Strain Name:

B6N;129-Egr1tm1Jmi/J

Stock Number:

012924

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Availability:

Repository- Live

Use Restrictions Apply, see Terms of Use
In this strain a coding exon upstream of the DNA-binding domain of the early growth response 1 (Egr1) gene is replaced with a neo cassette, abolishing gene function. These mice may be useful for studying carcinogenesis, inflammation, atherosclerosis, scleroderma, ischemic injury, tissue repair, fibrosis, matrix remodeling and wound healing.

Description

Strain Information

Type Congenic; Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   07-OCT-10
Specieslaboratory mouse
GenerationN27+N1F4 (05-MAR-13)
Generation Definitions
 
Donating Investigator Jeffrey Milbrandt,   Washington University in St. Louis

Description
In this strain a coding exon upstream of the DNA-binding domain of the early growth response 1 (Egr1) gene is replaced with a neo cassette, abolishing gene function. Homozygous Egr1-/- mice are viable and normal in size. Homozygous females are sterile, are absent of corpora lutea, and display a 30% reduction in the weight of the uterus. These mice exhibit an impaired inflammatory response, impaired wound healing, and attenuated dermal fibrosis after TGF-β or bleomycin stimulation. Macrophages from Egr1-/- mice showed reduced TNF-α secretion when stimulated with TGF-β. These mice may be useful for studying carcinogenesis, inflammation, atherosclerosis, scleroderma, ischemic injury, tissue repair, fibrosis, matrix remodeling and wound healing.

Development
A targeting vector was designed to place a neomycin resistance (neo) cassette into a coding exon upstream of the DNA-binding domain of the early growth response 1 (Egr1) gene. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl+-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and the resulting chimeric males were bred to C57BL/6NTac females to generate a colony of Egr1-/- mice. The Donating investigator confirms that these mice were backcrossed to C57BL/6NTac mice for 26 generations (see SNP note below). Upon arrival at The Jackson Laboratory, mice were bred to C57BL/6NJ (Stock No. 005304) for at least one generation to establish the colony.

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. 4 markers on 3 chromosomes, 6, 12, and 13, were found to be segregating, suggesting an incomplete backcross.

Control Information

  Control
   Wild-type from the colony
   005304 C57BL/6NJ (approximate)
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Egr1tm1Jmi/Egr1tm1Jmi

        B6.129-Egr1tm1Jmi
  • skeleton phenotype
  • abnormal trabecular bone morphology
    • increased cancellous bone formation   (MGI Ref ID J:62113)
  • decreased bone mineral density
    • decreased 10% by 4 months of age   (MGI Ref ID J:62113)
  • increased osteoclast cell number
    • elevated osteoclast formation regardless of estrogen levels   (MGI Ref ID J:51107)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • no atherosclerotic lesions at the root of the aorta   (MGI Ref ID J:96665)
  • liver/biliary system phenotype
  • *normal* liver/biliary system phenotype
    • galactoseamine/LPS induced liver injury is attenuated early   (MGI Ref ID J:128421)
    • less evidence of apoptosis   (MGI Ref ID J:128421)
    • very little hemorrhage   (MGI Ref ID J:128421)
    • no evidence of necrosis   (MGI Ref ID J:128421)
    • abnormal liver physiology
      • survive 7 hours rather than 6 hours after galactoseamine/LPS treatment   (MGI Ref ID J:128421)
      • extensive liver hemorrhage and hepatocyte apoptosis by 7 hours   (MGI Ref ID J:128421)
      • liver inflammation
        • neutrophiles in parenchyma 50% lower than in controls   (MGI Ref ID J:128421)
        • reduced extravasation of neutrophiles in liver   (MGI Ref ID J:128421)
  • homeostasis/metabolism phenotype
  • abnormal circulating alanine transaminase level
    • 30% less increase in alanine aminotransferase levels in plasma after galactoseamine/LPS treatment than in controls   (MGI Ref ID J:128421)
  • abnormal circulating tumor necrosis factor level
    • early increases after treatment with galactoseamine/LPS are similar to controls   (MGI Ref ID J:128421)
    • increase is 65% less 4 hours after treatment   (MGI Ref ID J:128421)
    • increase is 75% less 5.5 hours after treatment   (MGI Ref ID J:128421)
  • hematopoietic system phenotype
  • increased osteoclast cell number
    • elevated osteoclast formation regardless of estrogen levels   (MGI Ref ID J:51107)
  • immune system phenotype
  • abnormal circulating tumor necrosis factor level
    • early increases after treatment with galactoseamine/LPS are similar to controls   (MGI Ref ID J:128421)
    • increase is 65% less 4 hours after treatment   (MGI Ref ID J:128421)
    • increase is 75% less 5.5 hours after treatment   (MGI Ref ID J:128421)
  • increased osteoclast cell number
    • elevated osteoclast formation regardless of estrogen levels   (MGI Ref ID J:51107)
  • liver inflammation
    • neutrophiles in parenchyma 50% lower than in controls   (MGI Ref ID J:128421)
    • reduced extravasation of neutrophiles in liver   (MGI Ref ID J:128421)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Egr1tm1Jmi/Egr1tm1Jmi

