Fernandez-Rojo MA; Restall C; Ferguson C; Martel N; Martin S; Bosch M; Kassan A; Leong GM; Martin SD; McGee SL; Muscat GE; Anderson RL; Enrich C; Pol A; Parton RG. 2012. Caveolin-1 orchestrates the balance between glucose and lipid-dependent energy metabolism: implications for liver regeneration. Hepatology 55(5):1574-84. [PubMed: 22105343]  [MGI Ref ID J:202449]

Frank PG; Cheung MW; Pavlides S; Llaverias G; Park DS; Lisanti MP. 2006. Caveolin-1 and regulation of cellular cholesterol homeostasis. Am J Physiol Heart Circ Physiol 291(2):H677-86. [PubMed: 16603689]  [MGI Ref ID J:116292]

Frank PG; Lee H; Park DS; Tandon NN; Scherer PE; Lisanti MP. 2004. Genetic ablation of caveolin-1 confers protection against atherosclerosis. Arterioscler Thromb Vasc Biol 24(1):98-105. [PubMed: 14563650]  [MGI Ref ID J:101788]

Frank PG; Pavlides S; Cheung MW; Daumer K; Lisanti MP. 2008. Role of caveolin-1 in the regulation of lipoprotein metabolism. Am J Physiol Cell Physiol 295(1):C242-8. [PubMed: 18508910]  [MGI Ref ID J:138644]

Friedrich T; Richter B; Gaiser T; Weiss C; Janssen KP; Einwachter H; Schmid RM; Ebert MP; Burgermeister E. 2013. Deficiency of caveolin-1 in Apcmin/+ mice promotes colorectal tumorigenesis. Carcinogenesis 34(9):2109-18. [PubMed: 23640045]  [MGI Ref ID J:200094]

Gadjeva M; Paradis-Bleau C; Priebe GP; Fichorova R; Pier GB. 2010. Caveolin-1 modifies the immunity to Pseudomonas aeruginosa. J Immunol 184(1):296-302. [PubMed: 19949109]  [MGI Ref ID J:159000]

Garrean S; Gao XP; Brovkovych V; Shimizu J; Zhao YY; Vogel SM; Malik AB. 2006. Caveolin-1 regulates NF-kappaB activation and lung inflammatory response to sepsis induced by lipopolysaccharide. J Immunol 177(7):4853-60. [PubMed: 16982927]  [MGI Ref ID J:139304]

Gioiosa L; Raggi C; Ricceri L; Jasmin JF; Frank PG; Capozza F; Lisanti MP; Alleva E; Sargiacomo M; Laviola G. 2008. Altered emotionality, spatial memory and cholinergic function in caveolin-1 knock-out mice. Behav Brain Res 188(2):255-262. [PubMed: 18083242]  [MGI Ref ID J:131303]

Goetz JG; Minguet S; Navarro-Lerida I; Lazcano JJ; Samaniego R; Calvo E; Tello M; Osteso-Ibanez T; Pellinen T; Echarri A; Cerezo A; Klein-Szanto AJ; Garcia R; Keely PJ; Sanchez-Mateos P; Cukierman E; Del Pozo MA. 2011. Biomechanical remodeling of the microenvironment by stromal caveolin-1 favors tumor invasion and metastasis. Cell 146(1):148-63. [PubMed: 21729786]  [MGI Ref ID J:174768]

Gonzalez MI; Krizman-Genda E; Robinson MB. 2007. Caveolin-1 regulates the delivery and endocytosis of the glutamate transporter, excitatory amino acid carrier 1. J Biol Chem 282(41):29855-65. [PubMed: 17715130]  [MGI Ref ID J:126756]

Grande G; Rippe C; Rippe A; Rahman A; Sward K; Rippe B. 2009. Unaltered size selectivity of the glomerular filtration barrier in caveolin-1 knockout mice. Am J Physiol Renal Physiol 297(2):F257-62. [PubMed: 19474194]  [MGI Ref ID J:150730]

Grande-Garcia A; Echarri A; de Rooij J; Alderson NB; Waterman-Storer CM; Valdivielso JM; del Pozo MA. 2007. Caveolin-1 regulates cell polarization and directional migration through Src kinase and Rho GTPases. J Cell Biol 177(4):683-94. [PubMed: 17517963]  [MGI Ref ID J:134719]

Gu X; Fliesler SJ; Zhao YY; Stallcup WB; Cohen AW; Elliott MH. 2014. Loss of caveolin-1 causes blood-retinal barrier breakdown, venous enlargement, and mural cell alteration. Am J Pathol 184(2):541-55. [PubMed: 24326256]  [MGI Ref ID J:206305]

Guo Q; Shen N; Yuan K; Li J; Wu H; Zeng Y; Fox J 3rd; Bansal AK; Singh BB; Gao H; Wu M. 2012. Caveolin-1 plays a critical role in host immunity against Klebsiella pneumoniae by regulating STAT5 and Akt activity. Eur J Immunol 42(6):1500-11. [PubMed: 22678904]  [MGI Ref ID J:187758]

