Strain Name:

STOCK Tgfb1tm1Doe/J

Stock Number:

002098

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Availability:

Cryopreserved - Ready for recovery

Mice homozygous for Tgfb1tm1Doe mutation develop normally but die approximately two to three weeks after birth, dying within a few days of the onset of a wasting syndrome. Death is due to a massive inflammatory cell response and tissue necrosis. This strain may provide a model for human immune and inflammatory diseases such as autoimmune disease, transplant rejection and graft versus host reactions.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
 
Donating Investigator Thomas Doetschman,   University of Arizona

Appearance
black
Related Genotype: a/a

Description
It has been reported that mice homozygous for Tgfb1tm1Doe mutation develop normally but die approximately two to three weeks after birth. It was also reported that this strain shows a lower than expected number of homozygous births (~14% from heterozygous matings) suggesting that in utero death may occur. Homozygous mice usually die within a few days of the onset of a wasting syndrome. Death is due to a massive inflammatory cell response and tissue necrosis. A multifocal mixed inflammatory cell infiltration occurs into numerous organs, particularly the heart and stomach. Heterozygous mice do not differ from normal wildtype littermates. This strain may provide a model for human immune and inflammatory diseases such as autoimmune disease, transplant rejection and graft versus host reactions.

Development
The Tgfb1tm1Doe mutant strain was developed in the laboratory of Dr. Tom Doetschman at the University of Cincinnati College of Medicine. The vector targeted neo insertion into exon 6 of the Tgfb1 gene. the 129-derived D3 ES cell line was used. The genetic background of this strain is mixture of random bred CF1 mice, inbred 129 and inbred C57BL/6.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Tgfb1tm1Doe allele
002220   B6.129S2-Tgfb1tm1Doe/J
View Strains carrying   Tgfb1tm1Doe     (1 strain)

Strains carrying other alleles of Tgfb1
024931   129-Tgfb1tm1(Tgfb3)Kul/J
010721   STOCK Tgfb1tm2.1Doe/J
018624   STOCK Tgfb3tm2(Tgfb1)Vk/J
View Strains carrying other alleles of Tgfb1     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Sjogren Syndrome
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Camurati-Engelmann Disease; CAEND   (TGFB1)
Cystic Fibrosis; CF   (TGFB1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tgfb1tm1Doe/Tgfb1+

        involves: 129S2/SvPas * CF-1
  • homeostasis/metabolism phenotype
  • abnormal physiological response to xenobiotic
    • sevoflurane fails to protect heterozygotes against IR-induced renal tubular necrosis, unlike in wild-type controls   (MGI Ref ID J:137529)
    • sevoflurane also fails to protect primary cultures of renal proximal tubules against H2O2-induced necrosis, unlike in wild-type controls   (MGI Ref ID J:137529)
  • increased circulating creatinine level
    • heterozygotes subjected to renal ischemia-reperfusion (IR) under sevoflurane anesthesia display significantly higher plasma creatinine levels than wild-type mice subjected to renal IR under either sevoflurane or pentobarbital sodium anesthesia   (MGI Ref ID J:137529)
  • increased susceptibility to kidney reperfusion injury
    • heterozygotes are not protected against renal IR injury under anesthesia with sevoflurane (a volatile anesthetic), unlike similarly treated wild-type controls   (MGI Ref ID J:137529)
  • renal/urinary system phenotype
  • increased susceptibility to kidney reperfusion injury
    • heterozygotes are not protected against renal IR injury under anesthesia with sevoflurane (a volatile anesthetic), unlike similarly treated wild-type controls   (MGI Ref ID J:137529)
  • renal tubular necrosis
    • heterozygotes subjected to renal IR injury under sevoflurane anesthesia exhibit more severe renal tubular necrosis than similarly treated wild-type controls   (MGI Ref ID J:137529)
    • in culture, sevoflurane-treated proximal tubule cells isolated from heterozygous mice are not protected against H2O2-induced necrosis, unlike similarly treated wild-type proximal tubule cells   (MGI Ref ID J:137529)