        involves: 129
  • endocrine/exocrine gland phenotype
  • abnormal Leydig cell morphology
    • atrophic leydig cells; however, spermatogenesis is normal   (MGI Ref ID J:35132)
  • abnormal ovary morphology   (MGI Ref ID J:35132)
    • absent corpus luteum
      • ovaries were similar in weight to wild-type   (MGI Ref ID J:35132)
  • homeostasis/metabolism phenotype
  • abnormal circulating progesterone level
    • serum levels of progesterone are reduced, however serum levels of estradiol are normal   (MGI Ref ID J:35132)
  • abnormal vascular wound healing
    • less neointimal expansion seen 28 days after endothelial denudation of the femoral artery than in controls   (MGI Ref ID J:61294)
  • decreased luteinizing hormone level
    • LH undetected in females in the pituitary   (MGI Ref ID J:35132)
    • LH levels decreased in males in the pituitary   (MGI Ref ID J:35132)
    • LH levels did not increase after ovariectomy in the pituitary   (MGI Ref ID J:35132)
  • reproductive system phenotype
  • abnormal Leydig cell morphology
    • atrophic leydig cells; however, spermatogenesis is normal   (MGI Ref ID J:35132)
  • abnormal ovary morphology   (MGI Ref ID J:35132)
    • absent corpus luteum
      • ovaries were similar in weight to wild-type   (MGI Ref ID J:35132)
  • abnormal reproductive system physiology   (MGI Ref ID J:35132)
    • abnormal ovulation
      • females were anestrous   (MGI Ref ID J:35132)
      • ovulation could be induced by exogenous gonadotropins   (MGI Ref ID J:35132)
    • female infertility   (MGI Ref ID J:35132)
  • decreased uterus weight
    • ~30% the weight of wild-type uterus   (MGI Ref ID J:35132)
  • cardiovascular system phenotype
  • abnormal vascular wound healing
    • less neointimal expansion seen 28 days after endothelial denudation of the femoral artery than in controls   (MGI Ref ID J:61294)
  • cardiac fibrosis
    • fibrotic lesions in the heart regardless of treatment with adrenoreceptor agonists   (MGI Ref ID J:61294)
    • heart weight/body weight ratios are normal   (MGI Ref ID J:61294)