Guo YH; Hernandez I; Isermann B; Kang TB; Medved L; Sood R; Kerschen EJ; Holyst T; Mosesson MW; Weiler H. 2009. Caveolin-1-dependent apoptosis induced by fibrin degradation products. Blood 113(18):4431-9. [PubMed: 19074731]  [MGI Ref ID J:148438]

Hada N; Okayasu M; Ito J; Nakayachi M; Hayashida C; Kaneda T; Uchida N; Muramatsu T; Koike C; Masuhara M; Sato T; Hakeda Y. 2012. Receptor activator of NF-kappaB ligand-dependent expression of caveolin-1 in osteoclast precursors, and high dependency of osteoclastogenesis on exogenous lipoprotein. Bone 50(1):226-36. [PubMed: 22075210]  [MGI Ref ID J:180216]

Hansen CG; Shvets E; Howard G; Riento K; Nichols BJ. 2013. Deletion of cavin genes reveals tissue-specific mechanisms for morphogenesis of endothelial caveolae. Nat Commun 4:1831. [PubMed: 23652019]  [MGI Ref ID J:205741]

Hassan GS; Jasmin JF; Schubert W; Frank PG; Lisanti MP. 2004. Caveolin-1 deficiency stimulates neointima formation during vascular injury. Biochemistry 43(26):8312-21. [PubMed: 15222744]  [MGI Ref ID J:115492]

Hassan GS; Williams TM; Frank PG; Lisanti MP. 2006. Caveolin-1-deficient aortic smooth muscle cells show cell autonomous abnormalities in proliferation, migration, and endothelin-bases signal transduction Am J Physiol Heart Circ Physiol 290(6):H2393-401. [PubMed: 16415072]  [MGI Ref ID J:111840]

Head BP; Peart JN; Panneerselvam M; Yokoyama T; Pearn ML; Niesman IR; Bonds JA; Schilling JM; Miyanohara A; Headrick J; Ali SS; Roth DM; Patel PM; Patel HH. 2010. Loss of caveolin-1 accelerates neurodegeneration and aging. PLoS One 5(12):e15697. [PubMed: 21203469]  [MGI Ref ID J:168335]

Heimerl S; Liebisch G; Le Lay S; Bottcher A; Wiesner P; Lindtner S; Kurzchalia TV; Simons K; Schmitz G. 2008. Caveolin-1 deficiency alters plasma lipid and lipoprotein profiles in mice. Biochem Biophys Res Commun 367(4):826-33. [PubMed: 18191037]  [MGI Ref ID J:131294]

Hitkova I; Yuan G; Anderl F; Gerhard M; Kirchner T; Reu S; Rocken C; Schafer C; Schmid RM; Vogelmann R; Ebert MP; Burgermeister E. 2013. Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis. PLoS Pathog 9(4):e1003251. [PubMed: 23592983]  [MGI Ref ID J:196656]

Hu G; Ye RD; Dinauer MC; Malik AB; Minshall RD. 2008. Neutrophil caveolin-1 expression contributes to mechanism of lung inflammation and injury. Am J Physiol Lung Cell Mol Physiol 294(2):L178-86. [PubMed: 17993589]  [MGI Ref ID J:132206]

Ieronimakis N; Hays A; Reyes M. 2012. Bone marrow-derived cells do not engraft into skeletal muscle microvasculature but promote angiogenesis after acute injury. Exp Hematol 40(3):238-249.e3. [PubMed: 22155292]  [MGI Ref ID J:191531]

Jasmin JF; Malhotra S; Singh Dhallu M; Mercier I; Rosenbaum DM; Lisanti MP. 2007. Caveolin-1 deficiency increases cerebral ischemic injury. Circ Res 100(5):721-9. [PubMed: 17293479]  [MGI Ref ID J:133702]

Jasmin JF; Rengo G; Lymperopoulos A; Gupta R; Eaton GJ; Quann K; Gonzales DM; Mercier I; Koch WJ; Lisanti MP. 2011. Caveolin-1 Deficiency Exacerbates Cardiac Dysfunction and Reduces Survival in Mice with Myocardial Infarction. Am J Physiol Heart Circ Physiol :. [PubMed: 21297026]  [MGI Ref ID J:169602]

Jiao H; Zhang Y; Yan Z; Wang ZG; Liu G; Minshall RD; Malik AB; Hu G. 2013. Caveolin-1 Tyr14 phosphorylation induces interaction with TLR4 in endothelial cells and mediates MyD88-dependent signaling and sepsis-induced lung inflammation. J Immunol 191(12):6191-9. [PubMed: 24244013]  [MGI Ref ID J:207117]

Jin C; Shelburne CP; Li G; Potts EN; Riebe KJ; Sempowski GD; Foster WM; Abraham SN. 2011. Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation. J Clin Invest 121(3):941-55. [PubMed: 21285515]  [MGI Ref ID J:171819]

Jin Y; Kim HP; Cao J; Zhang M; Ifedigbo E; Choi AM. 2009. Caveolin-1 regulates the secretion and cytoprotection of Cyr61 in hyperoxic cell death. FASEB J 23(2):341-50. [PubMed: 18801924]  [MGI Ref ID J:146034]

