Strain Name:

B6.129S4-Timp1tm1Pds/J

Stock Number:

006243

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Availability:

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Homozygous females and hemizygous males have increased resistance to corneal and pulmonary infection, and have altered immune, hematopoietic, and vascular permeability. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, and antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
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Mating SystemHomozygote x Hemizygote         (Female x Male)   16-MAY-07
Specieslaboratory mouse
GenerationN12+F16 (12-DEC-13)
Generation Definitions
 
Donating Investigator Paul D. Soloway,   Cornell University

Description
Homozygous females and hemizygous males (the gene is X-linked) are viable and fertile. No endogenous transcript is detected in lung tissue from affected mice by Northern blot analysis.. Homozygous mice have increased resistance to corneal and pulmonary infection with P. aeruginosa, and have altered immune, hematopoietic, and vascular permeability in bleomycin-induced lung injury trials. Homozygotes also show increased and continued progression of aneurysm formation compared with wild-type mice in induced thoracic aortic aneurysm (TAA) models. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, as well as of P. aeruginosa resistance in individuals with unresolved, antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. Mice with this mutation have been published on many different genetic backgrounds. It should be noted that the phenotype could vary from that originally described. We will modify the strain description as published results become available.

Development
A targeting vector was designed to insert a neomycin resistance cassette into exon 3 of the endogenous gene on the X chromosome. The construct was electroporated into the 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The donating investigator reported that the resulting mutant mice were backcrossed to C57BL/6 inbred mice (see SNP note below) for more than 12 generations before arriving at The Jackson Laboratory.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, at least 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Timp1tm1Pds/Timp1tm1Pds

        involves: C57BL/6
  • immune system phenotype
  • decreased susceptibility to bacterial infection
    • 16 days after infection, inflammation is resolved and corneal integrity restored unlike in C57BL/6 wild-type mice   (MGI Ref ID J:94836)