Tgfb1tm1Doe/Tgfb1tm1Doe

        involves: 129S2/SvPas * CF1
  • mortality/aging
  • complete lethality at weaning
    • mice die around 3 weeks of age from wasting   (MGI Ref ID J:2892)
  • growth/size/body phenotype
  • cachexia
    • at ~3 weeks of age, mice exhibit severe wasting   (MGI Ref ID J:2892)
  • hematopoietic system phenotype
  • increased leukocyte cell number
    • average number of white blood cells is usually elevated in mutants   (MGI Ref ID J:2892)
  • small spleen
    • in most animals, spleens are smaller than in controls   (MGI Ref ID J:2892)
  • immune system phenotype
  • abnormal Peyer's patch morphology
    • Peyer's patches are fewer and possess less distinct germinal centers compared to normal controls   (MGI Ref ID J:2892)
  • abnormal inflammatory response
    • mild to moderate inflammation of serosa of internal organs (stomach, intestine, kidney, ovary, and testis) is seen in some mice   (MGI Ref ID J:2892)
    • brain inflammation
      • primarily (~80%) lymphocytic and plasmacytic inflammation   (MGI Ref ID J:2892)
    • eye inflammation
      • some mice show conjunctivitis, while others display inflammation of striated ocular muscle, or lacrimal gland inflammation   (MGI Ref ID J:2892)
      • conjunctivitis
        • seen in some animals prior to death   (MGI Ref ID J:2892)
    • heart inflammation
      • primarily (~80%) lymphocytic and plasmacytic inflammation; in some animals, inflammation involves pericardium, myocardium and endocardium of atria and ventricles   (MGI Ref ID J:2892)
    • liver inflammation
      • inflammatory cell infiltration is primarily periductal; granulocytes and lymphocytes are ~equal in number   (MGI Ref ID J:2892)
    • lung inflammation
      • primarily (~80%) lymphocytic and plasmacytic inflammation   (MGI Ref ID J:2892)
    • myositis
      • primarily (~80%) lymphocytic and plasmacytic inflammation; various muscles (diaphragm, masseter, leg)   (MGI Ref ID J:2892)
    • pancreas inflammation
      • inflammatory cell infiltration is primarily periductal; primarily (~80%) lymphocytic and plasmacytic inflammation; some degree of multifocal inflammation is seen in ~50% of animals   (MGI Ref ID J:2892)
    • salivary gland inflammation
      • inflammatory cell infiltration is primarily periductal; primarily (~80%) lymphocytic and plasmacytic inflammation; some degree of multifocal inflammatory cell infiltration is seen in ~50% of animals   (MGI Ref ID J:2892)
    • skin inflammation
      • seen in some animals prior to death   (MGI Ref ID J:2892)
    • stomach inflammation
      • inflammation is mainly granulocytic (60% neutrophils)   (MGI Ref ID J:2892)
  • enlarged lymph nodes
    • >60% of mice have slightly enlarged lymph nodes   (MGI Ref ID J:2892)
  • increased leukocyte cell number
    • average number of white blood cells is usually elevated in mutants   (MGI Ref ID J:2892)
  • small spleen
    • in most animals, spleens are smaller than in controls   (MGI Ref ID J:2892)
  • liver/biliary system phenotype
  • liver inflammation
    • inflammatory cell infiltration is primarily periductal; granulocytes and lymphocytes are ~equal in number   (MGI Ref ID J:2892)
  • multifocal hepatic necrosis
    • seen in some animals   (MGI Ref ID J:2892)
  • cardiovascular system phenotype
  • heart inflammation
    • primarily (~80%) lymphocytic and plasmacytic inflammation; in some animals, inflammation involves pericardium, myocardium and endocardium of atria and ventricles   (MGI Ref ID J:2892)
  • myocardial necrosis
    • variable degrees are observed   (MGI Ref ID J:2892)
  • muscle phenotype
  • abnormal diaphragm morphology
    • diaphragms show inflammation and necrosis severe enough to interfere with respiration   (MGI Ref ID J:2892)
  • myositis
    • primarily (~80%) lymphocytic and plasmacytic inflammation; various muscles (diaphragm, masseter, leg)   (MGI Ref ID J:2892)
  • endocrine/exocrine gland phenotype
  • pancreas inflammation
    • inflammatory cell infiltration is primarily periductal; primarily (~80%) lymphocytic and plasmacytic inflammation; some degree of multifocal inflammation is seen in ~50% of animals   (MGI Ref ID J:2892)
  • salivary gland inflammation
    • inflammatory cell infiltration is primarily periductal; primarily (~80%) lymphocytic and plasmacytic inflammation; some degree of multifocal inflammatory cell infiltration is seen in ~50% of animals   (MGI Ref ID J:2892)
  • digestive/alimentary phenotype
  • gastric necrosis
    • variable degrees are observed   (MGI Ref ID J:2892)
  • gastric ulcer
    • severe focal ulceration and/or hyperplasia of basal epithelial layer accompanies inflammation; non-glandular portion of stomach in most mice shows some degree of acanthosis and inflammatory cell infiltration   (MGI Ref ID J:2892)
  • salivary gland inflammation
    • inflammatory cell infiltration is primarily periductal; primarily (~80%) lymphocytic and plasmacytic inflammation; some degree of multifocal inflammatory cell infiltration is seen in ~50% of animals   (MGI Ref ID J:2892)
  • stomach inflammation
    • inflammation is mainly granulocytic (60% neutrophils)   (MGI Ref ID J:2892)
  • respiratory system phenotype
  • lung inflammation
    • primarily (~80%) lymphocytic and plasmacytic inflammation   (MGI Ref ID J:2892)
  • vision/eye phenotype
  • eye inflammation
    • some mice show conjunctivitis, while others display inflammation of striated ocular muscle, or lacrimal gland inflammation   (MGI Ref ID J:2892)
    • conjunctivitis
      • seen in some animals prior to death   (MGI Ref ID J:2892)
  • behavior/neurological phenotype
  • hunched posture
    • seen in some animals prior to death   (MGI Ref ID J:2892)
  • nervous system phenotype
  • brain inflammation
    • primarily (~80%) lymphocytic and plasmacytic inflammation   (MGI Ref ID J:2892)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • cytokine levels are comparable to controls   (MGI Ref ID J:2892)
  • integument phenotype
  • disheveled coat
    • seen in some animals prior to death   (MGI Ref ID J:2892)
  • skin inflammation
    • seen in some animals prior to death   (MGI Ref ID J:2892)