Jung K; Schlenz H; Krasteva G; Muhlfeld C. 2012. Alveolar Epithelial Type II Cells and Their Microenvironment in the Caveolin-1-Deficient Mouse. Anat Rec (Hoboken) 295(2):196-200. [PubMed: 22213628]  [MGI Ref ID J:179372]

Kawamori Y; Katayama Y; Asada N; Minagawa K; Sato M; Okamura A; Shimoyama M; Nakagawa K; Okano T; Tanimoto M; Kato S; Matsui T. 2010. Role for vitamin D receptor in the neuronal control of the hematopoietic stem cell niche. Blood 116(25):5528-35. [PubMed: 20813899]  [MGI Ref ID J:167420]

Lam RS; Nahirney D; Duszyk M. 2009. Cholesterol-dependent regulation of adenosine A(2A) receptor-mediated anion secretion in colon epithelial cells. Exp Cell Res 315(17):3028-35. [PubMed: 19523941]  [MGI Ref ID J:154892]

Le Lay S; Kurzchalia TV. 2005. Getting rid of caveolins: phenotypes of caveolin-deficient animals. Biochim Biophys Acta 1746(3):322-33. [PubMed: 16019085]  [MGI Ref ID J:104846]

Le Saux CJ; Teeters K; Miyasato SK; Hoffmann PR; Bollt O; Douet V; Shohet RV; Broide DH; Tam EK. 2008. Down-regulation of caveolin-1, an inhibitor of transforming growth factor-beta signaling, in acute allergen-induced airway remodeling. J Biol Chem 283(9):5760-8. [PubMed: 18056268]  [MGI Ref ID J:132297]

Le Saux O; Teeters K; Miyasato S; Choi J; Nakamatsu G; Richardson JA; Starcher B; Davis EC; Tam EK; Jourdan-Le Saux C. 2008. The role of caveolin-1 in pulmonary matrix remodeling and mechanical properties. Am J Physiol Lung Cell Mol Physiol 295(6):L1007-17. [PubMed: 18849439]  [MGI Ref ID J:143600]

Lee H; Park DS; Razani B; Russell RG; Pestell RG; Lisanti MP. 2002. Caveolin-1 mutations (P132L and null) and the pathogenesis of breast cancer: caveolin-1 (P132L) behaves in a dominant-negative manner and caveolin-1 (-/-) null mice show mammary epithelial cell hyperplasia. Am J Pathol 161(4):1357-69. [PubMed: 12368209]  [MGI Ref ID J:109251]

Li T; Sotgia F; Vuolo MA; Li M; Yang WC; Pestell RG; Sparano JA; Lisanti MP. 2006. Caveolin-1 mutations in human breast cancer: functional association with estrogen receptor alpha-positive status. Am J Pathol 168(6):1998-2013. [PubMed: 16723714]  [MGI Ref ID J:110117]

Li X; McClellan ME; Tanito M; Garteiser P; Towner R; Bissig D; Berkowitz BA; Fliesler SJ; Woodruff ML; Fain GL; Birch DG; Khan MS; Ash JD; Elliott MH. 2012. Loss of caveolin-1 impairs retinal function due to disturbance of subretinal microenvironment. J Biol Chem 287(20):16424-34. [PubMed: 22451674]  [MGI Ref ID J:185443]

Li Y; Lau WM; So KF; Tong Y; Shen J. 2011. Caveolin-1 promote astroglial differentiation of neural stem/progenitor cells through modulating Notch1/NICD and Hes1 expressions. Biochem Biophys Res Commun 407(3):517-24. [PubMed: 21414292]  [MGI Ref ID J:171932]

Li Z; Wermuth PJ; Benn BS; Lisanti MP; Jimenez SA. 2013. Caveolin-1 Deficiency Induces Spontaneous Endothelial-to-Mesenchymal Transition in Murine Pulmonary Endothelial Cells in Vitro. Am J Pathol 182(2):325-31. [PubMed: 23195429]  [MGI Ref ID J:192574]

Mahavadi S; Bhattacharya S; Kumar DP; Clay C; Ross G; Akbarali HI; Grider JR; Murthy KS. 2013. Increased PDE5 activity and decreased Rho kinase and PKC activities in colonic muscle from caveolin-1-/- mice impair the peristaltic reflex and propulsion. Am J Physiol Gastrointest Liver Physiol 305(12):G964-74. [PubMed: 24157969]  [MGI Ref ID J:210556]

Maniatis NA; Shinin V; Schraufnagel DE; Okada S; Vogel SM; Malik AB; Minshall RD. 2008. Increased pulmonary vascular resistance and defective pulmonary artery filling in caveolin-1-/- mice. Am J Physiol Lung Cell Mol Physiol 294(5):L865-73. [PubMed: 18192592]  [MGI Ref ID J:136587]

Marchiando AM; Shen L; Graham WV; Weber CR; Schwarz BT; Austin JR 2nd; Raleigh DR; Guan Y; Watson AJ; Montrose MH; Turner JR. 2010. Caveolin-1-dependent occludin endocytosis is required for TNF-induced tight junction regulation in vivo. J Cell Biol 189(1):111-26. [PubMed: 20351069]  [MGI Ref ID J:158798]