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

Timp1tm1Pds/Timp1tm1Pds

        involves: 129S4/SvJae
  • tumorigenesis
  • *normal* tumorigenesis
    • indistinguishable from wild type controls in metastasis assays indistinguishable from wild-type controls in metastasis assays   (MGI Ref ID J:43744)
  • growth/size/body phenotype
  • *normal* growth/size/body phenotype
    • body weight equivalent to control mice at same age   (MGI Ref ID J:40265)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • histologically normal ovaries   (MGI Ref ID J:40265)
    • number of healthy and atretic follicles equivalent to those in control mice   (MGI Ref ID J:40265)
    • serum estradiol concentrations equivalent to control mice   (MGI Ref ID J:40265)
    • ovary weight equivalent to control mice   (MGI Ref ID J:40265)
    • abnormal endometrial gland number
      • exhibit a significantly greater number of endometrial glands at P15 and P20; however, by P25, the number of glands is similar to wild-type, indicating accelerated endometrial gland formation   (MGI Ref ID J:96729)
    • abnormal estrous cycle
      • less than 50% exhibited normal estrus cycle   (MGI Ref ID J:64154)
      • abnormal estrus
        • decreased length of estrus period or failure to display estrus   (MGI Ref ID J:64154)
        • absent estrus   (MGI Ref ID J:64154)
        • short estrus   (MGI Ref ID J:64154)
      • prolonged proestrus
        • longer periods of proestrus   (MGI Ref ID J:64154)
    • abnormal uterus development
      • accelerated endometrial gland formation during early postnatal uterine development   (MGI Ref ID J:96729)
    • decreased litter size
      • when litters were produced, fewer pups per litter were born   (MGI Ref ID J:73618)
    • increased uterus weight
      • exhibit an increase in uterine wet weight at P5, P10 and P25   (MGI Ref ID J:96729)
      • mice that displayed normal estrus had uteri weighing significantly more than wild-type controls during estrus   (MGI Ref ID J:64154)
    • reduced female fertility
      • ~50% achieved pregnancy vs. 78% in wild-type controls   (MGI Ref ID J:73618)
      • those that did become pregnant produced fewer litters over a 12-month period than wild-type controls   (MGI Ref ID J:73618)
  • cardiovascular system phenotype
  • altered response to myocardial infarction
    • exhibit accelerated myocardial remodeling after myocardial infarction (coronary ligation) as indicated by increased left ventricular (LV) dilatation and LV dysfunction the accelerated remodeling can be rescued by MMP inhibition   (MGI Ref ID J:95572)
  • aortic aneurysm
    • homozygotes form significantly larger aneurysms than wild-type after elastase infusion to induce aneurysm formation (to model abdominal aortic aneurysm)   (MGI Ref ID J:101938)
    • homozygotes, unlike wild-type, also develop aneurysms following saline injection   (MGI Ref ID J:101938)
    • homozygotes show increased and continued progression of aneurysm formation compared with wild-type in a thoracic aortic aneurysm model (induced by calcium chloride treatment)   (MGI Ref ID J:102182)
  • increased left ventricle diastolic pressure
    • increased left ventricle end-diastolic pressure and volume vs. wild-type controls   (MGI Ref ID J:60524)
  • immune system phenotype
  • decreased susceptibility to bacterial infection
    • bacterial clearance following corneal infection is increased with 2 to 3 orders of magnitude fewer viable bacteria being found in mutant eyes 24 - 48 hours after infection   (MGI Ref ID J:94836)
  • hematopoietic system phenotype
  • *normal* hematopoietic system phenotype
    • normal blood cell counts and subtype distribution   (MGI Ref ID J:100411)
    • decreased bone marrow cell number
      • bone marrow cellularity is decreased by approximately 50% without changes in subtype composition   (MGI Ref ID J:100411)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • exhibit accelerated myocardial remodeling after myocardial infarction (coronary ligation) as indicated by increased left ventricular (LV) dilatation and LV dysfunction the accelerated remodeling can be rescued by MMP inhibition   (MGI Ref ID J:95572)
  • decreased circulating progesterone level
    • during estrus only   (MGI Ref ID J:64154)
  • increased circulating estradiol level
    • during estrus and diestrus   (MGI Ref ID J:64154)