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

Tgfb1tm1Doe/Tgfb1tm1Doe

        involves: 129S2/SvPas * BALB/c * CF-1
  • mortality/aging
  • complete postnatal lethality
    • mice survive average of 20.1 days after birth (range 8.5 - 39.5 days); rate of postnatal lethality is more severe on BALB/c background compared to 129/CF1 background animals survive on average 13.1 days after birth, rate of postnatal lethality is more severe on BALB/c background compared to 129/CF1 background   (MGI Ref ID J:69346)
  • partial prenatal lethality
    • bs ratio of homozygous to wild-type pups born is 0.64, in contrast to expected ratio of 1; less severe than on inbred BALB/c background   (MGI Ref ID J:69346)
  • liver/biliary system phenotype
  • *normal* liver/biliary system phenotype
    • at 11-12 days, livers appear normal relative to normal littermates   (MGI Ref ID J:69346)
    • liver inflammation
      • mice show mild periportal inflammation and no hepatocyte loss compared to animals on congenic BALB/c background   (MGI Ref ID J:69346)
  • immune system phenotype
  • heart inflammation
    • inflammatory lesions   (MGI Ref ID J:69346)
  • increased interferon-gamma secretion
    • liver CD4+ T cells in vitro produce large amounts of interferon gamma Ifng   (MGI Ref ID J:69346)
  • liver inflammation
    • mice show mild periportal inflammation and no hepatocyte loss compared to animals on congenic BALB/c background   (MGI Ref ID J:69346)
  • lung inflammation
    • inflammatory lesions   (MGI Ref ID J:69346)
  • cardiovascular system phenotype
  • heart inflammation
    • inflammatory lesions   (MGI Ref ID J:69346)
  • respiratory system phenotype
  • lung inflammation
    • inflammatory lesions   (MGI Ref ID J:69346)
  • homeostasis/metabolism phenotype
  • increased circulating alanine transaminase level
    • levels are elevated in plasma of 1/10 mice; incidence is lower than on BALB/c background   (MGI Ref ID J:69346)

Tgfb1tm1Doe/Tgfb1tm1Doe

        involves: 129S2/SvPas * CF-1
  • mortality/aging
  • complete lethality at weaning
    • due to multifocal inflammation, median survival of mutant mice is 21 days   (MGI Ref ID J:99033)

Tgfb1tm1Doe/Tgfb1tm1Doe

        C.129S2-Tgfb1tm1Doe
  • mortality/aging
  • partial postnatal lethality
    • mice survive average of 13.1 days after birth (range 8.5-39.5 days), longer than on mixed background   (MGI Ref ID J:69346)
  • partial prenatal lethality
    • ratio of homozygous to wild-type pups born is 0.24, in contrast to expected ratio of 1; more severe than on mixed background   (MGI Ref ID J:69346)
  • liver/biliary system phenotype
  • hepatic necrosis
    • widespread hepatocyte necrosis is seen at 11-12 days   (MGI Ref ID J:69346)
  • liver inflammation
    • extensive inflammation is observed in 11-12 day-old mice, while livers of mice on the 129/BALB/c/CF1 background appear normal at this age   (MGI Ref ID J:69346)
  • immune system phenotype
  • decreased CD4-positive T cell number
    • Cd4+ T cells in spleen are ~half the number in control mice   (MGI Ref ID J:69346)
  • heart inflammation
    • inflammatory lesions are seen   (MGI Ref ID J:69346)
  • increased CD4-positive T cell number
    • CD4+ T cells are ~7-fold more abundant in the liver compared to controls   (MGI Ref ID J:69346)
    • increased T-helper 1 cell number
      • livers contain abnormally high numbers of activated/effector Th1 cells   (MGI Ref ID J:69346)
  • increased interferon-gamma secretion
    • liver CD4+ T cells in vitro produce large amounts of interferon gamma Ifng   (MGI Ref ID J:69346)
  • liver inflammation
    • extensive inflammation is observed in 11-12 day-old mice, while livers of mice on the 129/BALB/c/CF1 background appear normal at this age   (MGI Ref ID J:69346)
  • hematopoietic system phenotype
  • decreased CD4-positive T cell number
    • Cd4+ T cells in spleen are ~half the number in control mice   (MGI Ref ID J:69346)
  • increased CD4-positive T cell number
    • CD4+ T cells are ~7-fold more abundant in the liver compared to controls   (MGI Ref ID J:69346)
    • increased T-helper 1 cell number
      • livers contain abnormally high numbers of activated/effector Th1 cells   (MGI Ref ID J:69346)
  • cardiovascular system phenotype
  • heart inflammation
    • inflammatory lesions are seen   (MGI Ref ID J:69346)
  • homeostasis/metabolism phenotype
  • increased circulating alanine transaminase level
    • bs levels are elevated in plasma of 8/10 11-14 day old mice   (MGI Ref ID J:69346)