Egr1tm1Jmi/Egr1tm1Jmi

        involves: 129 * C57BL/6
  • growth/size phenotype
  • postnatal growth retardation
  • liver/biliary system phenotype
  • *normal* liver/biliary system phenotype
    • ethanol feeding does not induce liver steatosis   (MGI Ref ID J:105638)
    • abnormal liver physiology   (MGI Ref ID J:105638)
      • decreased liver regeneration
        • hepatocellular proliferation after partial hepatectomy normal for first 36 hours   (MGI Ref ID J:93996)
        • proliferation is significantly reduced at 48 hours   (MGI Ref ID J:93996)
    • abnormal liver size
      • liver weight/body weight ratio does not increase with ethanol feeding as happens with controls   (MGI Ref ID J:105638)
    • increased liver triglyceride level
      • slightly elevated liver triglycerides with ethanol feeding   (MGI Ref ID J:105638)
  • cellular phenotype
  • abnormal mitosis
    • mitosis impaired between metaphase and anaphase   (MGI Ref ID J:93996)
    • decreased mitotic index
      • lower frequency of mitosis in the liver 48 hours after hepatectomy   (MGI Ref ID J:93996)
      • frequency of mitosis in the liver remains more or less constant from 48 to 72 hours after hepatectomy   (MGI Ref ID J:93996)
  • tumorigenesis
  • *normal* tumorigenesis
    • spontaneous tumors do not develop   (MGI Ref ID J:123870)
    • T cell derived lymphoma
      • ENU treatment at 4 and 20 weeks weeks results in T-cell lymphomas in 53% of mice compared to 26% of controls treated at 3 weeks and 10% of controls treated at 20 weeks   (MGI Ref ID J:123870)
      • mice with lymphomas do not develop myeloproliferative disease   (MGI Ref ID J:123870)
    • decreased tumor latency
      • mice treated with the mutagen DMBA and tumor promoter TPA develop skin tumors around 8 weeks rather than 12.5 weeks as in controls   (MGI Ref ID J:99386)
    • increased incidence of chemically-induced tumors
      • ENU treatment at 4 and 20 weeks weeks results in T-cell lymphomas in 53% of mice compared to 26% of controls treated at 3 weeks and 10% of controls treated at 20 weeks   (MGI Ref ID J:123870)
    • skin papilloma
      • skin tumors induced by treatment with DMBA and TPA appear to be papillomas   (MGI Ref ID J:99386)
  • homeostasis/metabolism phenotype
  • abnormal homeostasis   (MGI Ref ID J:105638)
    • abnormal circulating alanine transaminase level
      • serum alanine aminotransferase is not increased by ethanol feeding whereas levels increase 2 fold in controls   (MGI Ref ID J:105638)
    • abnormal tumor necrosis factor level
      • TNF alpha levels remain constant with ethanol feeding whereas they increase 20 fold in controls   (MGI Ref ID J:105638)
    • increased liver triglyceride level
      • slightly elevated liver triglycerides with ethanol feeding   (MGI Ref ID J:105638)
  • abnormal physiological response to xenobiotic
    • liver weight/body weight ratio does not increase with ethanol feeding as happens with controls   (MGI Ref ID J:105638)
    • serum alanine aminotransferase is not increased by ethanol feeding whereas levels increase 2 fold in controls   (MGI Ref ID J:105638)
    • TNF alpha levels remain constant with ethanol feeding whereas they increase 20 fold in controls   (MGI Ref ID J:105638)
    • no effect of ethanol diet on LPS sensitivity   (MGI Ref ID J:105638)
    • increased incidence of chemically-induced tumors
      • ENU treatment at 4 and 20 weeks weeks results in T-cell lymphomas in 53% of mice compared to 26% of controls treated at 3 weeks and 10% of controls treated at 20 weeks   (MGI Ref ID J:123870)
  • abnormal response to injury   (MGI Ref ID J:135238)
    • decreased cerebral infarction size
      • infarcts are much smaller in total area after temporary middle cerebral artery occlusion   (MGI Ref ID J:135238)
      • neurological deficits are mild   (MGI Ref ID J:135238)
      • less edema than in controls   (MGI Ref ID J:135238)
    • delayed wound healing
      • reduced rate of wound healing   (MGI Ref ID J:152898)
      • less collagen deposition   (MGI Ref ID J:152898)
      • fewer alpha smooth muscle cell positive myofibroblasts   (MGI Ref ID J:152898)
  • hematopoietic system phenotype
  • abnormal erythropoiesis
    • ineffective erythropoiesis in bone marrow and spleen   (MGI Ref ID J:123870)
  • abnormal hematopoietic stem cell morphology
    • two fold increase in hematopoietic stem cells in the S/G2-M phase of the cell cycle   (MGI Ref ID J:149801)
    • no buildup of stem cells in the bone marrow   (MGI Ref ID J:149801)
    • level of circulating hematopoietic stem cells is dramatically increased   (MGI Ref ID J:149801)
  • abnormal leukocyte morphology   (MGI Ref ID J:123870)
    • abnormal leukocyte cell number
      • mildly elevated   (MGI Ref ID J:123870)
      • increased lymphocyte cell number   (MGI Ref ID J:123870)
    • abnormal neutrophil morphology
      • dysplastic neutrophils in bone marrow and spleen   (MGI Ref ID J:123870)
  • decreased platelet cell number   (MGI Ref ID J:123870)
  • increased bone marrow cell number   (MGI Ref ID J:123870)
  • increased spleen weight
    • 15-20 fold increase in spleen weight   (MGI Ref ID J:123870)
    • expanded erythroid and myeloid cells in spleen   (MGI Ref ID J:123870)
  • immune system phenotype
  • *normal* immune system phenotype
    • no effect of ethanol diet on LPS sensitivity   (MGI Ref ID J:105638)
    • abnormal leukocyte morphology   (MGI Ref ID J:123870)
      • abnormal leukocyte cell number
        • mildly elevated   (MGI Ref ID J:123870)
        • increased lymphocyte cell number   (MGI Ref ID J:123870)
      • abnormal neutrophil morphology
        • dysplastic neutrophils in bone marrow and spleen   (MGI Ref ID J:123870)
    • abnormal microglial cell physiology
      • elevated numbers of activated microglial cells an macrophage but fewer than in controls   (MGI Ref ID J:135238)
    • abnormal tumor necrosis factor level
      • TNF alpha levels remain constant with ethanol feeding whereas they increase 20 fold in controls   (MGI Ref ID J:105638)
    • decreased inflammatory response
      • lower inflammatory response to four daily subcutaneous bleomycin injections   (MGI Ref ID J:152898)
      • lower inflammatory response to a single subcutaneous TGF beta injection   (MGI Ref ID J:152898)
    • increased spleen weight
      • 15-20 fold increase in spleen weight   (MGI Ref ID J:123870)
      • expanded erythroid and myeloid cells in spleen   (MGI Ref ID J:123870)
  • respiratory system phenotype
  • *normal* respiratory system phenotype
    • bleomycin induced lung pathologies are attenuated   (MGI Ref ID J:152898)
    • pulmonary fibrosis
      • number and size of subpleural and interstitial fibrotic foci is reduced   (MGI Ref ID J:152898)
      • diminished collagen accumulation   (MGI Ref ID J:152898)
      • pulmonary interstitial fibrosis
  • vision/eye phenotype
  • abnormal eye morphology   (MGI Ref ID J:123287)
    • abnormal cornea morphology
      • smaller radius of curvature at 40 days of age than in controls   (MGI Ref ID J:123287)
    • abnormal eye size
      • longer eyes (axial eye length) than controls at 42 days of age   (MGI Ref ID J:123287)
    • enlarged eye anterior chamber
      • deeper anterior chamber of the eye at 56 days of age   (MGI Ref ID J:123287)
  • abnormal vision
    • reduced refraction relative to controls   (MGI Ref ID J:123287)
  • nervous system phenotype
  • abnormal microglial cell physiology
    • elevated numbers of activated microglial cells an macrophage but fewer than in controls   (MGI Ref ID J:135238)
  • decreased cerebral infarction size
    • infarcts are much smaller in total area after temporary middle cerebral artery occlusion   (MGI Ref ID J:135238)
    • neurological deficits are mild   (MGI Ref ID J:135238)
    • less edema than in controls   (MGI Ref ID J:135238)
  • integument phenotype
  • skin papilloma
    • skin tumors induced by treatment with DMBA and TPA appear to be papillomas   (MGI Ref ID J:99386)
  • thick dermal layer
    • bleomycin induced dermal thickening more modest than in controls   (MGI Ref ID J:152898)
    • less sclerotic than controls   (MGI Ref ID J:152898)
    • less collagen accumulation   (MGI Ref ID J:152898)
    • reduced accumulation of alpha-smooth musclew actin myofibroblasts   (MGI Ref ID J:152898)
View Research Applications