Timp1tm1Pds/Timp1tm1Pds

        involves: 129S4/SvJae * C57BL/6
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • mutants show 76% survival rate 30 days after bleomycin treatment vs 100% in wild-type   (MGI Ref ID J:112941)
  • growth/size/body phenotype
  • weight loss
    • mutants show 33.3% weight reduction 7 days after bleomycin treatment vs 26.6% decrease observed in treated wild-type   (MGI Ref ID J:112941)
  • respiratory system phenotype
  • *normal* respiratory system phenotype
    • fibrotic response to lung injury is similar in mutants and wild type; Timp1-deficiency does not alter collagen accumulation fibrotic response to lung injury is similar in mutants and wild-type; Timp1-deficiency does not alter collagen accumulation   (MGI Ref ID J:112941)
    • neutrophil chemotactic activity is not different from wild type, following bleomycin treatment neutrophil chemotactic activity is not different from wild-type, following bleomycin treatment   (MGI Ref ID J:112941)
    • lung hemorrhage
      • at day 7, bleomycin-treated mutants show 3-fold higher concentrations of erythrocytes in BAL vs wild-type; number of erythrocytes per unit area of lung is >4-fold higher vs wild-type at day 7   (MGI Ref ID J:112941)
    • lung inflammation
      • tissue sections show extensive neutrophil accumulation at day7 after bleomycin treatment vs wild-type   (MGI Ref ID J:112941)
  • hematopoietic system phenotype
  • increased neutrophil cell number
    • percentage and concentration are 2-fold higher compared to wild-type by day 3 following treatment, and at day 7, concentration is 3.5-fold higher and percentage is 1.5 time higher compared to controls   (MGI Ref ID J:112941)
    • at day 7 after treatment, BAL neutrophil percentage and concentration are 3- and 10-fold higher in Timp1-null mice compared to Timp2-null animals; values for Timp2-null mice are similar to wild-type   (MGI Ref ID J:112941)
    • concentrations of alveolar macrophages or lymphocytes recovered from treated mutants are similar to those in treated wild-type   (MGI Ref ID J:112941)
  • immune system phenotype
  • increased neutrophil cell number
    • percentage and concentration are 2-fold higher compared to wild-type by day 3 following treatment, and at day 7, concentration is 3.5-fold higher and percentage is 1.5 time higher compared to controls   (MGI Ref ID J:112941)
    • at day 7 after treatment, BAL neutrophil percentage and concentration are 3- and 10-fold higher in Timp1-null mice compared to Timp2-null animals; values for Timp2-null mice are similar to wild-type   (MGI Ref ID J:112941)
    • concentrations of alveolar macrophages or lymphocytes recovered from treated mutants are similar to those in treated wild-type   (MGI Ref ID J:112941)
  • lung inflammation
    • tissue sections show extensive neutrophil accumulation at day7 after bleomycin treatment vs wild-type   (MGI Ref ID J:112941)
  • cardiovascular system phenotype
  • increased vascular permeability
    • pulmonary vaculature in bleomycin-treated mice shows greater leakage than similarly treated wild-type animals   (MGI Ref ID J:112941)
    • mice exposed to bleomycin display a large increase in albumin and IgM in bronchoalveolar lavage (BAL) compared with saline treated animals; albumin concentrations in BAL are increased >1.5-fold compared to treated wild-type mice at 2, 5, and 7 days after bleomycin treatment   (MGI Ref ID J:112941)
    • IgM concentrations also increase in the week following bleomycin, but it does not reach significance compared to wild-type   (MGI Ref ID J:112941)
  • lung hemorrhage
    • at day 7, bleomycin-treated mutants show 3-fold higher concentrations of erythrocytes in BAL vs wild-type; number of erythrocytes per unit area of lung is >4-fold higher vs wild-type at day 7   (MGI Ref ID J:112941)

Timp1tm1Pds/Y

        involves: 129S4/SvJae
  • cardiovascular system phenotype
  • altered response to myocardial infarction
    • exhibit accelerated myocardial remodeling after myocardial infarction (coronary ligation) as indicated by increased left ventricular (LV) dilatation and LV dysfunction the accelerated remodeling can be rescued by MMP inhibition   (MGI Ref ID J:95572)
  • aortic aneurysm
    • mutants form significantly larger aneurysms than wild-type after elastase infusion to induce aneurysm formation (to model abdominal aortic aneurysm)   (MGI Ref ID J:101938)
    • mutants, unlike wild-type, also develop aneurysms following saline injection   (MGI Ref ID J:101938)
    • hemizygotes show increased and continued progression of aneurysm formation compared with wild-type in a thoracic aortic aneurysm model (induced by calcium chloride treatment)   (MGI Ref ID J:102182)
  • increased left ventricle diastolic pressure
    • increased left ventricle end-diastolic pressure and volume vs. wild-type controls   (MGI Ref ID J:60524)
  • endocrine/exocrine gland phenotype
  • increased testis weight
    • increased testicular weight at day 21 after birth   (MGI Ref ID J:49303)
  • growth/size/body phenotype
  • *normal* growth/size/body phenotype
    • body weight equivalent to controls at same age   (MGI Ref ID J:49303)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • exhibit accelerated myocardial remodeling after myocardial infarction (coronary ligation) as indicated by increased left ventricular (LV) dilatation and LV dysfunction the accelerated remodeling can be rescued by MMP inhibition   (MGI Ref ID J:95572)
  • increased circulating testosterone level
    • only at day 21 after birth   (MGI Ref ID J:49303)
  • reproductive system phenotype
  • increased testis weight
    • increased testicular weight at day 21 after birth   (MGI Ref ID J:49303)