Tgfb1tm1Doe/Tgfb1tm1Doe

        involves: 129S2/SvPas
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mice exhibit normal numbers of dopaminergic neurons   (MGI Ref ID J:117465)
View Research Applications

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

Tgfb1tm1Doe related

Cancer Research
Growth Factors/Receptors/Cytokines

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
Growth Factors/Receptors/Cytokines
Inflammation

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tgfb1tm1Doe
Allele Name targeted mutation 1, Thomas Doetschman
Allele Type Targeted (Null/Knockout)
Common Name(s) TGFbeta1; Tgfb1-;
Mutation Made By Thomas Doetschman,   University of Arizona
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Tgfb1, transforming growth factor, beta 1
Chromosome 7
Gene Common Name(s) CED; DPD1; LAP; TGF-beta 1; TGF-beta1; TGFB; TGFbeta; TGFbeta1; Tgfb; Tgfb-1;
Molecular Note A neomycin resistance cassette was inserted into exon 6 of the gene, disrupting the production of a mature peptide. [MGI Ref ID J:2892]

Genotyping

Genotyping Information

Genotyping Protocols

NEOTD (Generic Neo), Standard PCR
Tgfb1tm1Doe, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Shull MM; Ormsby I; Kier AB; Pawlowski S; Diebold RJ; Yin M; Allen R; Sidman C; Proetzel G; Calvin D; Annunziata N; Doetschman T. 1992. Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease. Nature 359(6397):693-9. [PubMed: 1436033]  [MGI Ref ID J:2892]

Additional References

Boivin GP; O'Toole BA; Orsmby IE; Diebold RJ; Eis MJ; Doetschman T; Kier AB. 1995. Onset and progression of pathological lesions in transforming growth factor-beta 1-deficient mice. Am J Pathol 146(1):276-88. [PubMed: 7856734]  [MGI Ref ID J:22297]

Crowe MJ; Doetschman T; Greenhalgh DG. 2000. Delayed wound healing in immunodeficient TGF-beta1 knockout mice J Invest Dermatol 115(1):3-11. [PubMed: 10886500]  [MGI Ref ID J:63260]

Engle SJ; Hoying JB; Boivin GP; Ormsby I; Gartside PS; Doetschman T. 1999. Transforming growth factor beta1 suppresses nonmetastatic colon cancer at an early stage of tumorigenesis. Cancer Res 59(14):3379-86. [PubMed: 10416598]  [MGI Ref ID J:62324]

Engle SJ; Ormsby I; Pawlowski S; Boivin GP; Croft J; Balish E; Doetschman T. 2002. Elimination of Colon Cancer in Germ-free Transforming Growth Factor Beta 1-deficient Mice. Cancer Res 62(22):6362-6. [PubMed: 12438215]  [MGI Ref ID J:80209]

Fontaine RN; Gossett RE; Schroeder F; O'Toole BA; Doetschman T; Kier AB. 1996. Liver and intestinal fatty acid binding proteins in control and TGF beta 1 gene targeted deficient mice. Mol Cell Biochem 159(2):149-53. [PubMed: 8858565]  [MGI Ref ID J:35197]

Kallapur S; Ormsby I; Doetschman T. 1999. Strain dependency of TGFbeta1 function during embryogenesis. Mol Reprod Dev 52(4):341-9. [PubMed: 10092113]  [MGI Ref ID J:53366]

Kulkarni AB; Huh CG; Becker D; Geiser A; Lyght M; Flanders KC; Roberts AB; Sporn MB; Ward JM; Karlsson S. 1993. Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death. Proc Natl Acad Sci U S A 90(2):770-4. [PubMed: 8421714]  [MGI Ref ID J:50848]

Shull MM; Doetschman T. 1994. Transforming growth factor-beta 1 in reproduction and development. Mol Reprod Dev 39(2):239-46. [PubMed: 7826627]  [MGI Ref ID J:20858]