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

Cardiovascular Research
Atherosclerosis

Endocrine Deficiency Research
Skin Defects

Immunology, Inflammation and Autoimmunity Research

Internal/Organ Research
Wound Healing
      delayed/impaired

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Egr1tm1Jmi
Allele Name targeted mutation 1, Jeffrey Milbrandt
Allele Type Targeted (knock-out)
Common Name(s) Egr-10; Egr-1ko; Egr1-; NGFI-A-; egr-1-;
Mutation Made By Jeffrey Milbrandt,   Washington University in St. Louis
Strain of Origin129
Gene Symbol and Name Egr1, early growth response 1
Chromosome 18
Gene Common Name(s) A530045N19Rik; AT225; ETR103; Egr-1; G0S30; KROX-24; Krox-1; Krox-24; Krox24; Kruppel box 1; Kruppel box 24; NGF1-A; NGFI-A; NGFIA; Ngf1; Ngfi; RIKEN cDNA A530045N19 gene; TIS8; ZIF-268; ZNF225; Zenk; Zfp-6; Zif268; zinc finger protein 6;
General Note ES cell line = AB1 (129S7/SvEvBrd-Hprt+) or D3 (129S2/SvPas). Phenotypic Similarity to Human Syndrome: Myeloproliferative disorder J:123870 background involves: 129 * C57BL/6
Molecular Note The gene was disrupted by insertion of a PGK-neo cassette into a coding exon upstream of the DNA-binding domain via homologous recombination. The targeted mutation introduces several stop codons resulting protein truncation upstream of the DNA-binding domain. Gene expression and protein product were not observed in homozygous mutant ES cells. [MGI Ref ID J:24948]

Genotyping

Genotyping Information

Genotyping Protocols

Egr1tm1Jmi,

Separated MCA
Egr1tm1Jmi, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Lee SL; Tourtellotte LC; Wesselschmidt RL; Milbrandt J. 1995. Growth and differentiation proceeds normally in cells deficient in the immediate early gene NGFI-A. J Biol Chem 270(17):9971-7. [PubMed: 7730380]  [MGI Ref ID J:24948]

Additional References

Egr1tm1Jmi related

Abdulkadir SA; Qu Z; Garabedian E; Song SK; Peters TJ; Svaren J; Carbone JM; Naughton CK; Catalona WJ; Ackerman JJ; Gordon JI; Humphrey PA; Milbrandt J. 2001. Impaired prostate tumorigenesis in Egr1-deficient mice. Nat Med 7(1):101-7. [PubMed: 11135623]  [MGI Ref ID J:67125]

Albrecht C; Preusch MR; Hofmann G; Morris-Rosenfeld S; Blessing E; Rosenfeld ME; Katus HA; Bea F. 2010. Egr-1 deficiency in bone marrow-derived cells reduces atherosclerotic lesion formation in a hyperlipidaemic mouse model. Cardiovasc Res 86(2):321-9. [PubMed: 20110335]  [MGI Ref ID J:175882]

