Strain Name:

B6.129S4-Ccl2tm1Rol/J

Stock Number:

004434

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Mice that are homozygous for the targeted mutation show similar numbers of peritoneal macrophages, Kupffer cell and alveolar macrophages to those observed in wildtype mice. Thioglycollate induced peritonitis results in impaired recruitment of monocytes and macrophages to peritoneal cavity. Cellular recruitment to delayed-type hypersensitivity challenges and secondary granulomata is reduced. This mutant mouse strain represents a model that may be useful in studies related to leukocyte trafficking.

Description

Strain Information

Former Names B6.129S4-Scya2tm1Rol    (Changed: 15-DEC-04 )
MCP-1 -/-    (Changed: 15-DEC-04 )
Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
GenerationN10F?+N1F16 (14-AUG-14)
Generation Definitions
 
Donating Investigator Barrett J. Rollins,   Dana-Farber Cancer Inst, Harvard Med Sch

Description
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product is detected in lipopolysaccharide (LPS) -stimulated peritoneal macrophages isolated from homozygous mice. The numbers of peritoneal macrophages, Kupffer cell and alveolar macrophages were similar to levels found in wildtype mice. Thioglycollate induced peritonitis results in impaired recruitment of monocytes and macrophages to peritoneal cavity. Cellular recruitment to delayed-type hypersensitivity challenges and secondary granulomata is reduced. This mutant mouse strain represents a model that may be useful in studies related to leukocyte trafficking.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 2 and insert an inframe stop codon into exon 1. The construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice, and then backcrossed to C57BL/6 for ten generations.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Ccl2
016849   B6.Cg-Ccl2tm1.1Pame/J
014095   B6.Cg-Tg(GFAP-Ccl2)JE95Rmra/J
023347   B6N.129S1(FVB)-Ccl2tm1.2Tyos/J
View Strains carrying other alleles of Ccl2     (3 strains)

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).
Macular Degeneration, Age-Related, 2; ARMD2
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Chemokine, Cc Motif, Ligand 2; CCL2   (CCL2)
Human Immunodeficiency Virus Type 1, Susceptibility to   (CCL2)
Mycobacterium Tuberculosis, Susceptibility to   (CCL2)
Neural Tube Defects   (CCL2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ccl2tm1Rol/Ccl2tm1Rol