Marmon S; Hinchey J; Oh P; Cammer M; de Almeida CJ; Gunther L; Raine CS; Lisanti MP. 2009. Caveolin-1 expression determines the route of neutrophil extravasation through skin microvasculature. Am J Pathol 174(2):684-92. [PubMed: 19164603]  [MGI Ref ID J:144176]

Mattsson CL; Andersson ER; Nedergaard J. 2010. Differential involvement of caveolin-1 in brown adipocyte signaling: impaired beta3-adrenergic, but unaffected LPA, PDGF and EGF receptor signaling. Biochim Biophys Acta 1803(8):983-9. [PubMed: 20381543]  [MGI Ref ID J:165375]

Mattsson CL; Csikasz RI; Shabalina IG; Nedergaard J; Cannon B. 2010. Caveolin-1-ablated mice survive in cold by nonshivering thermogenesis despite desensitized adrenergic responsiveness. Am J Physiol Endocrinol Metab 299(3):E374-83. [PubMed: 20530737]  [MGI Ref ID J:170035]

Mayoral R; Valverde AM; Llorente Izquierdo C; Gonzalez-Rodriguez A; Bosca L; Martin-Sanz P. 2010. Impairment of transforming growth factor beta signaling in caveolin-1-deficient hepatocytes: role in liver regeneration. J Biol Chem 285(6):3633-42. [PubMed: 19966340]  [MGI Ref ID J:159769]

McGuire JF; Rouen S; Siegfreid E; Wright DE; Dobrowsky RT. 2009. Caveolin-1 and altered neuregulin signaling contribute to the pathophysiological progression of diabetic peripheral neuropathy. Diabetes 58(11):2677-86. [PubMed: 19675140]  [MGI Ref ID J:154381]

Medina FA; de Almeida CJ; Dew E; Li J; Bonuccelli G; Williams TM; Cohen AW; Pestell RG; Frank PG; Tanowitz HB; Lisanti MP. 2006. Caveolin-1-deficient mice show defects in innate immunity and inflammatory immune response during Salmonella enterica serovar Typhimurium infection. Infect Immun 74(12):6665-74. [PubMed: 16982844]  [MGI Ref ID J:115914]

Mercier I; Camacho J; Titchen K; Gonzales DM; Quann K; Bryant KG; Molchansky A; Milliman JN; Whitaker-Menezes D; Sotgia F; Jasmin JF; Schwarting R; Pestell RG; Blagosklonny MV; Lisanti MP. 2012. Caveolin-1 and Accelerated Host Aging in the Breast Tumor Microenvironment: Chemoprevention with Rapamycin, an mTOR Inhibitor and Anti-Aging Drug. Am J Pathol 181(1):278-93. [PubMed: 22698676]  [MGI Ref ID J:185581]

Mercier I; Casimiro MC; Zhou J; Wang C; Plymire C; Bryant KG; Daumer KM; Sotgia F; Bonuccelli G; Witkiewicz AK; Lin J; Tran TH; Milliman J; Frank PG; Jasmin JF; Rui H; Pestell RG; Lisanti MP. 2009. Genetic ablation of caveolin-1 drives estrogen-hypersensitivity and the development of DCIS-like mammary lesions. Am J Pathol 174(4):1172-90. [PubMed: 19342371]  [MGI Ref ID J:147439]

Milovanova T; Chatterjee S; Hawkins BJ; Hong N; Sorokina EM; Debolt K; Moore JS; Madesh M; Fisher AB. 2008. Caveolae are an essential component of the pathway for endothelial cell signaling associated with abrupt reduction of shear stress. Biochim Biophys Acta 1783(10):1866-75. [PubMed: 18573285]  [MGI Ref ID J:140780]

Mirza MK; Yuan J; Gao XP; Garrean S; Brovkovych V; Malik AB; Tiruppathi C; Zhao YY. 2010. Caveolin-1 deficiency dampens Toll-like receptor 4 signaling through eNOS activation. Am J Pathol 176(5):2344-51. [PubMed: 20304961]  [MGI Ref ID J:160770]

Miyasato SK; Loeffler J; Shohet R; Zhang J; Lindsey M; Le Saux CJ. 2011. Caveolin-1 modulates TGF-beta1 signaling in cardiac remodeling. Matrix Biol 30(5-6):318-29. [PubMed: 21641995]  [MGI Ref ID J:175660]

Morais C; Ebrahem Q; Anand-Apte B; Parat MO. 2012. Altered angiogenesis in caveolin-1 gene-deficient mice is restored by ablation of endothelial nitric oxide synthase. Am J Pathol 180(4):1702-14. [PubMed: 22322296]  [MGI Ref ID J:182003]

Mundy DI; Lopez AM; Posey KS; Chuang JC; Ramirez CM; Scherer PE; Turley SD. 2014. Impact of the loss of caveolin-1 on lung mass and cholesterol metabolism in mice with and without the lysosomal cholesterol transporter, Niemann-Pick type C1. Biochim Biophys Acta 1841(7):995-1002. [PubMed: 24747682]  [MGI Ref ID J:212556]