Allen K; Jaeschke H; Copple BL. 2011. Bile acids induce inflammatory genes in hepatocytes: a novel mechanism of inflammation during obstructive cholestasis. Am J Pathol 178(1):175-86. [PubMed: 21224055]  [MGI Ref ID J:168234]

Andrassy M; Belov D; Harja E; Zou YS; Leitges M; Katus HA; Nawroth PP; Yan SD; Schmidt AM; Yan SF. 2005. Central role of PKCbeta in neointimal expansion triggered by acute arterial injury. Circ Res 96(4):476-83. [PubMed: 15662033]  [MGI Ref ID J:106870]

Beck H; Semisch M; Culmsee C; Plesnila N; Hatzopoulos AK. 2008. Egr-1 regulates expression of the glial scar component phosphacan in astrocytes after experimental stroke. Am J Pathol 173(1):77-92. [PubMed: 18556777]  [MGI Ref ID J:137369]

Bettini M; Xi H; Milbrandt J; Kersh GJ. 2002. Thymocyte development in early growth response gene 1-deficient mice. J Immunol 169(4):1713-20. [PubMed: 12165491]  [MGI Ref ID J:78245]

Bieging KT; Fish K; Bondada S; Longnecker R. 2011. A shared gene expression signature in mouse models of EBV-associated and non-EBV-associated Burkitt lymphoma. Blood 118(26):6849-59. [PubMed: 22039254]  [MGI Ref ID J:179064]

Buitrago M; Lorenz K; Maass AH; Oberdorf-Maass S; Keller U; Schmitteckert EM; Ivashchenko Y; Lohse MJ; Engelhardt S. 2005. The transcriptional repressor Nab1 is a specific regulator of pathological cardiac hypertrophy. Nat Med 11(8):837-44. [PubMed: 16025126]  [MGI Ref ID J:100641]

Carter JH; Lefebvre JM; Wiest DL; Tourtellotte WG. 2007. Redundant role for early growth response transcriptional regulators in thymocyte differentiation and survival. J Immunol 178(11):6796-805. [PubMed: 17513727]  [MGI Ref ID J:142945]

Carter JH; Tourtellotte WG. 2007. Early growth response transcriptional regulators are dispensable for macrophage differentiation. J Immunol 178(5):3038-47. [PubMed: 17312150]  [MGI Ref ID J:144099]

Cenci S; Weitzmann MN; Gentile MA; Aisa MC; Pacifici R. 2000. M-CSF neutralization and egr-1 deficiency prevent ovariectomy-induced bone loss. J Clin Invest 105(9):1279-87. [PubMed: 10792003]  [MGI Ref ID J:62113]

Chen SH; Yao HW; Chen IT; Shieh B; Li C; Chen SH. 2008. Suppression of transcription factor early growth response 1 reduces herpes simplex virus lethality in mice. J Clin Invest 118(10):3470-7. [PubMed: 18769632]  [MGI Ref ID J:141166]

Cho SJ; Kang MJ; Homer RJ; Kang HR; Zhang X; Lee PJ; Elias JA; Lee CG. 2006. Role of early growth response-1 (Egr-1) in interleukin-13-induced inflammation and remodeling. J Biol Chem 281(12):8161-8. [PubMed: 16439363]  [MGI Ref ID J:110587]

Cornish EJ; Hurtgen BJ; McInnerney K; Burritt NL; Taylor RM; Jarvis JN; Wang SY; Burritt JB. 2008. Reduced nicotinamide adenine dinucleotide phosphate oxidase-independent resistance to Aspergillus fumigatus in alveolar macrophages. J Immunol 180(10):6854-67. [PubMed: 18453606]  [MGI Ref ID J:134869]

Dutta M; Kraus ZJ; Gomez-Rodriguez J; Hwang SH; Cannons JL; Cheng J; Lee SY; Wiest DL; Wakeland EK; Schwartzberg PL. 2013. A role for ly108 in the induction of promyelocytic zinc finger transcription factor in developing thymocytes. J Immunol 190(5):2121-8. [PubMed: 23355739]  [MGI Ref ID J:193308]

Gao X; Daugherty RL; Tourtellotte WG. 2007. Regulation of low affinity neurotrophin receptor (p75(NTR)) by early growth response (Egr) transcriptional regulators. Mol Cell Neurosci 36(4):501-14. [PubMed: 17916431]  [MGI Ref ID J:126322]

Gehrig A; Langmann T; Horling F; Janssen A; Bonin M; Walter M; Poths S; Weber BH. 2007. Genome-wide expression profiling of the retinoschisin-deficient retina in early postnatal mouse development. Invest Ophthalmol Vis Sci 48(2):891-900. [PubMed: 17251492]  [MGI Ref ID J:123330]

Gokey NG; Lopez-Anido C; Gillian-Daniel AL; Svaren J. 2011. Early growth response 1 (Egr1) regulates cholesterol biosynthetic gene expression. J Biol Chem 286(34):29501-10. [PubMed: 21712389]  [MGI Ref ID J:176629]