        B6.129S4-Ccl2tm1Rol
  • immune system phenotype
  • abnormal chemokine level
    • in thioglycollate- or zymosan- induced peritonitis models, no Ccl2 is detected while reduce levels of Ccl7 are present in peritoneal fluid   (MGI Ref ID J:151874)
    • 1 day after femoral artery excision, muscles accumulate more chemoattractants (KC and MIP-2) than in similarly treated wild-type mice   (MGI Ref ID J:118606)
  • abnormal cytokine secretion
    • MOG35-55-specific Th1 cytokine responses are diminished in mutants   (MGI Ref ID J:68145)
    • abnormal chemokine secretion
      • there is no Ccl2 (MCP-1) secretion by peritoneal macrophages activated in vitro compared to controls   (MGI Ref ID J:151874)
      • secretion of Ccl7 (MCP-3) and Ccl12 (MCP-5) is also dramatically reduced by these activated macrophages   (MGI Ref ID J:151874)
    • decreased interferon-gamma secretion
      • mutants exhibit reduced production of IFN-gamma in response to MOG35-55 induced EAE   (MGI Ref ID J:68145)
    • increased interleukin-10 secretion
      • mutants exhibit enhanced secretion of IL-10 in response to MOG35-55 induced EAE   (MGI Ref ID J:68145)
  • abnormal macrophage chemotaxis
    • the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice   (MGI Ref ID J:109290)
    • the total number of macrophages recruited is normal   (MGI Ref ID J:109290)
    • impaired macrophage chemotaxis
      • mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE   (MGI Ref ID J:68145)
      • only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls   (MGI Ref ID J:151874)
      • initially following femoral artery excision   (MGI Ref ID J:118606)
  • abnormal neutrophil physiology
    • the number of neutrophils recruited to the peritoneum in an induced peritonitis model is almost double that controls   (MGI Ref ID J:151874)
  • decreased leukocyte cell number
    • numbers of leukocytes isolated from CNS tissue during EAE attacks are about 1/3 of those from wild type mice with comparable EAE severity   (MGI Ref ID J:68145)
    • decreased macrophage cell number
      • age-dependent accumulation of macrophages in the choroids is less than in wild-type mice   (MGI Ref ID J:147328)
  • decreased susceptibility to experimental autoimmune encephalomyelitis
    • homozygotes are resistant to active experimental autoimmune encephalomyelitis (EAE) induction with MOG35-55, with delayed onset of disease, reduced inflammatory reaction including impaired recruitment of macrophages to the central nervous system (CNS), and faster and complete recovery   (MGI Ref ID J:68145)
    • adoptive transfer of primed T cells from wild-type mice to naive homozygous mutant recipients does not mediate clinical EAE, however wild-type mice receiving mutant T cells do develop clinical EAE   (MGI Ref ID J:68145)
  • increased CD4-positive, alpha beta T cell number
    • in an EAE model, mutants show an increase in proportion of CD4+ cells and reduction in CD11b+CD4- in the CNS leukocyte infiltrates compared to wild-type, although total numbers of T cells are not different   (MGI Ref ID J:68145)
  • increased IgG level
    • at 16 months, IgG is present in the retinal pigmented epithelium or choroids unlike in wild-type mice   (MGI Ref ID J:147328)
    • IgG light chain deposition in the retinal pigmented epithelium accumulates with age unlike in wild-type mice   (MGI Ref ID J:147328)
    • increased IgG1 level
      • significantly higher levels of anti-MOG35-55 IgG1 antibodies are seen in mutants compared to wild-type   (MGI Ref ID J:68145)
  • increased neutrophil cell number
    • 1 and 3 days after femoral artery excision, mice exhibit an earlier increase in neutrophil accumulation (measured by MPO activity) than in similarly treated wild-type mice   (MGI Ref ID J:118606)
  • increased osteoclast cell number
    • at P5 during tooth eruption   (MGI Ref ID J:109290)
    • peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice   (MGI Ref ID J:109290)
  • vision/eye phenotype
  • abnormal optic choroid morphology
    • age-dependent accumulation of macrophages in the choroids is less than in wild-type mice   (MGI Ref ID J:147328)
    • abnormal Bruch membrane morphology
      • the Bruch membrane is thickened compared to in wild-type mice after 9 months of age   (MGI Ref ID J:147328)
      • at 20 months, the outer Bruch membrane is breached by choriocapillary processes unlike in wild-type mice   (MGI Ref ID J:147328)
    • abnormal choriocapillaris morphology
      • at 16 months, mice exhibit dilation and attenuation of the choriocapillaris unlike wild-type mice   (MGI Ref ID J:147328)
    • choroidal neovascularization
      • at 15 to 19 months, mice exhibit intrachoroidal neovascularization with angiographic leakage unlike wild-type mice   (MGI Ref ID J:147328)
      • after 18 months, 4 of 15 mice exhibit choroidal neovascularization with angiographic leakage unlike in wild-type mice   (MGI Ref ID J:147328)
      • between 18 and 27 months, neovasculatization breaches the Bruch membrane and causes retinal pigmented epithelium and photoreceptor disruptions unlike in wild-type mice   (MGI Ref ID J:147328)
  • abnormal retinal pigment epithelium morphology
    • after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice   (MGI Ref ID J:147328)
    • at 16 months, mice exhibit attenuation of the retinal pigmented epithelium unlike in wild-type mice   (MGI Ref ID J:147328)
  • retinal degeneration
    • at 16 months, mice exhibit progressive outer retinal degeneration and confluent areas of visible atrophy unlike in wild-type mice   (MGI Ref ID J:147328)
    • at 18 months, mice exhibit geographic atrophy unlike in wild-type mice   (MGI Ref ID J:147328)
  • retinal deposits
    • after 9 months of age, mice exhibit subretinal deposits similar to drusen that increase with age unlike in wild-type mice   (MGI Ref ID J:147328)
  • retinal outer nuclear layer degeneration
  • retinal photoreceptor degeneration
  • behavior/neurological phenotype
  • abnormal conditioned taste aversion behavior
    • mice exhibit a stronger response to ethanol in an ethanol-induced conditioned taste aversion test compared with similarly treated wild-type mice   (MGI Ref ID J:102583)
    • however, saccharin consumption is normal   (MGI Ref ID J:102583)
  • alcohol aversion
    • in female mice   (MGI Ref ID J:102583)
  • alcohol preference
    • male mice exhibit a greater ethanol preference compared with wild-type (in post hoc analysis) mice, Ccr2tm1Mae homozygotes, and Ccl2tm1Rol Ccr2tm1Mae double homozygotes   (MGI Ref ID J:102583)
    • female mice exhibit a greater ethanol preference compared with Ccl2tm1Rol Ccr2tm1Mae double homozygotes and Ccr2tm1Mae homozygotes   (MGI Ref ID J:102583)
  • decreased alcohol consumption
    • in female mice compared with wild-type mice and Ccr2tm1Mae homozygotes   (MGI Ref ID J:102583)
  • impaired righting response
    • mice exhibit longer duration of ethanol-induced loss of righting response compared with similarly treated wild-type mice   (MGI Ref ID J:102583)
  • increased fluid intake
    • mice exhibit increased drinking of an ethanol solution compared with Ccl2tm1Rol Ccr2tm1Mae double homozygotes and Ccr2tm1Mae homozygotes   (MGI Ref ID J:102583)
    • mice exhibit increased drinking of a quinine solution compared with wild-type mice   (MGI Ref ID J:102583)
    • increased alcohol consumption
      • male mice consume more ethanol than wild-type (in post hoc analysis) mice and Ccl2tm1Rol Ccr2tm1Mae double homozygotes   (MGI Ref ID J:102583)
      • female mice consume more ethanol than Ccl2tm1Rol Ccr2tm1Mae double homozygotes   (MGI Ref ID J:102583)
  • cardiovascular system phenotype
  • abnormal blood circulation
    • following femoral artery excision, mice exhibit a delay in the restoration of perfusion compared with similarly treated wild-type mice   (MGI Ref ID J:118606)
  • abnormal choriocapillaris morphology
    • at 16 months, mice exhibit dilation and attenuation of the choriocapillaris unlike wild-type mice   (MGI Ref ID J:147328)
  • choroidal neovascularization
    • at 15 to 19 months, mice exhibit intrachoroidal neovascularization with angiographic leakage unlike wild-type mice   (MGI Ref ID J:147328)
    • after 18 months, 4 of 15 mice exhibit choroidal neovascularization with angiographic leakage unlike in wild-type mice   (MGI Ref ID J:147328)
    • between 18 and 27 months, neovasculatization breaches the Bruch membrane and causes retinal pigmented epithelium and photoreceptor disruptions unlike in wild-type mice   (MGI Ref ID J:147328)
  • nervous system phenotype
  • retinal photoreceptor degeneration
  • pigmentation phenotype
  • abnormal retinal pigment epithelium morphology
    • after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice   (MGI Ref ID J:147328)
    • at 16 months, mice exhibit attenuation of the retinal pigmented epithelium unlike in wild-type mice   (MGI Ref ID J:147328)
  • lipofuscinosis
    • after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice   (MGI Ref ID J:147328)
  • hematopoietic system phenotype
  • abnormal macrophage chemotaxis
    • the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice   (MGI Ref ID J:109290)
    • the total number of macrophages recruited is normal   (MGI Ref ID J:109290)
    • impaired macrophage chemotaxis
      • mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE   (MGI Ref ID J:68145)
      • only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls   (MGI Ref ID J:151874)
      • initially following femoral artery excision   (MGI Ref ID J:118606)
  • abnormal neutrophil physiology
    • the number of neutrophils recruited to the peritoneum in an induced peritonitis model is almost double that controls   (MGI Ref ID J:151874)
  • decreased leukocyte cell number
    • numbers of leukocytes isolated from CNS tissue during EAE attacks are about 1/3 of those from wild type mice with comparable EAE severity   (MGI Ref ID J:68145)
    • decreased macrophage cell number
      • age-dependent accumulation of macrophages in the choroids is less than in wild-type mice   (MGI Ref ID J:147328)
  • increased CD4-positive, alpha beta T cell number
    • in an EAE model, mutants show an increase in proportion of CD4+ cells and reduction in CD11b+CD4- in the CNS leukocyte infiltrates compared to wild-type, although total numbers of T cells are not different   (MGI Ref ID J:68145)
  • increased IgG level
    • at 16 months, IgG is present in the retinal pigmented epithelium or choroids unlike in wild-type mice   (MGI Ref ID J:147328)
    • IgG light chain deposition in the retinal pigmented epithelium accumulates with age unlike in wild-type mice   (MGI Ref ID J:147328)
    • increased IgG1 level
      • significantly higher levels of anti-MOG35-55 IgG1 antibodies are seen in mutants compared to wild-type   (MGI Ref ID J:68145)
  • increased neutrophil cell number
    • 1 and 3 days after femoral artery excision, mice exhibit an earlier increase in neutrophil accumulation (measured by MPO activity) than in similarly treated wild-type mice   (MGI Ref ID J:118606)
  • increased osteoclast cell number
    • at P5 during tooth eruption   (MGI Ref ID J:109290)
    • peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice   (MGI Ref ID J:109290)
  • homeostasis/metabolism phenotype
  • abnormal chemokine level
    • in thioglycollate- or zymosan- induced peritonitis models, no Ccl2 is detected while reduce levels of Ccl7 are present in peritoneal fluid   (MGI Ref ID J:151874)
    • 1 day after femoral artery excision, muscles accumulate more chemoattractants (KC and MIP-2) than in similarly treated wild-type mice   (MGI Ref ID J:118606)
  • abnormal response to injury
    • following femoral artery excision, mice exhibit a delay in the restoration of perfusion, extended period of increased ischemic muscle weight at day 1 and 7, earlier increase in neutrophil accumulation (measured by MPO activity) at day 1 and 3, increased chemoattractants (KC and MIP-2) levels at day 1, decreased accumulation of inflammatory infiltrate at day 3, delayed macrophage recruitment, large regions of necrotic muscle, increased adipocyte accumulation in the muscle, and impaired muscle regeneration compared with similarly treated wild-type mice   (MGI Ref ID J:118606)
  • decreased physiological sensitivity to xenobiotic
    • bleomycin-treated mice fail to exhibit skin fibrosis with normal collagen fibrils and few infiltrating macrophages and neutrophils unlike similarly treated wild-type mice   (MGI Ref ID J:110695)
  • craniofacial phenotype
  • accelerated tooth eruption
    • tooth eruption begins at P14 instead of P16 as in wild-type mice   (MGI Ref ID J:109290)
    • from P16 to P18, mice exhibit a 31-fold increase in erupted cusps compared with wild-type mice   (MGI Ref ID J:109290)
  • skeleton phenotype
  • increased osteoclast cell number
    • at P5 during tooth eruption   (MGI Ref ID J:109290)
    • peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice   (MGI Ref ID J:109290)
  • muscle phenotype
  • abnormal skeletal muscle morphology
    • following femoral artery excision, muscles accumulate more adipocytes than in similarly treated wild-type mice   (MGI Ref ID J:118606)
    • skeletal muscle necrosis
      • following femoral artery excision   (MGI Ref ID J:118606)
  • abnormal skeletal muscle regeneration
    • muscle regeneration, as measured by LDH and fiber size, is impaired following femoral artery excision   (MGI Ref ID J:118606)
  • increased muscle weight
    • after 1 and 7 days, mice subjected to femoral artery excision exhibit an extended period of increased ischemic muscle weight compared with similarly treated wild-type mice   (MGI Ref ID J:118606)
  • cellular phenotype
  • abnormal macrophage chemotaxis
    • the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice   (MGI Ref ID J:109290)
    • the total number of macrophages recruited is normal   (MGI Ref ID J:109290)
    • impaired macrophage chemotaxis
      • mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE   (MGI Ref ID J:68145)
      • only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls   (MGI Ref ID J:151874)
      • initially following femoral artery excision   (MGI Ref ID J:118606)
  • growth/size/body phenotype
  • accelerated tooth eruption
    • tooth eruption begins at P14 instead of P16 as in wild-type mice   (MGI Ref ID J:109290)
    • from P16 to P18, mice exhibit a 31-fold increase in erupted cusps compared with wild-type mice   (MGI Ref ID J:109290)