Timp1tm1Pds/Y

        involves: 129S4/SvJae * C57BL/6
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • whether or not infused with angiotensin II, mice exhibit normal heart rate   (MGI Ref ID J:211441)
    • abnormal systemic arterial blood pressure
      • following angiotensin II infusion, mice less of an increase in blood pressure compared with wild-type mice   (MGI Ref ID J:211441)
View Research Applications

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

Cardiovascular Research
Heart Abnormalities
      aortic aneurysms
Vascular Defects

Immunology, Inflammation and Autoimmunity Research
Cystic Fibrosis

Internal/Organ Research
Heart Abnormalities
      aortic aneurysms
Lung Defects

Research Tools
Cancer Research
Cardiovascular Research
Immunology, Inflammation and Autoimmunity Research
      genes regulating susceptibility to infectious disease and endotoxin

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Timp1tm1Pds
Allele Name targeted mutation 1, Paul D Soloway
Allele Type Targeted (Null/Knockout)
Common Name(s) TIMP-1-; TIMP-1KO; TIMP1KO; Timp1-; Timp1tm1Jae;
Mutation Made By Paul Soloway,   Cornell University
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Timp1, tissue inhibitor of metalloproteinase 1
Chromosome X
Gene Common Name(s) CLGI; Clgi; EPA; EPO; HCI; MGC:7143; TIMP; TIMP-1;
Molecular Note Insertion of a neomycin-thymidine kinase expression cassette resulted in a duplication of part of the gene (the second through the fifth coding exons, with the duplicated copies separated by the selectable markers), and inserted into the third coding exon a 21 bp sequence that placed a stop codon in each reading frame. Northern blot analyses failed to detect transcripts from this allele in lung, ovaries or embryonic fibroblasts. [MGI Ref ID J:43744] [MGI Ref ID J:94836]

Genotyping

Genotyping Information

Genotyping Protocols

Timp1tm1Pdsalternate2, High Resolution Melting


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Soloway PD; Alexander CM; Werb Z; Jaenisch R. 1996. Targeted mutagenesis of Timp-1 reveals that lung tumor invasion is influenced by Timp-1 genotype of the tumor but not by that of the host. Oncogene 13(11):2307-14. [PubMed: 8957071]  [MGI Ref ID J:43744]

Additional References

Timp1tm1Pds related

Aoki T; Kataoka H; Moriwaki T; Nozaki K; Hashimoto N. 2007. Role of TIMP-1 and TIMP-2 in the progression of cerebral aneurysms. Stroke 38(8):2337-45. [PubMed: 17569872]  [MGI Ref ID J:148151]

Basu R; Lee J; Morton JS; Takawale A; Fan D; Kandalam V; Wang X; Davidge ST; Kassiri Z. 2013. TIMP3 is the primary TIMP to regulate agonist-induced vascular remodelling and hypertension. Cardiovasc Res 98(3):360-71. [PubMed: 23524300]  [MGI Ref ID J:211441]

Chaillan FA; Rivera S; Marchetti E; Jourquin J; Werb Z; Soloway PD; Khrestchatisky M; Roman FS. 2006. Involvement of tissue inhibition of metalloproteinases-1 in learning and memory in mice. Behav Brain Res 173(2):191-8. [PubMed: 16860884]  [MGI Ref ID J:146049]

Chen P; Farivar AS; Mulligan MS; Madtes DK. 2006. Tissue inhibitor of metalloproteinase-1 deficiency abrogates obliterative airway disease after heterotopic tracheal transplantation. Am J Respir Cell Mol Biol 34(4):464-72. [PubMed: 16388023]  [MGI Ref ID J:120184]

Chen P; McGuire JK; Hackman RC; Kim KH; Black RA; Poindexter K; Yan W; Liu P; Chen AJ; Parks WC; Madtes DK. 2008. Tissue inhibitor of metalloproteinase-1 moderates airway re-epithelialization by regulating matrilysin activity. Am J Pathol 172(5):1256-70. [PubMed: 18385523]  [MGI Ref ID J:134273]