Gururajan M; Simmons A; Dasu T; Spear BT; Calulot C; Robertson DA; Wiest DL; Monroe JG; Bondada S. 2008. Early growth response genes regulate B cell development, proliferation, and immune response. J Immunol 181(7):4590-602. [PubMed: 18802061]  [MGI Ref ID J:141295]

Harja E; Bucciarelli LG; Lu Y; Stern DM; Zou YS; Schmidt AM; Yan SF. 2004. Early growth response-1 promotes atherogenesis: mice deficient in early growth response-1 and apolipoprotein E display decreased atherosclerosis and vascular inflammation. Circ Res 94(3):333-9. [PubMed: 14670837]  [MGI Ref ID J:96665]

Hu T; Gimferrer I; Simmons A; Wiest D; Alberola-Ila J. 2011. The Ras/MAPK Pathway Is Required for Generation of iNKT Cells. PLoS One 6(5):e19890. [PubMed: 21572967]  [MGI Ref ID J:172652]

Ingram JL; Antao-Menezes A; Mangum JB; Lyght O; Lee PJ; Elias JA; Bonner JC. 2006. Opposing actions of Stat1 and Stat6 on IL-13-induced up-regulation of early growth response-1 and platelet-derived growth factor ligands in pulmonary fibroblasts. J Immunol 177(6):4141-8. [PubMed: 16951379]  [MGI Ref ID J:138041]

Joslin JM; Fernald AA; Tennant TR; Davis EM; Kogan SC; Anastasi J; Crispino JD; Le Beau MM. 2007. Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders. Blood 110(2):719-26. [PubMed: 17420284]  [MGI Ref ID J:123870]

Kramer EL; Mushaben EM; Pastura PA; Acciani TH; Deutsch GH; Khurana Hershey GK; Korfhagen TR; Hardie WD; Whitsett JA; Le Cras TD. 2009. Early growth response-1 suppresses epidermal growth factor receptor-mediated airway hyperresponsiveness and lung remodeling in mice. Am J Respir Cell Mol Biol 41(4):415-25. [PubMed: 19188657]  [MGI Ref ID J:164707]

Krones-Herzig A; Mittal S; Yule K; Liang H; English C; Urcis R; Soni T; Adamson ED; Mercola D. 2005. Early growth response 1 acts as a tumor suppressor in vivo and in vitro via regulation of p53. Cancer Res 65(12):5133-43. [PubMed: 15958557]  [MGI Ref ID J:99386]

Lazarevic V; Zullo AJ; Schweitzer MN; Staton TL; Gallo EM; Crabtree GR; Glimcher LH. 2009. The gene encoding early growth response 2, a target of the transcription factor NFAT, is required for the development and maturation of natural killer T cells. Nat Immunol 10(3):306-13. [PubMed: 19169262]  [MGI Ref ID J:146134]

Lee CG; Cho SJ; Kang MJ; Chapoval SP; Lee PJ; Noble PW; Yehualaeshet T; Lu B; Flavell RA; Milbrandt J; Homer RJ; Elias JA. 2004. Early growth response gene 1-mediated apoptosis is essential for transforming growth factor beta1-induced pulmonary fibrosis. J Exp Med 200(3):377-89. [PubMed: 15289506]  [MGI Ref ID J:92469]

Lee SL; Sadovsky Y; Swirnoff AH; Polish JA; Goda P; Gavrilina G; Milbrandt J. 1996. Luteinizing hormone deficiency and female infertility in mice lacking the transcription factor NGFI-A (Egr-1). Science 273(5279):1219-21. [PubMed: 8703054]  [MGI Ref ID J:35132]

Lee SL; Wang Y; Milbrandt J. 1996. Unimpaired macrophage differentiation and activation in mice lacking the zinc finger transplantation factor NGFI-A (EGR1). Mol Cell Biol 16(8):4566-72. [PubMed: 8754857]  [MGI Ref ID J:34381]

Li B; Power MR; Lin TJ. 2006. De novo synthesis of early growth response factor-1 is required for the full responsiveness of mast cells to produce TNF and IL-13 by IgE and antigen stimulation. Blood 107(7):2814-20. [PubMed: 16317093]  [MGI Ref ID J:131243]

Li L; Carter J; Gao X; Whitehead J; Tourtellotte WG. 2005. The neuroplasticity-associated arc gene is a direct transcriptional target of early growth response (Egr) transcription factors. Mol Cell Biol 25(23):10286-300. [PubMed: 16287845]  [MGI Ref ID J:119883]

Liao Y; Shikapwashya ON; Shteyer E; Dieckgraefe BK; Hruz PW; Rudnick DA. 2004. Delayed hepatocellular mitotic progression and impaired liver regeneration in early growth response-1-deficient mice. J Biol Chem 279(41):43107-16. [PubMed: 15265859]  [MGI Ref ID J:93996]