Ccl2tm1Rol/Ccl2tm1Rol

        B6.129S4-Ccl2tm1Rol/J
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:126512)
    • abnormal gluconeogenesis
      • during hyperinsulinemic-euglycemic clamp analysis, mice fed a high fat diet exhibit a 3-fold increase in basal and clamp hepatic glucose production compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
    • decreased circulating insulin level
      • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
    • impaired glucose tolerance
      • at 14 and 27 weeks regardless of diet   (MGI Ref ID J:126512)
    • improved glucose tolerance
      • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
    • increased circulating glucose level
      • mild in fasting mice regardless of diet   (MGI Ref ID J:126512)
    • increased circulating insulin level
      • when fed a high fat diet   (MGI Ref ID J:126512)
    • increased insulin sensitivity
      • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
  • decreased adiponectin level
    • regardless of diet   (MGI Ref ID J:126512)
  • decreased circulating free fatty acid level
    • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
  • decreased susceptibility to neuronal excitotoxicity
    • mice treated with kainate acid exhibit decreased microglial accumulation and reduced neurodegeneration in the CA1 and CA3 pyramidal neurons compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
  • increased adiponectin level
    • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
  • increased circulating leptin level
    • when fed a high fat diet   (MGI Ref ID J:126512)
  • increased susceptibility to diet-induced obesity
    • when fed a high fat diet, mice exhibit a mildly enhanced weight gain compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
    • at 18 to 34 weeks, mice fed a high fat diet exhibit a 13% increase in body weight compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
  • adipose tissue phenotype
  • abnormal epididymal fat pad morphology
    • when fed a high fat diet, macrophage infiltration of the epididymal fat pad is reduced compared to in similarly treated wild-type mice   (MGI Ref ID J:110277)
  • abnormal gonadal fat pad morphology
    • mice fed a high fat diet exhibit a mild increase in macrophage infiltration of adipose tissue compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
    • however, macrophage numbers in subcutaneous fat when fed a standard diet is normal   (MGI Ref ID J:126512)
  • decreased fat cell size
    • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
  • increased percent body fat
    • 15% in mice fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
  • increased total fat pad weight
    • when fed a high fat diet   (MGI Ref ID J:126512)
  • liver/biliary system phenotype
  • decreased susceptibility to hepatic steatosis
    • when mice are fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:110277)
  • growth/size/body phenotype
  • decreased body weight
    • slightly when mice are fed a standard diet   (MGI Ref ID J:126512)
  • increased percent body fat
    • 15% in mice fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
  • increased susceptibility to diet-induced obesity
    • when fed a high fat diet, mice exhibit a mildly enhanced weight gain compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
    • at 18 to 34 weeks, mice fed a high fat diet exhibit a 13% increase in body weight compared with similarly treated wild-type mice   (MGI Ref ID J:126512)
  • nervous system phenotype
  • abnormal microglial cell physiology
    • mice treated with kainate acid exhibit decreased microglial accumulation compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
  • decreased susceptibility to neuronal excitotoxicity
    • mice treated with kainate acid exhibit decreased microglial accumulation and reduced neurodegeneration in the CA1 and CA3 pyramidal neurons compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
  • immune system phenotype
  • abnormal microglial cell physiology
    • mice treated with kainate acid exhibit decreased microglial accumulation compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
  • cellular phenotype
  • decreased susceptibility to neuronal excitotoxicity
    • mice treated with kainate acid exhibit decreased microglial accumulation and reduced neurodegeneration in the CA1 and CA3 pyramidal neurons compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
  • hematopoietic system phenotype
  • abnormal microglial cell physiology
    • mice treated with kainate acid exhibit decreased microglial accumulation compared with similarly treated wild-type mice   (MGI Ref ID J:141739)

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

Ccl2tm1Rol/Ccl2tm1Rol

        involves: 129S4/SvJae * 129X1/SvJ * C57BL/6
  • immune system phenotype
  • abnormal monocyte morphology
    • mutants are unable to recruit monocytes 72 hours after intraperitoneal thioglycollate administration despite normal numbers of circulating leukocytes and macrophages   (MGI Ref ID J:45920)
  • decreased interferon-gamma secretion
    • IFN-gamma secretion is 59% lower in mutant splenocytes   (MGI Ref ID J:45920)
  • decreased interleukin-4 secretion
    • IL-4 production is reduced in splenocytes   (MGI Ref ID J:45920)
  • decreased interleukin-5 secretion
    • IL-5 production is reduced in splenocytes   (MGI Ref ID J:45920)
  • decreased susceptibility to type IV hypersensitivity reaction
    • accumulation of F4/80+ monocytes in delayed-type hypersensitivity lesions is impaired, although the swelling response is normal   (MGI Ref ID J:45920)
    • development of secondary pulmonary granulomata in response to Schistosoma mansoni eggs in blunted   (MGI Ref ID J:45920)
  • impaired macrophage chemotaxis
    • impaired macrophage recruitment following intraperitoneal thioglycollate injection   (MGI Ref ID J:45920)
  • hematopoietic system phenotype
  • abnormal monocyte morphology
    • mutants are unable to recruit monocytes 72 hours after intraperitoneal thioglycollate administration despite normal numbers of circulating leukocytes and macrophages   (MGI Ref ID J:45920)
  • impaired macrophage chemotaxis
    • impaired macrophage recruitment following intraperitoneal thioglycollate injection   (MGI Ref ID J:45920)
  • cellular phenotype
  • impaired macrophage chemotaxis
    • impaired macrophage recruitment following intraperitoneal thioglycollate injection   (MGI Ref ID J:45920)

Ccl2tm1Rol/Ccl2tm1Rol

        involves: 129S4/SvJae * C57BL/6
  • mortality/aging
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • DNBS-treated mice do not exhibit an increase in mortality compared with similarly treated wild-type mice   (MGI Ref ID J:116878)
  • cardiovascular system phenotype
  • abnormal heart left ventricle morphology
    • following myocardial infarction, mice exhibit lower left ventricle end diastolic diameter compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
  • abnormal physiological neovascularization
    • ischemic capillary density relative to nonischemic density 30% lower than in controls   (MGI Ref ID J:107646)
    • poor recovery of blood flow after ischemia   (MGI Ref ID J:107646)
  • altered response to myocardial infarction
    • following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • following myocardial infarction, mice exhibit persistence of dead cardiomyocytes and delayed replacement with granulation compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • following myocardial infarction, mice exhibit decreased myofibroblast infiltration 3 days after reperfusion compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • following myocardial infarction, mice exhibit lower left ventricle end diastolic diameter compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • however, mice exhibit normal macrophage density, infarct size, and angiogenesis following myocardial infarction   (MGI Ref ID J:108533)
  • immune system phenotype
  • abnormal T cell physiology
    • following DNBS treatment, infiltration of CD3+ T cells in colonic tissue is decreased compared to in wild-type mice   (MGI Ref ID J:116878)
  • abnormal macrophage chemotaxis
    • in colonic tissue following DNBS treatment   (MGI Ref ID J:116878)
    • impaired macrophage chemotaxis
      • following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
      • however, macrophage density is normal 3 to 7 days following myocardial infarction   (MGI Ref ID J:108533)
  • decreased interferon-gamma secretion
    • in ConA-treated splenic cells of DNBS-treated mice   (MGI Ref ID J:116878)
  • decreased interleukin-1 beta secretion
    • in colonic tissue following DNBS treatment   (MGI Ref ID J:116878)
  • decreased interleukin-12b secretion
    • in colonic tissue following DNBS treatment   (MGI Ref ID J:116878)
  • decreased susceptibility to induced colitis
    • DNBS-treated mice exhibit reduced mucosal damage; less thickening of the colonic wall; less goblet cell depletion; fewer adhesions; reduced macrophage and CD3+ T cell infiltration; reduced IL1beta, IL12p40, and ConA-stimulated production; reduced numbers of 5-HT-expressing enterochromaffin cells, and no increase in mortality compared with similarly treated wild-type mice   (MGI Ref ID J:116878)
  • tumorigenesis
  • decreased incidence of tumors by chemical induction
    • DMBA and TPA-treated mice exhibit 50% fewer skin tumors than similarly treated wild-type mice   (MGI Ref ID J:56068)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • following myocardial infarction, mice exhibit persistence of dead cardiomyocytes and delayed replacement with granulation compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • following myocardial infarction, mice exhibit decreased myofibroblast infiltration 3 days after reperfusion compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • following myocardial infarction, mice exhibit lower left ventricle end diastolic diameter compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
    • however, mice exhibit normal macrophage density, infarct size, and angiogenesis following myocardial infarction   (MGI Ref ID J:108533)
  • decreased incidence of tumors by chemical induction
    • DMBA and TPA-treated mice exhibit 50% fewer skin tumors than similarly treated wild-type mice   (MGI Ref ID J:56068)
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • DNBS-treated mice do not exhibit an increase in mortality compared with similarly treated wild-type mice   (MGI Ref ID J:116878)
  • digestive/alimentary phenotype
  • decreased susceptibility to induced colitis
    • DNBS-treated mice exhibit reduced mucosal damage; less thickening of the colonic wall; less goblet cell depletion; fewer adhesions; reduced macrophage and CD3+ T cell infiltration; reduced IL1beta, IL12p40, and ConA-stimulated production; reduced numbers of 5-HT-expressing enterochromaffin cells, and no increase in mortality compared with similarly treated wild-type mice   (MGI Ref ID J:116878)
  • cellular phenotype
  • abnormal macrophage chemotaxis
    • in colonic tissue following DNBS treatment   (MGI Ref ID J:116878)
    • impaired macrophage chemotaxis
      • following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
      • however, macrophage density is normal 3 to 7 days following myocardial infarction   (MGI Ref ID J:108533)
  • hematopoietic system phenotype
  • abnormal T cell physiology
    • following DNBS treatment, infiltration of CD3+ T cells in colonic tissue is decreased compared to in wild-type mice   (MGI Ref ID J:116878)
  • abnormal macrophage chemotaxis
    • in colonic tissue following DNBS treatment   (MGI Ref ID J:116878)
    • impaired macrophage chemotaxis
      • following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice   (MGI Ref ID J:108533)
      • however, macrophage density is normal 3 to 7 days following myocardial infarction   (MGI Ref ID J:108533)