Creemers EE; Davis JN; Parkhurst AM; Leenders P; Dowdy KB; Hapke E; Hauet AM; Escobar PG; Cleutjens JP; Smits JF; Daemen MJ; Zile MR; Spinale FG. 2003. Deficiency of TIMP-1 exacerbates LV remodeling after myocardial infarction in mice. Am J Physiol Heart Circ Physiol 284(1):H364-71. [PubMed: 12388239]  [MGI Ref ID J:89953]

Crocker SJ; Frausto RF; Whitmire JK; Benning N; Milner R; Whitton JL. 2007. Amelioration of coxsackievirus B3-mediated myocarditis by inhibition of tissue inhibitors of matrix metalloproteinase-1. Am J Pathol 171(6):1762-73. [PubMed: 18055551]  [MGI Ref ID J:128961]

Crocker SJ; Whitmire JK; Frausto RF; Chertboonmuang P; Soloway PD; Whitton JL; Campbell IL. 2006. Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Am J Pathol 169(6):2104-16. [PubMed: 17148673]  [MGI Ref ID J:116220]

Eddy AA; Kim H; Lopez-Guisa J; Oda T; Soloway PD. 2000. Interstitial fibrosis in mice with overload proteinuria: deficiency of TIMP-1 is not protective. Kidney Int 58(2):618-28. [PubMed: 10916085]  [MGI Ref ID J:79425]

English JL; Kassiri Z; Koskivirta I; Atkinson SJ; Di Grappa M; Soloway PD; Nagase H; Vuorio E; Murphy G; Khokha R. 2006. Individual Timp deficiencies differentially impact pro-MMP-2 activation. J Biol Chem 281(15):10337-46. [PubMed: 16469749]  [MGI Ref ID J:112210]

Eskandari MK; Vijungco JD; Flores A; Borensztajn J; Shively V; Pearce WH. 2005. Enhanced abdominal aortic aneurysm in TIMP-1-deficient mice. J Surg Res 123(2):289-93. [PubMed: 15680392]  [MGI Ref ID J:101938]

Fowell AJ; Collins JE; Duncombe DR; Pickering JA; Rosenberg WM; Benyon RC. 2011. Silencing tissue inhibitors of metalloproteinases (TIMPs) with short interfering RNA reveals a role for TIMP-1 in hepatic stellate cell proliferation. Biochem Biophys Res Commun 407(2):277-82. [PubMed: 21300026]  [MGI Ref ID J:171964]

Gerin I; Louis GW; Zhang X; Prestwich TC; Kumar TR; Myers MG Jr; Macdougald OA; Nothnick WB. 2009. Hyperphagia and obesity in female mice lacking tissue inhibitor of metalloproteinase-1. Endocrinology 150(4):1697-704. [PubMed: 19036876]  [MGI Ref ID J:158084]

Harslund J; Nielsen OL; Brunner N; Offenberg H. 2007. Gender-dependent physiological implications of combined PAI-1 and TIMP-1 gene deficiency characterized in a mouse model. Am J Physiol Regul Integr Comp Physiol 293(4):R1630-9. [PubMed: 17652357]  [MGI Ref ID J:145130]

Ikonomidis JS; Gibson WC; Butler JE; McClister DM; Sweterlitsch SE; Thompson RP; Mukherjee R; Spinale FG. 2004. Effects of deletion of the tissue inhibitor of matrix metalloproteinases-1 gene on the progression of murine thoracic aortic aneurysms. Circulation 110(11 Suppl 1):II268-73. [PubMed: 15364874]  [MGI Ref ID J:102182]

Ikonomidis JS; Hendrick JW; Parkhurst AM; Herron AR; Escobar PG; Dowdy KB; Stroud RE; Hapke E; Zile MR; Spinale FG. 2005. Accelerated LV remodeling after myocardial infarction in TIMP-1-deficient mice: effects of exogenous MMP inhibition. Am J Physiol Heart Circ Physiol 288(1):H149-58. [PubMed: 15598866]  [MGI Ref ID J:95572]