Tgfb1tm1Doe related

Azhar M; Runyan RB; Gard C; Sanford LP; Miller ML; Andringa A; Pawlowski S; Rajan S; Doetschman T. 2009. Ligand-specific function of transforming growth factor beta in epithelial-mesenchymal transition in heart development. Dev Dyn 238(2):431-42. [PubMed: 19161227]  [MGI Ref ID J:144180]

Azhar M; Yin M; Bommireddy R; Duffy JJ; Yang J; Pawlowski SA; Boivin GP; Engle SJ; Sanford LP; Grisham C; Singh RR; Babcock GF; Doetschman T. 2009. Generation of mice with a conditional allele for transforming growth factor beta 1 gene. Genesis 47(6):423-31. [PubMed: 19415629]  [MGI Ref ID J:150024]

Barone KS; Tolarova DD; Ormsby I; Doetschman T; Michael JG. 1998. Induction of oral tolerance in TGF-beta 1 null mice. J Immunol 161(1):154-60. [PubMed: 9647219]  [MGI Ref ID J:110924]

Boivin GP; O'Toole BA; Orsmby IE; Diebold RJ; Eis MJ; Doetschman T; Kier AB. 1995. Onset and progression of pathological lesions in transforming growth factor-beta 1-deficient mice. Am J Pathol 146(1):276-88. [PubMed: 7856734]  [MGI Ref ID J:22297]

Bommireddy R; Babcock GF; Singh RR; Doetschman T. 2008. TGFbeta1 deficiency does not affect the generation and maintenance of CD4(+)CD25(+)FOXP3(+) putative T(reg) cells, but causes their numerical inadequacy and loss of regulatory function. Clin Immunol 127(2):206-13. [PubMed: 18308639]  [MGI Ref ID J:133597]

Bommireddy R; Engle SJ; Ormsby I; Boivin GP; Babcock GF; Doetschman T. 2004. Elimination of both CD4(+) and CD8(+) T cells but not B cells eliminates inflammation and prolongs the survival of TGFbeta1-deficient mice. Cell Immunol 232(1-2):96-104. [PubMed: 15922720]  [MGI Ref ID J:99033]

Bommireddy R; Ormsby I; Yin M; Boivin GP; Babcock GF; Doetschman T. 2003. TGF beta 1 inhibits Ca2+-calcineurin-mediated activation in thymocytes. J Immunol 170(7):3645-52. [PubMed: 12646629]  [MGI Ref ID J:110914]

Brooks WW; Conrad CH. 2000. Myocardial fibrosis in transforming growth factor beta(1)Heterozygous mice J Mol Cell Cardiol 32(2):187-95. [PubMed: 10722796]  [MGI Ref ID J:61255]

Capron C; Lacout C; Lecluse Y; Jalbert V; Chagraoui H; Charrier S; Galy A; Bennaceur-Griscelli A; Cramer-Borde E; Vainchenker W. 2010. A major role of TGF-beta1 in the homing capacities of murine hematopoietic stem cell/progenitors. Blood 116(8):1244-53. [PubMed: 20489054]  [MGI Ref ID J:163490]

Chang JL; Brauer DS; Johnson J; Chen CG; Akil O; Balooch G; Humphrey MB; Chin EN; Porter AE; Butcher K; Ritchie RO; Schneider RA; Lalwani A; Derynck R; Marshall GW; Marshall SJ; Lustig L; Alliston T. 2010. Tissue-specific calibration of extracellular matrix material properties by transforming growth factor-beta and Runx2 in bone is required for hearing. EMBO Rep 11(10):765-71. [PubMed: 20847738]  [MGI Ref ID J:168154]

Ciric B; El-behi M; Cabrera R; Zhang GX; Rostami A. 2009. IL-23 drives pathogenic IL-17-producing CD8+ T cells. J Immunol 182(9):5296-305. [PubMed: 19380776]  [MGI Ref ID J:150310]

Crawford SE; Stellmach V; Murphy-Ullrich JE; Ribeiro SM; Lawler J; Hynes RO; Boivin GP; Bouck N. 1998. Thrombospondin-1 is a major activator of TGF-beta1 in vivo. Cell 93(7):1159-70. [PubMed: 9657149]  [MGI Ref ID J:48446]

Cripps JG; Celaj S; Burdick M; Strieter RM; Gorham JD. 2012. Liver inflammation in a mouse model of Th1 hepatitis despite the absence of invariant NKT cells or the Th1 chemokine receptors CXCR3 and CCR5. Lab Invest 92(10):1461-71. [PubMed: 22906987]  [MGI Ref ID J:189898]

Crowe MJ; Doetschman T; Greenhalgh DG. 2000. Delayed wound healing in immunodeficient TGF-beta1 knockout mice J Invest Dermatol 115(1):3-11. [PubMed: 10886500]  [MGI Ref ID J:63260]

Diebold RJ; Eis MJ; Yin M; Ormsby I; Boivin GP; Darrow BJ; Saffitz JE; Doetschman T. 1995. Early-onset multifocal inflammation in the transforming growth factor beta 1-null mouse is lymphocyte mediated. Proc Natl Acad Sci U S A 92(26):12215-9. [PubMed: 8618872]  [MGI Ref ID J:99717]