Ccl2tm1Rol/Ccl2tm1Rol

        involves: 129S4/SvJae
  • mortality/aging
  • increased susceptibility to infection induced morbidity/mortality
    • following infection with the parasite T. cruzi, mice exhibit earlier and increased lethality compared with similarly treated wild-type mice   (MGI Ref ID J:155025)
  • immune system phenotype
  • abnormal macrophage physiology
    • activated macrophage clear trypomastigotes less efficiently than wild-type cells   (MGI Ref ID J:155025)
    • impaired macrophage chemotaxis
      • to the lungs of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • abnormal monocyte morphology
    • 7/4bri and 7/4dim cells are decreased in blood by 50%   (MGI Ref ID J:121281)
    • intraperitoneal thioglycollate challenge leads to an increase in 7/4bri cells   (MGI Ref ID J:121281)
  • decreased inflammatory response
    • following infection with T. cruzi, mice exhibit decreased focal infiltration of leukocytes (recruitment of activated CD8+ cells and monocytes) in the heart and liver compared with similarly treated wild-type mice   (MGI Ref ID J:155025)
  • decreased lymphocyte cell number
    • in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • decreased macrophage cell number
    • in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • increased circulating interferon-gamma level
    • following infection with T. cruzi   (MGI Ref ID J:155025)
  • increased circulating interleukin-10 level
    • following infection with T. cruzi   (MGI Ref ID J:155025)
  • increased circulating tumor necrosis factor level
    • following infection with T. cruzi   (MGI Ref ID J:155025)
  • increased susceptibility to infection induced morbidity/mortality
    • following infection with the parasite T. cruzi, mice exhibit earlier and increased lethality compared with similarly treated wild-type mice   (MGI Ref ID J:155025)
  • increased susceptibility to parasitic infection
    • mice infected with T. cruzi exhibit increased mortality; prostration, vasodilation and rough hair close to the time of death; increased plasma TNF, IFN-gamma, and IL10 levels; increased tissue parasitic burden with reduced focal leukocyte infiltration; and unlike in similarly treated wild-type mice   (MGI Ref ID J:155025)
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • mice are protected from bleomycin-induced lung fibrosis with fewer recruited alveolar macrophages and lymphocytes in the lungs compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • increased circulating interferon-gamma level
    • following infection with T. cruzi   (MGI Ref ID J:155025)
  • increased circulating interleukin-10 level
    • following infection with T. cruzi   (MGI Ref ID J:155025)
  • increased circulating tumor necrosis factor level
    • following infection with T. cruzi   (MGI Ref ID J:155025)
  • hematopoietic system phenotype
  • abnormal macrophage physiology
    • activated macrophage clear trypomastigotes less efficiently than wild-type cells   (MGI Ref ID J:155025)
    • impaired macrophage chemotaxis
      • to the lungs of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • abnormal monocyte morphology
    • 7/4bri and 7/4dim cells are decreased in blood by 50%   (MGI Ref ID J:121281)
    • intraperitoneal thioglycollate challenge leads to an increase in 7/4bri cells   (MGI Ref ID J:121281)
  • decreased lymphocyte cell number
    • in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • decreased macrophage cell number
    • in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • behavior/neurological phenotype
  • abnormal posture
    • following infection with T. cruzi, mice exhibit prostration as they near death unlike similarly treated wild-type mice   (MGI Ref ID J:155025)
  • cardiovascular system phenotype
  • increased vasodilation
    • following infection with T. cruzi as mice near death   (MGI Ref ID J:155025)
  • muscle phenotype
  • increased vasodilation
    • following infection with T. cruzi as mice near death   (MGI Ref ID J:155025)
  • cellular phenotype
  • impaired macrophage chemotaxis
    • to the lungs of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)

Ccl2tm1Rol/Ccl2tm1Rol

        SJL.129S4-Ccl2tm1Rol
  • immune system phenotype
  • decreased susceptibility to experimental autoimmune encephalomyelitis
    • homozygotes exhibit attenuated severity of PLP-induced EAE and reduced number of relapses compared to wild-type   (MGI Ref ID J:68145)

Ccl2tm1Rol/Ccl2tm1Rol

        (129S4/SvJae x C57BL/6)F1
  • hematopoietic system phenotype
  • decreased macrophage cell number
    • following induction of nephrotoxic serum nephritis, mice exhibit reduced macrophage accumulation in the interstitium and adjacent to damaged tubules compared with similarly treated wild-type mice   (MGI Ref ID J:119615)
    • however, the number macrophages in the glomeruli is normal following induction of nephrotoxic serum nephritis   (MGI Ref ID J:119615)
  • homeostasis/metabolism phenotype
  • abnormal response to injury
    • following induction of nephrotoxic serum nephritis, mice exhibit reduced tubule damage and macrophage accumulation compared with similarly treated wild-type mice   (MGI Ref ID J:119615)
    • however, mice exhibit normal IgG/C3 deposition, proteinuria, glomerular macrophage accumulation, and glomerular damage following induction of nephrotoxic serum nephritis   (MGI Ref ID J:119615)
  • immune system phenotype
  • decreased macrophage cell number
    • following induction of nephrotoxic serum nephritis, mice exhibit reduced macrophage accumulation in the interstitium and adjacent to damaged tubules compared with similarly treated wild-type mice   (MGI Ref ID J:119615)
    • however, the number macrophages in the glomeruli is normal following induction of nephrotoxic serum nephritis   (MGI Ref ID J:119615)

Ccl2tm1Rol/Ccl2tm1Rol

        involves: 129S4/SvJae * C57BL/6 * SJL
  • homeostasis/metabolism phenotype
  • delayed wound healing
    • at day 3 following injury, re-epithelialization is delayed with decreased vascular density at the injury compared to in similarly treated wild-type mice   (MGI Ref ID J:70862)
    • complete wound healing takes twice as long as in wild-type mice   (MGI Ref ID J:70862)
    • however, macrophage accumulation at the site of injury is normal   (MGI Ref ID J:70862)
  • cardiovascular system phenotype
  • decreased angiogenesis
    • during wound healing   (MGI Ref ID J:70862)
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Research Applications
This mouse can be used to support research in many areas including:

Ccl2tm1Rol related

Cancer Research
Growth Factors/Receptors/Cytokines

Immunology, Inflammation and Autoimmunity Research
Inflammation

Internal/Organ Research
Wound Healing
      delayed/impaired

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ccl2tm1Rol
Allele Name targeted mutation 1, Barrett J Rollins
Allele Type Targeted (Null/Knockout)
Common Name(s) (MCP)1-; CCL2-; CCL2KO; MCP-1-; MCP-1KO; Scya2-;
Mutation Made By Barrett Rollins,   Dana-Farber Cancer Inst, Harvard Med Sch
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Ccl2, chemokine (C-C motif) ligand 2
Chromosome 11
Gene Common Name(s) AI323594; CKb10; HC11; MCAF; MCP-1; MCP-4; MCP1; NCC-1; NCC1; SCYA13; SCYL1; SMC-CF; Scya2; Sigje; expressed sequence AI323594; monocyte chemoattractant protein-1; monocyte chemotactic protein; small inducible cytokine A2; small inducible gene JE;
General Note Phenotypic Similarity to Human Syndrome: Age-related macular degeneration (J:126935, J:147328).

Phenotypic Similarity to Human Syndrome: Macular Degeneration, Geographic Atrophy, Dry Type (J:200877)

Molecular Note A small deletion and an in frame stop codon were created in exon 1. A PGK-neomycin resistance cassette was also inserted into exon 2. Secreted protein was not detected in stimulated peritoneal macrophages from homozygous mutant mice. [MGI Ref ID J:45920]

Genotyping

Genotyping Information

Genotyping Protocols

Ccl2tm1Rol, Melt Curve Analysis
Crb1rd8End Point, End Point Analysis
Ccl2tm1Rol, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Ccl2tm1Rol related

Abonia JP; Austen KF; Rollins BJ; Joshi SK; Flavell RA; Kuziel WA; Koni PA; Gurish MF. 2005. Constitutive homing of mast cell progenitors to the intestine depends on autologous expression of the chemokine receptor CXCR2. Blood 105(11):4308-13. [PubMed: 15705791]  [MGI Ref ID J:98967]

Akiyama K; Chen C; Wang D; Xu X; Qu C; Yamaza T; Cai T; Chen W; Sun L; Shi S. 2012. Mesenchymal-stem-cell-induced immunoregulation involves FAS-ligand-/FAS-mediated T cell apoptosis. Cell Stem Cell 10(5):544-55. [PubMed: 22542159]  [MGI Ref ID J:185809]

Amano SU; Cohen JL; Vangala P; Tencerova M; Nicoloro SM; Yawe JC; Shen Y; Czech MP; Aouadi M. 2014. Local proliferation of macrophages contributes to obesity-associated adipose tissue inflammation. Cell Metab 19(1):162-71. [PubMed: 24374218]  [MGI Ref ID J:210550]

Ambati J; Anand A; Fernandez S; Sakurai E; Lynn BC; Kuziel WA; Rollins BJ; Ambati BK. 2003. An animal model of age-related macular degeneration in senescent Ccl-2- or Ccr-2-deficient mice. Nat Med 9(11):1390-7. [PubMed: 14566334]  [MGI Ref ID J:147328]

Aoki T; Kataoka H; Ishibashi R; Nozaki K; Egashira K; Hashimoto N. 2009. Impact of monocyte chemoattractant protein-1 deficiency on cerebral aneurysm formation. Stroke 40(3):942-51. [PubMed: 19164781]  [MGI Ref ID J:169983]

Babcock AA; Toft-Hansen H; Owens T. 2008. Signaling through MyD88 regulates leukocyte recruitment after brain injury. J Immunol 181(9):6481-90. [PubMed: 18941239]  [MGI Ref ID J:140719]

Bai Y; Liu R; Huang D; La Cava A; Tang YY; Iwakura Y; Campagnolo DI; Vollmer TL; Ransohoff RM; Shi FD. 2008. CCL2 recruitment of IL-6-producing CD11b(+) monocytes to the draining lymph nodes during the initiation of Th17-dependent B cell-mediated autoimmunity. Eur J Immunol 38(7):1877-88. [PubMed: 18581322]  [MGI Ref ID J:137386]

Balamayooran G; Batra S; Balamayooran T; Cai S; Jeyaseelan S. 2011. Monocyte Chemoattractant Protein 1 Regulates Pulmonary Host Defense via Neutrophil Recruitment during Escherichia coli Infection. Infect Immun 79(7):2567-77. [PubMed: 21518788]  [MGI Ref ID J:173485]

Balamayooran G; Batra S; Theivanthiran B; Cai S; Pacher P; Jeyaseelan S. 2012. Intrapulmonary G-CSF Rescues Neutrophil Recruitment to the Lung and Neutrophil Release to Blood in Gram-Negative Bacterial Infection in MCP-1-/- Mice. J Immunol 189(12):5849-59. [PubMed: 23129755]  [MGI Ref ID J:190969]

Bandukwala HS; Clay BS; Tong J; Mody PD; Cannon JL; Shilling RA; Verbeek JS; Weinstock JV; Solway J; Sperling AI. 2007. Signaling through Fc gamma RIII is required for optimal T helper type (Th)2 responses and Th2-mediated airway inflammation. J Exp Med 204(8):1875-89. [PubMed: 17664287]  [MGI Ref ID J:125951]

Baran CP; Opalek JM; McMaken S; Newland CA; O'Brien JM Jr; Hunter MG; Bringardner BD; Monick MM; Brigstock DR; Stromberg PC; Hunninghake GW; Marsh CB. 2007. Important roles for macrophage colony-stimulating factor, CC chemokine ligand 2, and mononuclear phagocytes in the pathogenesis of pulmonary fibrosis. Am J Respir Crit Care Med 176(1):78-89. [PubMed: 17431224]  [MGI Ref ID J:147697]

Barlic J; Murphy PM. 2007. Chemokine regulation of atherosclerosis. J Leukoc Biol 82(2):226-36. [PubMed: 17329566]  [MGI Ref ID J:123530]

Basu RK; Donaworth E; Wheeler DS; Devarajan P; Wong HR. 2011. Antecedent acute kidney injury worsens subsequent endotoxin-induced lung inflammation in a two-hit mouse model. Am J Physiol Renal Physiol 301(3):F597-604. [PubMed: 21677147]  [MGI Ref ID J:175640]

Behm CZ; Kaufmann BA; Carr C; Lankford M; Sanders JM; Rose CE; Kaul S; Lindner JR. 2008. Molecular imaging of endothelial vascular cell adhesion molecule-1 expression and inflammatory cell recruitment during vasculogenesis and ischemia-mediated arteriogenesis. Circulation 117(22):2902-11. [PubMed: 18506006]  [MGI Ref ID J:155083]

Birkner K; Steiner B; Rinkler C; Kern Y; Aichele P; Bogdan C; von Loewenich FD. 2008. The elimination of Anaplasma phagocytophilum requires CD4(+) T cells, but is independent of Th1 cytokines and a wide spectrum of effector mechanisms. Eur J Immunol 38(12):3395-3410. [PubMed: 19039769]  [MGI Ref ID J:141369]

Bitsaktsis C; Winslow G. 2006. Fatal recall responses mediated by CD8 T cells during intracellular bacterial challenge infection. J Immunol 177(7):4644-51. [PubMed: 16982903]  [MGI Ref ID J:139316]

Blednov YA; Bergeson SE; Walker D; Ferreira VM; Kuziel WA; Harris RA. 2005. Perturbation of chemokine networks by gene deletion alters the reinforcing actions of ethanol. Behav Brain Res 165(1):110-25. [PubMed: 16105698]  [MGI Ref ID J:102583]

Buczynski BW; Yee M; Paige Lawrence B; O'Reilly MA. 2012. Lung development and the host response to influenza A virus are altered by different doses of neonatal oxygen in mice. Am J Physiol Lung Cell Mol Physiol 302(10):L1078-87. [PubMed: 22408042]  [MGI Ref ID J:190174]