Jourquin J; Tremblay E; Bernard A; Charton G; Chaillan FA; Marchetti E; Roman FS; Soloway PD; Dive V; Yiotakis A; Khrestchatisky M; Rivera S. 2005. Tissue inhibitor of metalloproteinases-1 (TIMP-1) modulates neuronal death, axonal plasticity, and learning and memory. Eur J Neurosci 22(10):2569-78. [PubMed: 16307599]  [MGI Ref ID J:104315]

Kadri Z; Maouche-Chretien L; Rooke HM; Orkin SH; Romeo PH; Mayeux P; Leboulch P; Chretien S. 2005. Phosphatidylinositol 3-kinase/Akt induced by erythropoietin renders the erythroid differentiation factor GATA-1 competent for TIMP-1 gene transactivation. Mol Cell Biol 25(17):7412-22. [PubMed: 16107690]  [MGI Ref ID J:100411]

Kim H; Oda T; Lopez-Guisa J; Wing D; Edwards DR; Soloway PD; Eddy AA. 2001. TIMP-1 deficiency does not attenuate interstitial fibrosis in obstructive nephropathy. J Am Soc Nephrol 12(4):736-48. [PubMed: 11274235]  [MGI Ref ID J:79423]

Kim KH; Burkhart K; Chen P; Frevert CW; Randolph-Habecker J; Hackman RC; Soloway PD; Madtes DK. 2005. Tissue inhibitor of metalloproteinase-1 deficiency amplifies acute lung injury in bleomycin-exposed mice. Am J Respir Cell Mol Biol 33(3):271-9. [PubMed: 15947421]  [MGI Ref ID J:112941]

Lee MM; Yoon BJ; Osiewicz K; Preston M; Bundy B; van Heeckeren AM; Werb Z; Soloway PD. 2005. Tissue inhibitor of metalloproteinase 1 regulates resistance to infection. Infect Immun 73(1):661-5. [PubMed: 15618213]  [MGI Ref ID J:94836]

Lemaitre V; Soloway PD; D'Armiento J. 2003. Increased medial degradation with pseudo-aneurysm formation in apolipoprotein E-knockout mice deficient in tissue inhibitor of metalloproteinases-1. Circulation 107(2):333-8. [PubMed: 12538437]  [MGI Ref ID J:103082]

Lijnen HR; Demeulemeester D; Van Hoef B; Collen D; Maquoi E. 2003. Deficiency of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) impairs nutritionally induced obesity in mice. Thromb Haemost 89(2):249-55. [PubMed: 12574803]  [MGI Ref ID J:113258]

Lijnen HR; Soloway P; Collen D. 1999. Tissue inhibitor of matrix metalloproteinases-1 impairs arterial neointima formation after vascular injury in mice. Circ Res 85(12):1186-91. [PubMed: 10590246]  [MGI Ref ID J:79424]

Moore CS; Milner R; Nishiyama A; Frausto RF; Serwanski DR; Pagarigan RR; Whitton JL; Miller RH; Crocker SJ. 2011. Astrocytic Tissue Inhibitor of Metalloproteinase-1 (TIMP-1) Promotes Oligodendrocyte Differentiation and Enhances CNS Myelination. J Neurosci 31(16):6247-54. [PubMed: 21508247]  [MGI Ref ID J:171600]

Mukherjee R; Parkhurst AM; Mingoia JT; Sweterlitsch SE; Leiser JS; Escobar GP; Spinale FG; Saul JP. 2004. Myocardial remodeling after discrete radiofrequency injury: effects of tissue inhibitor of matrix metalloproteinase-1 gene deletion. Am J Physiol Heart Circ Physiol 286(4):H1242-7. [PubMed: 14630637]  [MGI Ref ID J:95607]