Do JS; Fink PJ; Li L; Spolski R; Robinson J; Leonard WJ; Letterio JJ; Min B. 2010. Cutting edge: spontaneous development of IL-17-producing gamma delta T cells in the thymus occurs via a TGF-beta 1-dependent mechanism. J Immunol 184(4):1675-9. [PubMed: 20061408]  [MGI Ref ID J:159493]

Engle SJ; Hoying JB; Boivin GP; Ormsby I; Gartside PS; Doetschman T. 1999. Transforming growth factor beta1 suppresses nonmetastatic colon cancer at an early stage of tumorigenesis. Cancer Res 59(14):3379-86. [PubMed: 10416598]  [MGI Ref ID J:62324]

Engle SJ; Ormsby I; Pawlowski S; Boivin GP; Croft J; Balish E; Doetschman T. 2002. Elimination of Colon Cancer in Germ-free Transforming Growth Factor Beta 1-deficient Mice. Cancer Res 62(22):6362-6. [PubMed: 12438215]  [MGI Ref ID J:80209]

Filvaroff E; Erlebacher A; Ye J; Gitelman SE; Lotz J; Heillman M; Derynck R. 1999. Inhibition of TGF-beta receptor signaling in osteoblasts leads to decreased bone remodeling and increased trabecular bone mass. Development 126(19):4267-79. [PubMed: 10477295]  [MGI Ref ID J:57333]

Foitzik K; Lindner G; Mueller-Roever S; Maurer M; Botchkareva N; Botchkarev V; Handjiski B; Metz M; Hibino T; Soma T; Dotto GP; Paus R. 2000. Control of murine hair follicle regression (catagen) by TGF-beta1 in vivo. FASEB J 14(5):752-60. [PubMed: 10744631]  [MGI Ref ID J:61470]

Foitzik K; Paus R; Doetschman T; Dotto GP. 1999. The TGF-beta2 isoform is both a required and sufficient inducer of murine hair follicle morphogenesis. Dev Biol 212(2):278-89. [PubMed: 10433821]  [MGI Ref ID J:56937]

Gorham JD; Lin JT; Sung JL; Rudner LA; French MA. 2001. Genetic regulation of autoimmune disease: balb/c background tgf-beta1-deficient mice develop necroinflammatory ifn-gamma-dependent hepatitis. J Immunol 166(10):6413-22. [PubMed: 11342667]  [MGI Ref ID J:69346]

Hoying JB; Yin M; Diebold R; Ormsby I; Becker A; Doetschman T. 1999. Transforming growth factor beta1 enhances platelet aggregation through a non-transcriptional effect on the fibrinogen receptor. J Biol Chem 274(43):31008-13. [PubMed: 10521498]  [MGI Ref ID J:115127]

Hull ML; Johan MZ; Hodge WL; Robertson SA; Ingman WV. 2012. Host-derived TGFB1 deficiency suppresses lesion development in a mouse model of endometriosis. Am J Pathol 180(3):880-7. [PubMed: 22210480]  [MGI Ref ID J:181959]

Ingman WV; Robertson SA. 2008. Mammary gland development in transforming growth factor beta1 null mutant mice: systemic and epithelial effects. Biol Reprod 79(4):711-7. [PubMed: 18614704]  [MGI Ref ID J:140882]

Ingman WV; Robertson SA. 2007. Transforming growth factor-beta1 null mutation causes infertility in male mice associated with testosterone deficiency and sexual dysfunction. Endocrinology 148(8):4032-43. [PubMed: 17478551]  [MGI Ref ID J:129629]

Ingman WV; Robker RL; Woittiez K; Robertson SA. 2006. Null mutation in transforming growth factor beta1 disrupts ovarian function and causes oocyte incompetence and early embryo arrest. Endocrinology 147(2):835-45. [PubMed: 16269452]  [MGI Ref ID J:129446]

Kallapur S; Ormsby I; Doetschman T. 1999. Strain dependency of TGFbeta1 function during embryogenesis. Mol Reprod Dev 52(4):341-9. [PubMed: 10092113]  [MGI Ref ID J:53366]

Kim CH. 2006. Migration and function of FoxP3+ regulatory T cells in the hematolymphoid system. Exp Hematol 34(8):1033-40. [PubMed: 16863909]  [MGI Ref ID J:111905]

Krause TJ; Katz D; Wheeler CJ; Ebner S; McKinnon RD. 1999. Increased levels of surgical adhesions in TGFbeta1 heterozygous mice. J Invest Surg 12(1):31-8. [PubMed: 10084677]  [MGI Ref ID J:103445]