Cao X; Liu M; Tuo J; Shen D; Chan CC. 2010. The effects of quercetin in cultured human RPE cells under oxidative stress and in Ccl2/Cx3cr1 double deficient mice. Exp Eye Res 91(1):15-25. [PubMed: 20361964]  [MGI Ref ID J:164130]

Capoccia BJ; Gregory AD; Link DC. 2008. Recruitment of the inflammatory subset of monocytes to sites of ischemia induces angiogenesis in a monocyte chemoattractant protein-1-dependent fashion. J Leukoc Biol 84(3):760-8. [PubMed: 18550788]  [MGI Ref ID J:138153]

Chan CC; Ross RJ; Shen D; Ding X; Majumdar Z; Bojanowski CM; Zhou M; Salem N Jr; Bonner R; Tuo J. 2008. Ccl2/Cx3cr1-deficient mice: an animal model for age-related macular degeneration. Ophthalmic Res 40(3-4):124-8. [PubMed: 18421225]  [MGI Ref ID J:190363]

Chen M; Forrester JV; Xu H. 2011. Dysregulation in retinal para-inflammation and age-related retinal degeneration in CCL2 or CCR2 deficient mice. PLoS One 6(8):e22818. [PubMed: 21850237]  [MGI Ref ID J:176516]

Chen M; Hombrebueno JR; Luo C; Penalva R; Zhao J; Colhoun L; Pandi SP; Forrester JV; Xu H. 2013. Age- and light-dependent development of localised retinal atrophy in CCL2(-/-)CX3CR1(GFP/GFP) mice. PLoS One 8(4):e61381. [PubMed: 23637822]  [MGI Ref ID J:200877]

Chen M; Zhao J; Luo C; Pandi SP; Penalva RG; Fitzgerald DC; Xu H. 2012. Para-inflammation-mediated retinal recruitment of bone marrow-derived myeloid cells following whole-body irradiation is CCL2 dependent. Glia 60(5):833-42. [PubMed: 22362506]  [MGI Ref ID J:181628]

Cho Y; Cao X; Shen D; Tuo J; Parver LM; Rickles FR; Chan CC. 2011. Evidence for enhanced tissue factor expression in age-related macular degeneration. Lab Invest 91(4):519-26. [PubMed: 21042291]  [MGI Ref ID J:170290]

Chow FY; Nikolic-Paterson DJ; Ozols E; Atkins RC; Rollin BJ; Tesch GH. 2006. Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice. Kidney Int 69(1):73-80. [PubMed: 16374426]  [MGI Ref ID J:136515]

Cochain C; Rodero MP; Vilar J; Recalde A; Richart AL; Loinard C; Zouggari Y; Guerin C; Duriez M; Combadiere B; Poupel L; Levy BI; Mallat Z; Combadiere C; Silvestre JS. 2010. Regulation of monocyte subset systemic levels by distinct chemokine receptors controls post-ischaemic neovascularization. Cardiovasc Res 88(1):186-95. [PubMed: 20501509]  [MGI Ref ID J:182115]

Collington SJ; Hallgren J; Pease JE; Jones TG; Rollins BJ; Westwick J; Austen KF; Williams TJ; Gurish MF; Weller CL. 2010. The role of the CCL2/CCR2 axis in mouse mast cell migration in vitro and in vivo. J Immunol 184(11):6114-23. [PubMed: 20427772]  [MGI Ref ID J:161229]

Conrad SM; Strauss-Ayali D; Field AE; Mack M; Mosser DM. 2007. Leishmania-derived murine monocyte chemoattractant protein 1 enhances the recruitment of a restrictive population of CC chemokine receptor 2-positive macrophages. Infect Immun 75(2):653-65. [PubMed: 17088347]  [MGI Ref ID J:117724]

D'Avila H; Melo RC; Parreira GG; Werneck-Barroso E; Castro-Faria-Neto HC; Bozza PT. 2006. Mycobacterium bovis bacillus Calmette-Guerin induces TLR2-mediated formation of lipid bodies: intracellular domains for eicosanoid synthesis in vivo. J Immunol 176(5):3087-97. [PubMed: 16493068]  [MGI Ref ID J:129415]

D'Mello C ; Le T ; Swain MG. 2009. Cerebral microglia recruit monocytes into the brain in response to tumor necrosis factoralpha signaling during peripheral organ inflammation. J Neurosci 29(7):2089-102. [PubMed: 19228962]  [MGI Ref ID J:146590]

Daley-Bauer LP; Wynn GM; Mocarski ES. 2012. Cytomegalovirus impairs antiviral CD8+ T cell immunity by recruiting inflammatory monocytes. Immunity 37(1):122-33. [PubMed: 22840843]  [MGI Ref ID J:187387]

Davies MH; Stempel AJ; Powers MR. 2008. MCP-1 deficiency delays regression of pathologic retinal neovascularization in a model of ischemic retinopathy. Invest Ophthalmol Vis Sci 49(9):4195-202. [PubMed: 18487365]  [MGI Ref ID J:141687]

DePaolo RW; Rollins BJ; Kuziel W; Karpus WJ. 2003. CC chemokine ligand 2 and its receptor regulate mucosal production of IL-12 and TGF-beta in high dose oral tolerance. J Immunol 171(7):3560-7. [PubMed: 14500652]  [MGI Ref ID J:85628]

DeSchoolmeester ML; Little MC; Rollins BJ; Else KJ. 2003. Absence of CC Chemokine Ligand 2 Results in an Altered Th1/Th2 Cytokine Balance and Failure to Expel Trichuris muris Infection. J Immunol 170(9):4693-700. [PubMed: 12707348]  [MGI Ref ID J:82997]

Deng GM; Liu L; Kyttaris VC; Tsokos GC. 2010. Lupus serum IgG induces skin inflammation through the TNFR1 signaling pathway. J Immunol 184(12):7154-61. [PubMed: 20483718]  [MGI Ref ID J:161156]

Dessing MC; de Vos AF; Florquin S; van der Poll T. 2006. Monocyte chemoattractant protein 1 does not contribute to protective immunity against pneumococcal pneumonia. Infect Immun 74(12):7021-3. [PubMed: 16982835]  [MGI Ref ID J:115915]

Dessing MC; van der Sluijs KF; Florquin S; van der Poll T. 2007. Monocyte chemoattractant protein 1 contributes to an adequate immune response in influenza pneumonia. Clin Immunol 125(3):328-36. [PubMed: 17827068]  [MGI Ref ID J:128006]

Dewald O; Zymek P; Winkelmann K; Koerting A; Ren G; Abou-Khamis T; Michael LH; Rollins BJ; Entman ML; Frangogiannis NG. 2005. CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts. Circ Res 96(8):881-9. [PubMed: 15774854]  [MGI Ref ID J:108533]

Ding X; Patel M; Shen D; Herzlich AA; Cao X; Villasmil R; Klupsch K; Tuo J; Downward J; Chan CC. 2009. Enhanced HtrA2/Omi expression in oxidative injury to retinal pigment epithelial cells and murine models of neurodegeneration. Invest Ophthalmol Vis Sci 50(10):4957-66. [PubMed: 19443712]  [MGI Ref ID J:154545]

Dogan RN; Elhofy A; Karpus WJ. 2008. Production of CCL2 by central nervous system cells regulates development of murine experimental autoimmune encephalomyelitis through the recruitment of TNF- and iNOS-expressing macrophages and myeloid dendritic cells. J Immunol 180(11):7376-84. [PubMed: 18490737]  [MGI Ref ID J:136335]

Drobits B; Holcmann M; Amberg N; Swiecki M; Grundtner R; Hammer M; Colonna M; Sibilia M. 2012. Imiquimod clears tumors in mice independent of adaptive immunity by converting pDCs into tumor-killing effector cells. J Clin Invest 122(2):575-85. [PubMed: 22251703]  [MGI Ref ID J:184497]

Dunay IR; Damatta RA; Fux B; Presti R; Greco S; Colonna M; Sibley LD. 2008. Gr1(+) Inflammatory Monocytes Are Required for Mucosal Resistance to the Pathogen Toxoplasma gondii. Immunity 29(2):306-17. [PubMed: 18691912]  [MGI Ref ID J:139568]