Nothnick WB. 2001. Disruption of the tissue inhibitor of metalloproteinase-1 gene in reproductive-age female mice is associated with estrous cycle stage-specific increases in stromelysin messenger RNA expression and activity. Biol Reprod 65(6):1780-8. [PubMed: 11717141]  [MGI Ref ID J:72869]

Nothnick WB. 2000. Disruption of the tissue inhibitor of metalloproteinase-1 gene results in altered reproductive cyclicity and uterine morphology in reproductive-Age female mice Biol Reprod 63(3):905-12. [PubMed: 10952938]  [MGI Ref ID J:64154]

Nothnick WB. 2001. Reduction in reproductive lifespan of tissue inhibitor of metalloproteinase 1 (TIMP-1)-deficient female mice. Reproduction 122(6):923-7. [PubMed: 11732988]  [MGI Ref ID J:73618]

Nothnick WB. 2003. Tissue inhibitor of metalloproteinase-1 (TIMP-1) deficient mice display reduced serum progesterone levels during corpus luteum development. Endocrinology 144(1):5-8. [PubMed: 12488323]  [MGI Ref ID J:81405]

Nothnick WB; Soloway P; Curry TE Jr. 1997. Assessment of the role of tissue inhibitor of metalloproteinase-1 (TIMP-1) during the periovulatory period in female mice lacking a functional TIMP-1 gene. Biol Reprod 56(5):1181-8. [PubMed: 9160717]  [MGI Ref ID J:40265]

Nothnick WB; Soloway PD; Curry TE Jr. 1998. Pattern of messenger ribonucleic acid expression of tissue inhibitors of metalloproteinases (TIMPs) during testicular maturation in male mice lacking a functional TIMP-1 gene. Biol Reprod 59(2):364-70. [PubMed: 9687309]  [MGI Ref ID J:49303]

Nothnick WB; Zhang X; Zhou HE. 2004. Steroidal regulation of uterine edema and tissue inhibitors of metalloproteinase (TIMP)-3 messenger RNA expression is altered in TIMP-1-deficient mice. Biol Reprod 70(2):500-8. [PubMed: 14568914]  [MGI Ref ID J:96726]

Ogier C; Creidy R; Boucraut J; Soloway PD; Khrestchatisky M; Rivera S. 2005. Astrocyte reactivity to Fas activation is attenuated in TIMP-1 deficient mice, an in vitro study. BMC Neurosci 6(1):68. [PubMed: 16316466]  [MGI Ref ID J:123445]

Osawa Y; Suetsugu A; Matsushima-Nishiwaki R; Yasuda I; Saibara T; Moriwaki H; Seishima M; Kozawa O. 2013. Liver acid sphingomyelinase inhibits growth of metastatic colon cancer. J Clin Invest :. [PubMed: 23298833]  [MGI Ref ID J:194498]

Osiewicz K; McGarry M; Soloway PD. 1999. Hyper-resistance to infection in TIMP-1-deficient mice is neutrophil dependent but not immune cell autonomous. Ann N Y Acad Sci 878:494-6. [PubMed: 10415752]  [MGI Ref ID J:79559]

Perez SE; Cano DA; Dao-Pick T; Rougier JP; Werb Z; Hebrok M. 2005. Matrix metalloproteinases 2 and 9 are dispensable for pancreatic islet formation and function in vivo. Diabetes 54(3):694-701. [PubMed: 15734845]  [MGI Ref ID J:105134]

Pierno S; Camerino GM; Cannone M; Liantonio A; De Bellis M; Digennaro C; Gramegna G; De Luca A; Germinario E; Danieli-Betto D; Betto R; Dobrowolny G; Rizzuto E; Musaro A; Desaphy JF; Camerino DC. 2013. Paracrine effects of IGF-1 overexpression on the functional decline due to skeletal muscle disuse: molecular and functional evaluation in hindlimb unloaded MLC/mIgf-1 transgenic mice. PLoS One 8(6):e65167. [PubMed: 23755187]  [MGI Ref ID J:204253]