Lee HT; Chen SW; Doetschman TC; Deng C; D'Agati VD; Kim M. 2008. Sevoflurane protects against renal ischemia and reperfusion injury in mice via the transforming growth factor-beta1 pathway. Am J Physiol Renal Physiol 295(1):F128-36. [PubMed: 18434384]  [MGI Ref ID J:137529]

Letterio JJ; Bottinger EP. 1998. TGF-beta knockout and dominant-negative receptor transgenic mice. Miner Electrolyte Metab 24(2-3):161-7. [PubMed: 9525700]  [MGI Ref ID J:46776]

Lin JT; Kitzmiller TJ; Cates JM; Gorham JD. 2005. MHC-independent genetic regulation of liver damage in a mouse model of autoimmune hepatocellular injury. Lab Invest 85(4):550-61. [PubMed: 15696185]  [MGI Ref ID J:98233]

Lin JT; Martin SL; Xia L; Gorham JD. 2005. TGF-beta 1 uses distinct mechanisms to inhibit IFN-gamma expression in CD4+ T cells at priming and at recall: differential involvement of Stat4 and T-bet. J Immunol 174(10):5950-8. [PubMed: 15879087]  [MGI Ref ID J:98993]

Makwana M; Jones LL; Cuthill D; Heuer H; Bohatschek M; Hristova M; Friedrichsen S; Ormsby I; Bueringer D; Koppius A; Bauer K; Doetschman T; Raivich G. 2007. Endogenous transforming growth factor beta1 suppresses inflammation and promotes survival in adult CNS. J Neurosci 27(42):11201-13. [PubMed: 17942715]  [MGI Ref ID J:126068]

McLennan IS; Koishi K. 2004. Fetal and maternal transforming growth factor-beta 1 may combine to maintain pregnancy in mice. Biol Reprod 70(6):1614-8. [PubMed: 14766723]  [MGI Ref ID J:96993]

McLennan IS; Poussart Y; Koishi K. 2000. Development of skeletal muscles in transforming growth factor-beta 1 (TGF-beta1) null-mutant mice. Dev Dyn 217(3):250-6. [PubMed: 10741419]  [MGI Ref ID J:108018]

Memon MA; Anway MD; Covert TR; Uzumcu M; Skinner MK. 2008. Transforming growth factor beta (TGFbeta1, TGFbeta2 and TGFbeta3) null-mutant phenotypes in embryonic gonadal development. Mol Cell Endocrinol 294(1-2):70-80. [PubMed: 18790002]  [MGI Ref ID J:145458]

Nemeth K; Keane-Myers A; Brown JM; Metcalfe DD; Gorham JD; Bundoc VG; Hodges MG; Jelinek I; Madala S; Karpati S; Mezey E. 2010. Bone marrow stromal cells use TGF-beta to suppress allergic responses in a mouse model of ragweed-induced asthma. Proc Natl Acad Sci U S A 107(12):5652-7. [PubMed: 20231466]  [MGI Ref ID J:158920]

Pangas SA. 2012. Regulation of the ovarian reserve by members of the transforming growth factor beta family. Mol Reprod Dev 79(10):666-79. [PubMed: 22847922]  [MGI Ref ID J:190579]

Perez-Lorenzo R; Markell LM; Hogan KA; Yuspa SH; Glick AB. 2010. Transforming growth factor beta1 enhances tumor promotion in mouse skin carcinogenesis. Carcinogenesis 31(6):1116-23. [PubMed: 20172950]  [MGI Ref ID J:160717]

Robinson RT; French MA; Kitzmiller TJ; Gorham JD. 2006. Restriction of the CD4+ T-cell receptor repertoire prevents immune pathology in TGF-beta1 knockout mice. Lab Invest 86(8):815-28. [PubMed: 16751781]  [MGI Ref ID J:119226]

Robinson RT; Gorham JD. 2007. TGF-beta 1 regulates antigen-specific CD4+ T cell responses in the periphery. J Immunol 179(1):71-9. [PubMed: 17579023]  [MGI Ref ID J:149425]

Robinson RT; Wang J; Cripps JG; Milks MW; English KA; Pearson TA; Gorham JD. 2009. End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas. J Immunol 182(5):3278-84. [PubMed: 19234226]  [MGI Ref ID J:146230]

Rudner LA; Lin JT; Park IK; Cates JM; Dyer DA; Franz DM; French MA; Duncan EM; White HD; Gorham JD. 2003. Necroinflammatory Liver Disease in BALB/c Background, TGF-beta1-Deficient Mice Requires CD4(+) T Cells. J Immunol 170(9):4785-92. [PubMed: 12707360]  [MGI Ref ID J:83022]

Saika S; Saika S; Liu CY; Azhar M; Sanford LP; Doetschman T; Gendron RL; Kao CW; Kao WW. 2001. TGFbeta2 in corneal morphogenesis during mouse embryonic development. Dev Biol 240(2):419-32. [PubMed: 11784073]  [MGI Ref ID J:73681]