Noel J; Wang H; Hong N; Tao JQ; Yu K; Sorokina EM; Debolt K; Heayn M; Rizzo V; Delisser H; Fisher AB; Chatterjee S. 2013. PECAM-1 and caveolae form the mechanosensing complex necessary for NOX2 activation and angiogenic signaling with stopped flow in pulmonary endothelium. Am J Physiol Lung Cell Mol Physiol 305(11):L805-18. [PubMed: 24077950]  [MGI Ref ID J:210194]

Nuno DW; England SK; Lamping KG. 2012. RhoA localization with caveolin-1 regulates vascular contractions to serotonin. Am J Physiol Regul Integr Comp Physiol 303(9):R959-67. [PubMed: 22955057]  [MGI Ref ID J:190458]

Pani B; Liu X; Bollimuntha S; Cheng KT; Niesman IR; Zheng C; Achen VR; Patel HH; Ambudkar IS; Singh BB. 2013. Impairment of TRPC1-STIM1 channel assembly and AQP5 translocation compromise agonist-stimulated fluid secretion in mice lacking caveolin1. J Cell Sci 126(Pt 2):667-75. [PubMed: 23203809]  [MGI Ref ID J:200237]

Park DS; Cohen AW; Frank PG; Razani B; Lee H; Williams TM; Chandra M; Shirani J; De Souza AP; Tang B; Jelicks LA; Factor SM; Weiss LM; Tanowitz HB; Lisanti MP. 2003. Caveolin-1 Null (-/-) Mice Show Dramatic Reductions in Life Span. Biochemistry 42(51):15124-15131. [PubMed: 14690422]  [MGI Ref ID J:87282]

Park DS; Lee H; Frank PG; Razani B; Nguyen AV; Parlow AF; Russell RG; Hulit J; Pestell RG; Lisanti MP. 2002. Caveolin-1-deficient mice show accelerated mammary gland development during pregnancy, premature lactation, and hyperactivation of the Jak-2/STAT5a signaling cascade. Mol Biol Cell 13(10):3416-30. [PubMed: 12388746]  [MGI Ref ID J:120010]

Park DS; Woodman SE; Schubert W; Cohen AW; Frank PG; Chandra M; Shirani J; Razani B; Tang B; Jelicks LA; Factor SM; Weiss LM; Tanowitz HB; Lisanti MP. 2002. Caveolin-1/3 double-knockout mice are viable, but lack both muscle and non-muscle caveolae, and develop a severe cardiomyopathic phenotype. Am J Pathol 160(6):2207-17. [PubMed: 12057923]  [MGI Ref ID J:77372]

Petriello MC; Han SG; Newsome BJ; Hennig B. 2014. PCB 126 toxicity is modulated by cross-talk between caveolae and Nrf2 signaling. Toxicol Appl Pharmacol 277(2):192-9. [PubMed: 24709675]  [MGI Ref ID J:212118]

Pojoga LH; Adamova Z; Kumar A; Stennett AK; Romero JR; Adler GK; Williams GH; Khalil RA. 2010. Sensitivity of NOS-dependent vascular relaxation pathway to mineralocorticoid receptor blockade in caveolin-1-deficient mice. Am J Physiol Heart Circ Physiol 298(6):H1776-88. [PubMed: 20363891]  [MGI Ref ID J:160449]

Pojoga LH; Yao TM; Sinha S; Ross RL; Lin JC; Raffetto JD; Adler GK; Williams GH; Khalil RA. 2008. Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice. Am J Physiol Heart Circ Physiol 294(3):H1258-65. [PubMed: 18178722]  [MGI Ref ID J:132392]

Razani B; Combs TP; Wang XB; Frank PG; Park DS; Russell RG; Li M; Tang B; Jelicks LA; Scherer PE; Lisanti MP. 2002. Caveolin-1-deficient Mice Are Lean, Resistant to Diet-induced Obesity, and Show Hypertriglyceridemia with Adipocyte Abnormalities. J Biol Chem 277(10):8635-47. [PubMed: 11739396]  [MGI Ref ID J:75192]

Razani B; Lisanti MP. 2001. Caveolin-deficient mice: insights into caveolar function human disease. J Clin Invest 108(11):1553-61. [PubMed: 11733547]  [MGI Ref ID J:73209]

Roelandt T; Giddelo C; Heughebaert C; Denecker G; Hupe M; Crumrine D; Kusuma A; Haftek M; Roseeuw D; Declercq W; Feingold KR; Elias PM; Hachem JP. 2009. The 'caveolae brake hypothesis' and the epidermal barrier. J Invest Dermatol 129(4):927-36. [PubMed: 19005485]  [MGI Ref ID J:150227]

Romanenko VG; Roser KS; Melvin JE; Begenisich T. 2009. The role of cell cholesterol and the cytoskeleton in the interaction between IK1 and maxi-K channels. Am J Physiol Cell Physiol 296(4):C878-88. [PubMed: 19176762]  [MGI Ref ID J:149700]