Eguchi K; Manabe I; Oishi-Tanaka Y; Ohsugi M; Kono N; Ogata F; Yagi N; Ohto U; Kimoto M; Miyake K; Tobe K; Arai H; Kadowaki T; Nagai R. 2012. Saturated fatty acid and TLR signaling link beta cell dysfunction and islet inflammation. Cell Metab 15(4):518-33. [PubMed: 22465073]  [MGI Ref ID J:184209]

Felton LM; Cunningham C; Rankine EL; Waters S; Boche D; Perry VH. 2005. MCP-1 and murine prion disease: separation of early behavioural dysfunction from overt clinical disease. Neurobiol Dis 20(2):283-95. [PubMed: 15886005]  [MGI Ref ID J:102784]

Ferreira AM; Takagawa S; Fresco R; Zhu X; Varga J; DiPietro LA. 2006. Diminished induction of skin fibrosis in mice with MCP-1 deficiency. J Invest Dermatol 126(8):1900-8. [PubMed: 16691201]  [MGI Ref ID J:110695]

Fischer S; Kleinschnitz C; Muller M; Kobsar I; Ip CW; Rollins B; Martini R. 2008. Monocyte chemoattractant protein-1 is a pathogenic component in a model for a hereditary peripheral neuropathy. Mol Cell Neurosci 37(2):359-66. [PubMed: 18326085]  [MGI Ref ID J:133028]

Frangogiannis NG; Dewald O; Xia Y; Ren G; Haudek S; Leucker T; Kraemer D; Taffet G; Rollins BJ; Entman ML. 2007. Critical role of monocyte chemoattractant protein-1/CC chemokine ligand 2 in the pathogenesis of ischemic cardiomyopathy. Circulation 115(5):584-92. [PubMed: 17283277]  [MGI Ref ID J:130611]

Ge S; Song L; Serwanski DR; Kuziel WA; Pachter JS. 2008. Transcellular transport of CCL2 across brain microvascular endothelial cells. J Neurochem 104(5):1219-32. [PubMed: 18289346]  [MGI Ref ID J:131712]

Godefroy D; Gosselin RD; Yasutake A; Fujimura M; Combadiere C; Maury-Brachet R; Laclau M; Rakwal R; Melik-Parsadaniantz S; Bourdineaud JP; Rostene W. 2012. The chemokine CCL2 protects against methylmercury neurotoxicity. Toxicol Sci 125(1):209-18. [PubMed: 21976372]  [MGI Ref ID J:183564]

Gonnella PA; Kodali D; Weiner HL. 2003. Induction of low dose oral tolerance in monocyte chemoattractant protein-1- and CCR2-deficient mice. J Immunol 170(5):2316-22. [PubMed: 12594253]  [MGI Ref ID J:82016]

Goodyear A; Jones A; Troyer R; Bielefeldt-Ohmann H; Dow S. 2010. Critical protective role for MCP-1 in pneumonic Burkholderia mallei infection. J Immunol 184(3):1445-54. [PubMed: 20042590]  [MGI Ref ID J:159498]

Graves DT; Alsulaimani F; Ding Y; Marks SC Jr. 2002. Developmentally regulated monocyte recruitment and bone resorption are modulated by functional deletion of the monocytic chemoattractant protein-1 gene. Bone 31(2):282-7. [PubMed: 12151080]  [MGI Ref ID J:109290]

Gregory JL; Morand EF; McKeown SJ; Ralph JA; Hall P; Yang YH; McColl SR; Hickey MJ. 2006. Macrophage migration inhibitory factor induces macrophage recruitment via CC chemokine ligand 2. J Immunol 177(11):8072-9. [PubMed: 17114481]  [MGI Ref ID J:140686]

Groh J; Heinl K; Kohl B; Wessig C; Greeske J; Fischer S; Martini R. 2010. Attenuation of MCP-1/CCL2 expression ameliorates neuropathy in a mouse model for Charcot-Marie-Tooth 1X. Hum Mol Genet 19(18):3530-43. [PubMed: 20591826]  [MGI Ref ID J:163173]

Gu L; Okada Y; Clinton SK; Gerard C; Sukhova GK; Libby P; Rollins BJ. 1998. Absence of monocyte chemoattractant protein-1 reduces atherosclerosis in low density lipoprotein receptor-deficient mice. Mol Cell 2(2):275-81. [PubMed: 9734366]  [MGI Ref ID J:75837]

Gu L; Tseng S; Horner RM; Tam C; Loda M; Rollins BJ. 2000. Control of TH2 polarization by the chemokine monocyte chemoattractant protein-1. Nature 404(6776):407-11. [PubMed: 10746730]  [MGI Ref ID J:61420]

Held KS; Chen BP; Kuziel WA; Rollins BJ; Lane TE. 2004. Differential roles of CCL2 and CCR2 in host defense to coronavirus infection. Virology 329(2):251-60. [PubMed: 15518805]  [MGI Ref ID J:102446]

Henderson RB; Hobbs JA; Mathies M; Hogg N. 2003. Rapid recruitment of inflammatory monocytes is independent of neutrophil migration. Blood 102(1):328-35. [PubMed: 12623845]  [MGI Ref ID J:115516]

Hokeness KL; Kuziel WA; Biron CA; Salazar-Mather TP. 2005. Monocyte chemoattractant protein-1 and CCR2 interactions are required for IFN-alpha/beta-induced inflammatory responses and antiviral defense in liver. J Immunol 174(3):1549-56. [PubMed: 15661915]  [MGI Ref ID J:96407]

Huang D; Wang J; Kivisakk P; Rollins BJ; Ransohoff RM. 2001. Absence of monocyte chemoattractant protein 1 in mice leads to decreased local macrophage recruitment and antigen-specific t helper cell type 1 immune response in experimental autoimmune encephalomyelitis. J Exp Med 193(6):713-26. [PubMed: 11257138]  [MGI Ref ID J:68145]

Inouye KE; Shi H; Howard JK; Daly CH; Lord GM; Rollins BJ; Flier JS. 2007. Absence of CC chemokine ligand 2 does not limit obesity-associated infiltration of macrophages into adipose tissue. Diabetes 56(9):2242-50. [PubMed: 17473219]  [MGI Ref ID J:126512]

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Takahashi M; Galligan C; Tessarollo L; Yoshimura T. 2009. Monocyte chemoattractant protein-1 (MCP-1), not MCP-3, is the primary chemokine required for monocyte recruitment in mouse peritonitis induced with thioglycollate or zymosan A. J Immunol 183(5):3463-71. [PubMed: 19641140]  [MGI Ref ID J:151874]

Takaoka M; Suzuki H; Shioda S; Sekikawa K; Saito Y; Nagai R; Sata M. 2010. Endovascular injury induces rapid phenotypic changes in perivascular adipose tissue. Arterioscler Thromb Vasc Biol 30(8):1576-82. [PubMed: 20489168]  [MGI Ref ID J:179555]

Takeda A; Baffi JZ; Kleinman ME; Cho WG; Nozaki M; Yamada K; Kaneko H; Albuquerque RJ; Dridi S; Saito K; Raisler BJ; Budd SJ; Geisen P; Munitz A; Ambati BK; Green MG; Ishibashi T; Wright JD; Humbles AA; Gerard CJ; Ogura Y; Pan Y; Smith JR; Grisanti S; Hartnett ME; Rothenberg ME; Ambati J. 2009. CCR3 is a target for age-related macular degeneration diagnosis and therapy. Nature 460(7252):225-30. [PubMed: 19525930]  [MGI Ref ID J:150352]

Tarabra E; Giunti S; Barutta F; Salvidio G; Burt D; Deferrari G; Gambino R; Vergola D; Pinach S; Perin PC; Camussi G; Gruden G. 2009. Effect of the monocyte chemoattractant protein-1/CC chemokine receptor 2 system on nephrin expression in streptozotocin-treated mice and human cultured podocytes. Diabetes 58(9):2109-18. [PubMed: 19587356]  [MGI Ref ID J:154400]

Tesch GH; Schwarting A; Kinoshita K; Lan HY; Rollins BJ; Kelley VR. 1999. Monocyte chemoattractant protein-1 promotes macrophage-mediated tubular injury, but not glomerular injury, in nephrotoxic serum nephritis. J Clin Invest 103(1):73-80. [PubMed: 9884336]  [MGI Ref ID J:119615]