Rossi L; Ergen AV; Goodell MA. 2011. TIMP-1 deficiency subverts cell-cycle dynamics in murine long-term HSCs. Blood 117(24):6479-88. [PubMed: 21521782]  [MGI Ref ID J:174818]

Roten L; Nemoto S; Simsic J; Coker ML; Rao V; Baicu S; Defreyte G; Soloway PJ; Zile MR; Spinale FG. 2000. Effects of gene deletion of the tissue inhibitor of the matrix metalloproteinase-type 1 (TIMP-1) on left ventricular geometry and function in mice J Mol Cell Cardiol 32(1):109-20. [PubMed: 10652195]  [MGI Ref ID J:60524]

Sands MF; Ohtake PJ; Mahajan SD; Takyar SS; Aalinkeel R; Fang YV; Blume JW; Mullan BA; Sykes DE; Lachina S; Knight PR; Schwartz SA. 2009. Tissue inhibitor of metalloproteinase-1 modulates allergic lung inflammation in murine asthma. Clin Immunol 130(2):186-98. [PubMed: 18955015]  [MGI Ref ID J:144080]

Silence J; Collen D; Lijnen HR. 2002. Reduced atherosclerotic plaque but enhanced aneurysm formation in mice with inactivation of the tissue inhibitor of metalloproteinase-1 (TIMP-1) gene. Circ Res 90(8):897-903. [PubMed: 11988491]  [MGI Ref ID J:109733]

Vaillant B; Chiaramonte MG; Cheever AW; Soloway PD; Wynn TA. 2001. Regulation of hepatic fibrosis and extracellular matrix genes by the th response: new insight into the role of tissue inhibitors of matrix metalloproteinases. J Immunol 167(12):7017-26. [PubMed: 11739522]  [MGI Ref ID J:73095]

Wiseman BS; Sternlicht MD; Lund LR; Alexander CM; Mott J; Bissell MJ; Soloway P; Itohara S; Werb Z. 2003. Site-specific inductive and inhibitory activities of MMP-2 and MMP-3 orchestrate mammary gland branching morphogenesis. J Cell Biol 162(6):1123-33. [PubMed: 12975354]  [MGI Ref ID J:85503]

Yamada E; Tobe T; Yamada H; Okamoto N; Zack DJ; Werb Z; Soloway PD; Campochiaro PA. 2001. TIMP-1 promotes VEGF-induced neovascularization in the retina. Histol Histopathol 16(1):87-97. [PubMed: 11193216]  [MGI Ref ID J:79536]

Zhang X; Hoang E; Nothnick WB. 2009. Estrogen-induced uterine abnormalities in TIMP-1 deficient mice are associated with elevated plasmin activity and reduced expression of the novel uterine plasmin protease inhibitor serpinb7. Mol Reprod Dev 76(2):160-72. [PubMed: 18537133]  [MGI Ref ID J:144441]

Zhou HE; Zhang X; Nothnick WB. 2004. Disruption of the TIMP-1 gene product is associated with accelerated endometrial gland formation during early postnatal uterine development. Biol Reprod 71(2):534-9. [PubMed: 15084483]  [MGI Ref ID J:96729]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, homozygous females are bred to hemizygous males.
Mating SystemHomozygote x Hemizygote         (Female x Male)   16-MAY-07
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 $239.00MaleHemizygous for Timp1tm1Pds  
$239.00FemaleHomozygous for Timp1tm1Pds  
Price per Pair (US dollars $)Pair Genotype
$478.00Homozygous for Timp1tm1Pds x Hemizygous for Timp1tm1Pds  

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.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70MaleHemizygous for Timp1tm1Pds  
$310.70FemaleHomozygous for Timp1tm1Pds  
Price per Pair (US dollars $)Pair Genotype
$621.40Homozygous for Timp1tm1Pds x Hemizygous for Timp1tm1Pds  

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.

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
   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


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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