Rosengren BI; Rippe A; Rippe C; Venturoli D; Sward K; Rippe B. 2006. Transvascular protein transport in mice lacking endothelial caveolae. Am J Physiol Heart Circ Physiol 291(3):H1371-7. [PubMed: 16501011]  [MGI Ref ID J:116286]

Rubin J; Schwartz Z; Boyan BD; Fan X; Case N; Sen B; Drab M; Smith D; Aleman M; Wong KL; Yao H; Jo H; Gross TS. 2007. Caveolin-1 knockout mice have increased bone size and stiffness. J Bone Miner Res 22(9):1408-18. [PubMed: 17550335]  [MGI Ref ID J:141361]

Schubert W; Frank PG; Razani B; Park DS; Chow CW; Lisanti MP. 2001. Caveolae-deficient Endothelial Cells Show Defects in the Uptake and Transport of Albumin in Vivo. J Biol Chem 276(52):48619-22. [PubMed: 11689550]  [MGI Ref ID J:73489]

Schubert W; Frank PG; Woodman SE; Hyogo H; Cohen DE; Chow CW; Lisanti MP. 2002. Microvascular hyperpermeability in caveolin-1 (-/-) knock-out mice. Treatment with a specific nitric-oxide synthase inhibitor, L-name, restores normal microvascular permeability in Cav-1 null mice. J Biol Chem 277(42):40091-8. [PubMed: 12167625]  [MGI Ref ID J:79595]

Schubert W; Sotgia F; Cohen AW; Capozza F; Bonuccelli G; Bruno C; Minetti C; Bonilla E; Dimauro S; Lisanti MP. 2007. Caveolin-1(-/-)- and caveolin-2(-/-)-deficient mice both display numerous skeletal muscle abnormalities, with tubular aggregate formation. Am J Pathol 170(1):316-33. [PubMed: 17200204]  [MGI Ref ID J:117199]

Senou M; Costa MJ; Massart C; Thimmesch M; Khalifa C; Poncin S; Boucquey M; Gerard AC; Audinot JN; Dessy C; Ruf J; Feron O; Devuyst O; Guiot Y; Dumont JE; Van Sande J; Many MC. 2009. Role of caveolin-1 in thyroid phenotype, cell homeostasis, and hormone synthesis: in vivo study of caveolin-1 knockout mice. Am J Physiol Endocrinol Metab 297(2):E438-51. [PubMed: 19435853]  [MGI Ref ID J:151165]

Shivshankar P; Brampton C; Miyasato S; Kasper M; Thannickal VJ; Le Saux CJ. 2012. Caveolin-1 deficiency protects from pulmonary fibrosis by modulating epithelial cell senescence in mice. Am J Respir Cell Mol Biol 47(1):28-36. [PubMed: 22362388]  [MGI Ref ID J:199776]

Singleton PA; Mirzapoiazova T; Guo Y; Sammani S; Mambetsariev N; Lennon FE; Moreno-Vinasco L; Garcia JG. 2010. High-molecular-weight hyaluronan is a novel inhibitor of pulmonary vascular leakiness. Am J Physiol Lung Cell Mol Physiol 299(5):L639-51. [PubMed: 20709728]  [MGI Ref ID J:165733]

Singleton PA; Pendyala S; Gorshkova IA; Mambetsariev N; Moitra J; Garcia JG; Natarajan V. 2009. Dynamin 2 and c-Abl are novel regulators of hyperoxia-mediated NADPH oxidase activation and reactive oxygen species production in caveolin-enriched microdomains of the endothelium. J Biol Chem 284(50):34964-75. [PubMed: 19833721]  [MGI Ref ID J:158213]

Sotgia F; Rui H; Bonuccelli G; Mercier I; Pestell RG; Lisanti MP. 2006. Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Cancer Res 66(22):10647-51. [PubMed: 17108100]  [MGI Ref ID J:116126]

Sotgia F; Williams TM; Schubert W; Medina F; Minetti C; Pestell RG; Lisanti MP. 2006. Caveolin-1 deficiency (-/-) conveys premalignant alterations in mammary epithelia, with abnormal lumen formation, growth factor independence, and cell invasiveness. Am J Pathol 168(1):292-309. [PubMed: 16400031]  [MGI Ref ID J:104439]

Sun Y; Hu G; Zhang X; Minshall RD. 2009. Phosphorylation of caveolin-1 regulates oxidant-induced pulmonary vascular permeability via paracellular and transcellular pathways. Circ Res 105(7):676-85, 15 p following 685. [PubMed: 19713536]  [MGI Ref ID J:169962]

Sundivakkam PC; Kwiatek AM; Sharma TT; Minshall RD; Malik AB; Tiruppathi C. 2009. Caveolin-1 scaffold domain interacts with TRPC1 and IP3R3 to regulate Ca2+ store release-induced Ca2+ entry in endothelial cells. Am J Physiol Cell Physiol 296(3):C403-13. [PubMed: 19052258]  [MGI Ref ID J:146324]