McMullen MR; Pritchard MT; Wang Q; Millward CA; Croniger CM; Nagy LE. 2005. Early growth response-1 transcription factor is essential for ethanol-induced fatty liver injury in mice. Gastroenterology 128(7):2066-76. [PubMed: 15940638]  [MGI Ref ID J:105638]

McNeil LK; Starr TK; Hogquist KA. 2005. A requirement for sustained ERK signaling during thymocyte positive selection in vivo. Proc Natl Acad Sci U S A 102(38):13574-9. [PubMed: 16174747]  [MGI Ref ID J:101416]

Min IM; Pietramaggiori G; Kim FS; Passegue E; Stevenson KE; Wagers AJ. 2008. The transcription factor EGR1 controls both the proliferation and localization of hematopoietic stem cells. Cell Stem Cell 2(4):380-91. [PubMed: 18397757]  [MGI Ref ID J:149801]

Pritchard MT; Nagy LE. 2010. Hepatic fibrosis is enhanced and accompanied by robust oval cell activation after chronic carbon tetrachloride administration to Egr-1-deficient mice. Am J Pathol 176(6):2743-52. [PubMed: 20395449]  [MGI Ref ID J:161334]

Pritchard MT; Roychowdhury S; McMullen MR; Guo L; Arteel GE; Nagy LE. 2007. Early growth response-1 contributes to galactosamine/lipopolysaccharide-induced acute liver injury in mice. Am J Physiol Gastrointest Liver Physiol 293(6):G1124-33. [PubMed: 17916644]  [MGI Ref ID J:128421]

Ramana CV; Cheng GS; Kumar A; Kwon HJ; Enelow RI. 2009. Role of alveolar epithelial early growth response-1 (Egr-1) in CD8+ T cell-mediated lung injury. Mol Immunol 47(2-3):623-31. [PubMed: 19786304]  [MGI Ref ID J:155228]

Reumann MK; Strachna O; Yagerman S; Torrecilla D; Kim J; Doty SB; Lukashova L; Boskey AL; Mayer-Kuckuk P. 2011. Loss of transcription factor early growth response gene 1 results in impaired endochondral bone repair. Bone 49(4):743-52. [PubMed: 21726677]  [MGI Ref ID J:176477]

Saadane N; Alpert L; Chalifour LE. 2000. Altered molecular response to adrenoreceptor-induced cardiac hypertrophy in Egr-1-deficient mice. Am J Physiol Heart Circ Physiol 278(3):H796-805. [PubMed: 10710348]  [MGI Ref ID J:61294]

Schippert R; Burkhardt E; Feldkaemper M; Schaeffel F. 2007. Relative axial myopia in Egr-1 (ZENK) knockout mice. Invest Ophthalmol Vis Sci 48(1):11-7. [PubMed: 17197510]  [MGI Ref ID J:123287]

Schmidt J; Stoffels B; Moore BA; Chanthaphavong RS; Mazie AR; Buchholz BM; Bauer AJ. 2008. Proinflammatory role of leukocyte-derived Egr-1 in the development of murine postoperative ileus. Gastroenterology 135(3):926-36, 936.e1-2. [PubMed: 18652830]  [MGI Ref ID J:141988]

Schnell FJ; Kersh GJ. 2005. Control of recent thymic emigrant survival by positive selection signals and early growth response gene 1. J Immunol 175(4):2270-7. [PubMed: 16081795]  [MGI Ref ID J:107510]

Schnell FJ; Zoller AL; Patel SR; Williams IR; Kersh GJ. 2006. Early growth response gene 1 provides negative feedback to inhibit entry of progenitor cells into the thymus. J Immunol 176(8):4740-7. [PubMed: 16585567]  [MGI Ref ID J:131188]

Singh A; Svaren J; Grayson J; Suresh M. 2004. CD8 T cell responses to lymphocytic choriomeningitis virus in early growth response gene 1-deficient mice. J Immunol 173(6):3855-62. [PubMed: 15356133]  [MGI Ref ID J:92763]

Srivastava S; Weitzmann MN; Kimble RB; Rizzo M; Zahner M; Milbrandt J; Ross FP; Pacifici R. 1998. Estrogen blocks M-CSF gene expression and osteoclast formation by regulating phosphorylation of Egr-1 and its interaction with Sp-1. J Clin Invest 102(10):1850-9. [PubMed: 9819371]  [MGI Ref ID J:51107]

Sullivan BP; Cui W; Copple BL; Luyendyk JP. 2012. Early growth response factor-1 limits biliary fibrosis in a model of xenobiotic-induced cholestasis in mice. Toxicol Sci 126(1):267-74. [PubMed: 22094456]  [MGI Ref ID J:183661]