Saito H; Shultz LD; Sinha M; Papaconstantinou J. 1999. Induction of the alpha(1)-antichymotrypsin gene in the brain associated with TGF-beta1 deficiency or systemic administration of endotoxin. Biochem Biophys Res Commun 263(2):270-5. [PubMed: 10491283]  [MGI Ref ID J:57876]

Saxena V; Lienesch DW; Zhou M; Bommireddy R; Azhar M; Doetschman T; Singh RR. 2008. Dual roles of immunoregulatory cytokine TGF-beta in the pathogenesis of autoimmunity-mediated organ damage. J Immunol 180(3):1903-12. [PubMed: 18209088]  [MGI Ref ID J:131622]

Scherf W; Burdach S; Hansen G. 2005. Reduced expression of transforming growth factor beta 1 exacerbates pathology in an experimental asthma model. Eur J Immunol 35(1):198-206. [PubMed: 15593298]  [MGI Ref ID J:95223]

Schultz JJ; Witt SA; Glascock BJ; Nieman ML; Reiser PJ; Nix SL; Kimball TR; Doetschman T. 2002. TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II. J Clin Invest 109(6):787-96. [PubMed: 11901187]  [MGI Ref ID J:124825]

Shibahara K; Ota M; Horiguchi M; Yoshinaga K; Melamed J; Rifkin DB. 2013. Production of gastrointestinal tumors in mice by modulating latent TGF-beta1 activation. Cancer Res 73(1):459-68. [PubMed: 23117884]  [MGI Ref ID J:194125]

Shull MM; Doetschman T. 1994. Transforming growth factor-beta 1 in reproduction and development. Mol Reprod Dev 39(2):239-46. [PubMed: 7826627]  [MGI Ref ID J:20858]

Sun X; Robertson SA; Ingman WV. 2013. Regulation of epithelial cell turnover and macrophage phenotype by epithelial cell-derived transforming growth factor beta1 in the mammary gland. Cytokine 61(2):377-88. [PubMed: 23290315]  [MGI Ref ID J:197873]

Tang Y; Wu X; Lei W; Pang L; Wan C; Shi Z; Zhao L; Nagy TR; Peng X; Hu J; Feng X; Van Hul W; Wan M; Cao X. 2009. TGF-beta1-induced migration of bone mesenchymal stem cells couples bone resorption with formation. Nat Med 15(7):757-65. [PubMed: 19584867]  [MGI Ref ID J:151616]

TeKippe M; Harrison DE; Chen J. 2003. Expansion of hematopoietic stem cell phenotype and activity in Trp53-null mice. Exp Hematol 31(6):521-7. [PubMed: 12829028]  [MGI Ref ID J:115677]

Wara AK; Foo S; Croce K; Sun X; Icli B; Tesmenitsky Y; Esen F; Lee JS; Subramaniam M; Spelsberg TC; Lev EI; Leshem-Lev D; Pande RL; Creager MA; Rosenzweig A; Feinberg MW. 2011. TGF-beta1 signaling and Kruppel-like factor 10 regulate bone marrow-derived proangiogenic cell differentiation, function, and neovascularization. Blood 118(24):6450-60. [PubMed: 21828131]  [MGI Ref ID J:179035]

Wu X; Pang L; Lei W; Lu W; Li J; Li Z; Frassica FJ; Chen X; Wan M; Cao X. 2010. Inhibition of Sca-1-positive skeletal stem cell recruitment by alendronate blunts the anabolic effects of parathyroid hormone on bone remodeling. Cell Stem Cell 7(5):571-80. [PubMed: 21040899]  [MGI Ref ID J:167538]

Yano T; Ito K; Fukamachi H; Chi XZ; Wee HJ; Inoue K; Ida H; Bouillet P; Strasser A; Bae SC; Ito Y. 2006. The RUNX3 tumor suppressor upregulates Bim in gastric epithelial cells undergoing transforming growth factor beta-induced apoptosis. Mol Cell Biol 26(12):4474-88. [PubMed: 16738314]  [MGI Ref ID J:109611]

Zhang J; Pho V; Bonasera SJ; Holtzman J; Tang AT; Hellmuth J; Tang S; Janak PH; Tecott LH; Huang EJ. 2007. Essential function of HIPK2 in TGFbeta-dependent survival of midbrain dopamine neurons. Nat Neurosci 10(1):77-86. [PubMed: 17159989]  [MGI Ref ID J:117465]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryThis Tgfb1tm1Doe strain is maintained by mating heterozygousmice to normal wildtype siblings. Heterozygous mice and normal wildtype siblings may be ordered. Homozygotes usually die by two to three weeks of age and therefore are not available. Expected coat color from breeding:Black

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   Wild-type from the colony
 
  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.


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The Jackson Laboratory's Genotype Promise

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

Terms of Use


General Terms and Conditions


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General inquiries regarding Terms of Use

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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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