Suzuki Y; Yamamura H; Ohya S; Imaizumi Y. 2013. Caveolin-1 facilitates the direct coupling between large conductance Ca2+-activated K+ (BKCa) and Cav1.2 Ca2+ channels and their clustering to regulate membrane excitability in vascular myocytes. J Biol Chem 288(51):36750-61. [PubMed: 24202214]  [MGI Ref ID J:207193]

Takayasu Y; Takeuchi K; Kumari R; Bennett MV; Zukin RS; Francesconi A. 2010. Caveolin-1 knockout mice exhibit impaired induction of mGluR-dependent long-term depression at CA3-CA1 synapses. Proc Natl Acad Sci U S A :. [PubMed: 21098662]  [MGI Ref ID J:167146]

Tkachenko E; Tse D; Sideleva O; Deharvengt SJ; Luciano MR; Xu Y; McGarry CL; Chidlow J; Pilch PF; Sessa WC; Toomre DK; Stan RV. 2012. Caveolae, fenestrae and transendothelial channels retain PV1 on the surface of endothelial cells. PLoS One 7(3):e32655. [PubMed: 22403691]  [MGI Ref ID J:186939]

Tomassian T; Humphries LA; Liu SD; Silva O; Brooks DG; Miceli MC. 2011. Caveolin-1 orchestrates TCR synaptic polarity, signal specificity, and function in CD8 T cells. J Immunol 187(6):2993-3002. [PubMed: 21849673]  [MGI Ref ID J:179237]

Trushina E; Canaria CA; Lee DY; McMurray CT. 2014. Loss of caveolin-1 expression in knock-in mouse model of Huntington's disease suppresses pathophysiology in vivo. Hum Mol Genet 23(1):129-44. [PubMed: 24021477]  [MGI Ref ID J:203116]

Trushina E; Du Charme J; Parisi J; McMurray CT. 2006. Neurological abnormalities in caveolin-1 knock out mice. Behav Brain Res 172(1):24-32. [PubMed: 16750274]  [MGI Ref ID J:110712]

Uemura T; Stringer DE; Blohm-Mangone KA; Gerner EW. 2010. Polyamine transport is mediated by both endocytic and solute carrier transport mechanisms in the gastrointestinal tract. Am J Physiol Gastrointest Liver Physiol 299(2):G517-22. [PubMed: 20522643]  [MGI Ref ID J:163345]

Volonte D; McTiernan CF; Drab M; Kasper M; Galbiati F. 2008. Caveolin-1 and caveolin-3 form heterooligomeric complexes in atrial cardiac myocytes that are required for doxorubicin-induced apoptosis. Am J Physiol Heart Circ Physiol 294(1):H392-401. [PubMed: 17982011]  [MGI Ref ID J:132310]

Wang H; Wang AX; Barrett EJ. 2011. Caveolin-1 is required for vascular endothelial insulin uptake. Am J Physiol Endocrinol Metab 300(1):E134-44. [PubMed: 20959538]  [MGI Ref ID J:172328]

Wang MD; Kiss RS; Franklin V; McBride HM; Whitman SC; Marcel YL. 2007. Different cellular traffic of LDL-cholesterol and acetylated LDL-cholesterol leads to distinct reverse cholesterol transport pathways. J Lipid Res 48(3):633-45. [PubMed: 17148552]  [MGI Ref ID J:120283]

Wang XM; Kim HP; Nakahira K; Ryter SW; Choi AM. 2009. The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1. J Immunol 182(6):3809-18. [PubMed: 19265160]  [MGI Ref ID J:145914]

Wantha S; Alard JE; Megens RT; van der Does AM; Doring Y; Drechsler M; Pham CT; Wang MW; Wang JM; Gallo RL; von Hundelshausen P; Lindbom L; Hackeng T; Weber C; Soehnlein O. 2013. Neutrophil-derived cathelicidin promotes adhesion of classical monocytes. Circ Res 112(5):792-801. [PubMed: 23283724]  [MGI Ref ID J:212860]

Williams TM; Cheung MW; Park DS; Razani B; Cohen AW; Muller WJ; Di Vizio D; Chopra NG; Pestell RG; Lisanti MP. 2003. Loss of caveolin-1 gene expression accelerates the development of dysplastic mammary lesions in tumor-prone transgenic mice. Mol Biol Cell 14(3):1027-42. [PubMed: 12631721]  [MGI Ref ID J:132472]

Williams TM; Hassan GS; Li J; Cohen AW; Medina F; Frank PG; Pestell RG; Di Vizio D; Loda M; Lisanti MP. 2005. Caveolin-1 promotes tumor progression in an autochthonous mouse model of prostate cancer: genetic ablation of Cav-1 delays advanced prostate tumor development in tramp mice. J Biol Chem 280(26):25134-45. [PubMed: 15802273]  [MGI Ref ID J:133066]

Williams TM; Lee H; Cheung MW; Cohen AW; Razani B; Iyengar P; Scherer PE; Pestell RG; Lisanti MP. 2004. Combined loss of INK4a and caveolin-1 synergistically enhances cell proliferation and oncogene-induced tumorigenesis: role of INK4a/CAV-1 in mammary epithelial cell hyperplasia. J Biol Chem 279(23):24745-56. [PubMed: 15044451]  [MGI Ref ID J:90334]