Tsou CL; Peters W; Si Y; Slaymaker S; Aslanian AM; Weisberg SP; Mack M; Charo IF. 2007. Critical roles for CCR2 and MCP-3 in monocyte mobilization from bone marrow and recruitment to inflammatory sites. J Clin Invest 117(4):902-9. [PubMed: 17364026]  [MGI Ref ID J:121281]

Tuaillon N; Shen DF; Berger RB; Lu B; Rollins BJ; Chan CC. 2002. MCP-1 expression in endotoxin-induced uveitis. Invest Ophthalmol Vis Sci 43(5):1493-8. [PubMed: 11980865]  [MGI Ref ID J:119434]

Tuo J; Bojanowski CM; Zhou M; Shen D; Ross RJ; Rosenberg KI; Cameron DJ; Yin C; Kowalak JA; Zhuang Z; Zhang K; Chan CC. 2007. Murine ccl2/cx3cr1 deficiency results in retinal lesions mimicking human age-related macular degeneration. Invest Ophthalmol Vis Sci 48(8):3827-36. [PubMed: 17652758]  [MGI Ref ID J:126935]

Tuo J; Ross RJ; Herzlich AA; Shen D; Ding X; Zhou M; Coon SL; Hussein N; Salem N Jr; Chan CC. 2009. A high omega-3 fatty acid diet reduces retinal lesions in a murine model of macular degeneration. Am J Pathol 175(2):799-807. [PubMed: 19608872]  [MGI Ref ID J:150955]

Van de Veire S; Stalmans I; Heindryckx F; Oura H; Tijeras-Raballand A; Schmidt T; Loges S; Albrecht I; Jonckx B; Vinckier S; Van Steenkiste C; Tugues S; Rolny C; De Mol M; Dettori D; Hainaud P; Coenegrachts L; Contreres JO; Van Bergen T; Cuervo H; Xiao WH; Le Henaff C; Buysschaert I; Kharabi Masouleh B; Geerts A; Schomber T; Bonnin P; Lambert V; Haustraete J; Zacchigna S; Rakic JM; Jimenez W; Noel A; Giacca M; Colle I; Foidart JM; Tobelem G; Morales-Ruiz M; Vilar J; Maxwell P; Vinores SA; Carmeliet G; Dew. 2010. Further pharmacological and genetic evidence for the efficacy of PlGF inhibition in cancer and eye disease. Cell 141(1):178-90. [PubMed: 20371353]  [MGI Ref ID J:160745]

Vasudevan K; Raber J; Sztein J. 2010. Fertility comparison between wild type and transgenic mice by in vitro fertilization. Transgenic Res 19(4):587-94. [PubMed: 19844803]  [MGI Ref ID J:163583]

Verma V; Sauer T; Chan CC; Zhou M; Zhang C; Maminishkis A; Shen D; Tuo J. 2008. Constancy of ERp29 expression in cultured retinal pigment epithelial cells in the Ccl2/Cx3cr1 deficient mouse model of age-related macular degeneration. Curr Eye Res 33(8):701-7. [PubMed: 18696346]  [MGI Ref ID J:140475]

Vessey KA; Greferath U; Jobling AI; Phipps JA; Ho T; Waugh M; Fletcher EL. 2012. Ccl2/Cx3cr1 knockout mice have inner retinal dysfunction but are not an accelerated model of AMD. Invest Ophthalmol Vis Sci 53(12):7833-46. [PubMed: 23074204]  [MGI Ref ID J:214216]

Waddell A; Ahrens R; Steinbrecher K; Donovan B; Rothenberg ME; Munitz A; Hogan SP. 2011. Colonic eosinophilic inflammation in experimental colitis is mediated by Ly6C(high) CCR2(+) inflammatory monocyte/macrophage-derived CCL11. J Immunol 186(10):5993-6003. [PubMed: 21498668]  [MGI Ref ID J:173219]

Waeckel L; Mallat Z; Potteaux S; Combadiere C; Clergue M; Duriez M; Bao L; Gerard C; Rollins BJ; Tedgui A; Levy BI; Silvestre JS. 2005. Impairment in postischemic neovascularization in mice lacking the CXC chemokine receptor 3. Circ Res 96(5):576-82. [PubMed: 15718500]  [MGI Ref ID J:107646]

Wang T; Dai H; Wan N; Moore Y; Dai Z. 2008. The Role for Monocyte Chemoattractant Protein-1 in the Generation and Function of Memory CD8+ T Cells. J Immunol 180(5):2886-93. [PubMed: 18292510]  [MGI Ref ID J:131543]

Wang Y; Abu-Asab MS; Yu CR; Tang Z; Shen D; Tuo J; Li X; Chan CC. 2014. Platelet-derived growth factor (PDGF)-C inhibits neuroretinal apoptosis in a murine model of focal retinal degeneration. Lab Invest 94(6):674-82. [PubMed: 24709779]  [MGI Ref ID J:210964]

Winter C; Herbold W; Maus R; Langer F; Briles DE; Paton JC; Welte T; Maus UA. 2009. Important role for CC chemokine ligand 2-dependent lung mononuclear phagocyte recruitment to inhibit sepsis in mice infected with Streptococcus pneumoniae. J Immunol 182(8):4931-7. [PubMed: 19342672]  [MGI Ref ID J:147500]

Woloszynek JC; Coleman T; Semenkovich CF; Sands MS. 2007. Lysosomal dysfunction results in altered energy balance. J Biol Chem 282(49):35765-71. [PubMed: 17911106]  [MGI Ref ID J:129210]

Wong VW; Rustad KC; Akaishi S; Sorkin M; Glotzbach JP; Januszyk M; Nelson ER; Levi K; Paterno J; Vial IN; Kuang AA; Longaker MT; Gurtner GC. 2012. Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling. Nat Med 18(1):148-52. [PubMed: 22157678]  [MGI Ref ID J:180795]

Yao Y; Tsirka SE. 2012. The CCL2-CCR2 system affects the progression and clearance of intracerebral hemorrhage. Glia 60(6):908-18. [PubMed: 22419223]  [MGI Ref ID J:183881]

Ye Z; Uittenbogaard AM; Cohen DA; Kaplan AM; Ambati J; Straley SC. 2011. Distinct CCR2(+) Gr1(+) cells control growth of the Yersinia pestis DeltayopM mutant in liver and spleen during systemic plague. Infect Immun 79(2):674-87. [PubMed: 21149593]  [MGI Ref ID J:169036]

Yuda K; Takahashi H; Inoue T; Ueta T; Iriyama A; Kadonosono K; Tamaki Y; Aburatani H; Nagai R; Yanagi Y. 2012. Adrenomedullin Inhibits Choroidal Neovascularization via CCL2 in the Retinal Pigment Epithelium. Am J Pathol 181(4):1464-72. [PubMed: 22841816]  [MGI Ref ID J:188706]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX8

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, homozygous mice may be bred together. The expected coat color is Black.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
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

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $152.30Female or MaleHomozygous for Ccl2tm1Rol  
4 weeks $152.30Female or MaleHomozygous for Ccl2tm1Rol  
5 weeks $152.30Female or MaleHomozygous for Ccl2tm1Rol  
6 weeks $155.75Female or MaleHomozygous for Ccl2tm1Rol  
7 weeks $159.20Female or MaleHomozygous for Ccl2tm1Rol  
8 weeks $162.65Female or MaleHomozygous for Ccl2tm1Rol  
Price per Pair (US dollars $)Pair Genotype
$311.50Homozygous for Ccl2tm1Rol x Homozygous for Ccl2tm1Rol  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

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

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $198.00Female or MaleHomozygous for Ccl2tm1Rol  
4 weeks $198.00Female or MaleHomozygous for Ccl2tm1Rol  
5 weeks $198.00Female or MaleHomozygous for Ccl2tm1Rol  
6 weeks $202.50Female or MaleHomozygous for Ccl2tm1Rol  
7 weeks $207.00Female or MaleHomozygous for Ccl2tm1Rol  
8 weeks $211.50Female or MaleHomozygous for Ccl2tm1Rol  
Price per Pair (US dollars $)Pair Genotype
$405.00Homozygous for Ccl2tm1Rol x Homozygous for Ccl2tm1Rol  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

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

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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.


See Terms of Use tab for General Terms and Conditions


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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

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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