Tourtellotte WG; Nagarajan R; Bartke A; Milbrandt J. 2000. Functional compensation by Egr4 in Egr1-dependent luteinizing hormone regulation and Leydig cell steroidogenesis. Mol Cell Biol 20(14):5261-8. [PubMed: 10866682]  [MGI Ref ID J:63084]

Tureyen K; Brooks N; Bowen K; Svaren J; Vemuganti R. 2008. Transcription factor early growth response-1 induction mediates inflammatory gene expression and brain damage following transient focal ischemia. J Neurochem 105(4):1313-24. [PubMed: 18208539]  [MGI Ref ID J:135238]

Wang C; Dostanic S; Servant N; Chalifour LE. 2005. Egr-1 negatively regulates expression of the sodium-calcium exchanger-1 in cardiomyocytes in vitro and in vivo. Cardiovasc Res 65(1):187-94. [PubMed: 15621046]  [MGI Ref ID J:134626]

Wu M; Melichian DS; de la Garza M; Gruner K; Bhattacharyya S; Barr L; Nair A; Shahrara S; Sporn PH; Mustoe TA; Tourtellotte WG; Varga J. 2009. Essential roles for early growth response transcription factor Egr-1 in tissue fibrosis and wound healing. Am J Pathol 175(3):1041-55. [PubMed: 19679873]  [MGI Ref ID J:152898]

Yan SF; Fujita T; Lu J; Okada K; Shan Zou Y; Mackman N; Pinsky DJ; Stern DM. 2000. Egr-1, a master switch coordinating upregulation of divergent gene families underlying ischemic stress Nat Med 6(12):1355-61. [PubMed: 11100120]  [MGI Ref ID J:66141]

Yang YJ; Chen W; Edgar A; Li B; Molkentin JD; Berman JN; Lin TJ. 2009. Rcan1 negatively regulates Fc epsilonRI-mediated signaling and mast cell function. J Exp Med 206(1):195-207. [PubMed: 19124655]  [MGI Ref ID J:144026]

Yao H; Duan M; Buch S. 2011. Cocaine-mediated induction of platelet-derived growth factor: implication for increased vascular permeability. Blood 117(8):2538-47. [PubMed: 21148086]  [MGI Ref ID J:169571]

Yao HW; Chen SH; Li C; Tung YY; Chen SH. 2012. Suppression of transcription factor early growth response 1 reduces herpes simplex virus 1-induced corneal disease in mice. J Virol 86(16):8559-67. [PubMed: 22647700]  [MGI Ref ID J:186165]

Yasuoka H; Hsu E; Ruiz XD; Steinman RA; Choi AM; Feghali-Bostwick CA. 2009. The fibrotic phenotype induced by IGFBP-5 is regulated by MAPK activation and egr-1-dependent and -independent mechanisms. Am J Pathol 175(2):605-15. [PubMed: 19628764]  [MGI Ref ID J:150940]

Yu J; Baron V; Mercola D; Mustelin T; Adamson ED. 2007. A network of p73, p53 and Egr1 is required for efficient apoptosis in tumor cells. Cell Death Differ 14(3):436-46. [PubMed: 16990849]  [MGI Ref ID J:132337]

Zaiou M; Azrolan N; Hayek T; Wang H; Wu L; Haghpassand M; Cizman B; Madaio MP; Milbrandt J; Marsh JB; Breslow JL; Fisher EA. 1998. The full induction of human apoprotein A-I gene expression by the experimental nephrotic syndrome in transgenic mice depends on cis-acting elements in the proximal 256 base-pair promoter region and the trans-acting factor early growth response factor 1. J Clin Invest 101(8):1699-707. [PubMed: 9541501]  [MGI Ref ID J:118791]

Zheng D; Butler LS; McNamara JO. 1998. Kindling and associated mossy fibre sprouting are not affected in mice deficient of NGFI-A/ NGFI-B genes. Neuroscience 83(1):251-8. [PubMed: 9466414]  [MGI Ref ID J:47060]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous mice may be bred to wildtype mice from the colony. Homozygous females are sterile.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   07-OCT-10
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 $232.00Female or MaleHeterozygous for Egr1tm1Jmi  
$232.00Female or MaleHomozygous for Egr1tm1Jmi  
Price per Pair (US dollars $)Pair Genotype
$464.00Heterozygous for Egr1tm1Jmi x Heterozygous for Egr1tm1Jmi  

Standard Supply

Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $301.60Female or MaleHeterozygous for Egr1tm1Jmi  
$301.60Female or MaleHomozygous for Egr1tm1Jmi  
Price per Pair (US dollars $)Pair Genotype
$603.20Heterozygous for Egr1tm1Jmi x Heterozygous for Egr1tm1Jmi  

Standard Supply

Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.

Control Information

  Control
   Wild-type from the colony
   005304 C57BL/6NJ (approximate)
 
  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
fax:207-288-6655

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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