Williams TM; Medina F; Badano I; Hazan RB; Hutchinson J; Muller WJ; Chopra NG; Scherer PE; Pestell RG; Lisanti MP. 2004. Caveolin-1 gene disruption promotes mammary tumorigenesis and dramatically enhances lung metastasis in vivo. Role of Cav-1 in cell invasiveness and matrix metalloproteinase (MMP-2/9) secretion. J Biol Chem 279(49):51630-46. [PubMed: 15355971]  [MGI Ref ID J:95195]

Williams TM; Sotgia F; Lee H; Hassan G; Di Vizio D; Bonuccelli G; Capozza F; Mercier I; Rui H; Pestell RG; Lisanti MP. 2006. Stromal and epithelial caveolin-1 both confer a protective effect against mammary hyperplasia and tumorigenesis: caveolin-1 antagonizes cyclin d1 function in mammary epithelial cells. Am J Pathol 169(5):1784-801. [PubMed: 17071600]  [MGI Ref ID J:114569]

Woodman SE; Ashton AW; Schubert W; Lee H; Williams TM; Medina FA; Wyckoff JB; Combs TP; Lisanti MP. 2003. Caveolin-1 knockout mice show an impaired angiogenic response to exogenous stimuli. Am J Pathol 162(6):2059-68. [PubMed: 12759260]  [MGI Ref ID J:109484]

Yang B; Radel C; Hughes D; Kelemen S; Rizzo V. 2011. p190 RhoGTPase-activating protein links the beta1 integrin/caveolin-1 mechanosignaling complex to RhoA and actin remodeling. Arterioscler Thromb Vasc Biol 31(2):376-83. [PubMed: 21051664]  [MGI Ref ID J:184189]

Yuan K; Huang C; Fox J; Gaid M; Weaver A; Li G; Singh BB; Gao H; Wu M. 2011. Elevated Inflammatory Response in Caveolin-1-deficient Mice with Pseudomonas aeruginosa Infection Is Mediated by STAT3 Protein and Nuclear Factor {kappa}B (NF-{kappa}B). J Biol Chem 286(24):21814-25. [PubMed: 21515682]  [MGI Ref ID J:173648]

Zaas DW; Swan ZD; Brown BJ; Li G; Randell SH; Degan S; Sunday ME; Wright JR; Abraham SN. 2009. Counteracting signaling activities in lipid rafts associated with the invasion of lung epithelial cells by Pseudomonas aeruginosa. J Biol Chem 284(15):9955-64. [PubMed: 19211560]  [MGI Ref ID J:149065]

Zhang M; Lee SJ; An C; Xu JF; Joshi B; Nabi IR; Choi AM; Jin Y. 2011. Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis. Free Radic Biol Med 50(10):1252-62. [PubMed: 21382479]  [MGI Ref ID J:171939]

Zhang PX; Murray TS; Villella VR; Ferrari E; Esposito S; D'Souza A; Raia V; Maiuri L; Krause DS; Egan ME; Bruscia EM. 2013. Reduced caveolin-1 promotes hyperinflammation due to abnormal heme oxygenase-1 localization in lipopolysaccharide-challenged macrophages with dysfunctional cystic fibrosis transmembrane conductance regulator. J Immunol 190(10):5196-206. [PubMed: 23606537]  [MGI Ref ID J:202542]

Zhang Y; Peng F; Gao B; Ingram AJ; Krepinsky JC. 2012. High glucose-induced RhoA activation requires caveolae and PKCbeta1-mediated ROS generation. Am J Physiol Renal Physiol 302(1):F159-72. [PubMed: 21975875]  [MGI Ref ID J:180093]

Zhao YY; Zhao YD; Mirza MK; Huang JH; Potula HH; Vogel SM; Brovkovych V; Yuan JX; Wharton J; Malik AB. 2009. Persistent eNOS activation secondary to caveolin-1 deficiency induces pulmonary hypertension in mice and humans through PKG nitration. J Clin Invest 119(7):2009-18. [PubMed: 19487814]  [MGI Ref ID J:152579]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB27

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice can be bred as homozygotes. The donating investigator noted diminished reproductive performance as the backcross to C57BL/6J background progressed and backcrossed to a 129S6/SvEv background for 1 generation. The mice are now maintained as homozygotes and are primarily a mix of 129 and C57BL/6, but a minor contribution from the SJL background (contributed from the originating ES cell line) should not be discounted. Coat color expected from breeding: Black and Agouti.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHomozygous for Cav1tm1Mls  
Price per Pair (US dollars $)Pair Genotype
$399.80Homozygous for Cav1tm1Mls x Homozygous for Cav1tm1Mls  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHomozygous for Cav1tm1Mls  
Price per Pair (US dollars $)Pair Genotype
$519.80Homozygous for Cav1tm1Mls x Homozygous for Cav1tm1Mls  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Important Note

Note that this allele is also available on a C57BL/6J congenic background (Stock No. 007083).

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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