Strain Name:

C3H/HeJ

Stock Number:

000659

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      Cell Line: C3H/HeJ AC386/GrsrJ mES cells
      Cell Line: C3H/HeJ-PB151.24 mES cells
      Cell Line: C3H/HeJ-PRX-C3H #2 mES cells

Common Names: C3;     C3H Heston;    
C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, infectious disease, sensorineural, and cardiovascular biology research. A spontaneous mutation occurred in C3H/HeJ at the lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4Lps-d) making C3H/HeJ mice more resistant to endotoxin. C3H/HeJ (Tlr4Lps-d) mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica.

Description

Strain Information

Former Names C3H/HeJ-Pde6brd1    (Changed: 19-MAR-08 )
Type Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Type Inbred Strain;
Additional information on Inbred Strains.
Visit our online Nomenclature tutorial.
Mating SystemSibling x Sibling         (Female x Male)   01-MAR-06
Breeding Considerations This strain is an exceptional breeder.
Specieslaboratory mouse
H2 Haplotypek
GenerationF258pF261 (14-AUG-14)
Generation Definitions

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Appearance
agouti
Related Genotype: A/A

Important Note
This strain does not carry mouse mammary tumor virus (MMTV). See JAX® NOTES, May 2000, No. 480. This strain is homozygous for retinal degeneration allele Pde6brd1, the defective lipopolysaccharide response allele Tlr4Lps-d, and for a chromosomal inversion on Chromosome 6. A sighted alternative is Stock No. 003648, C3Sn.BLiA-Pde6b+/DnJ.

Description
C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. White belly spots, ranging in phenotype from a few white hairs to a defined spot are common in C3H/HeJ mice. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). C3H/HeJ mice spontaneously develop alopecia areata (AA) at a reported incidence of approximately 0.25% by 5 months of age. In older mice (12-18 months old), incidences as high as approximately 20% are reported. Females as young as 3-5 months can develop AA, but onset typically is delayed until after 6 months in males. Alopecia areata can be surgically-induced by grafting a small piece of skin from an older, donor animal with AA onto a younger, isogenic C3H/HeJ recipient.

A spontaneous mutation occurred in C3H/HeJ at the lipopolysaccharide response locus (later identified as a mutation in the toll-like receptor 4 gene, Tlr4Lps-d) making C3H/HeJ mice endotoxin resistant. C3H/HeJ (Tlr4Lps-d) mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica. Mice infected with Salmonella exhibit delayed chemokine production, impaired nitric oxide generation and attenuated cellular immune responses. Mortality in infected mice appears to result from enhanced bacterial growth within the liver Kupffer cell network (Vazquez-Torres et al., 2004). The C3H/HeJ substrain is homozygous for an inversion on Chromosome 6 (symbol: In(6)1J). The inversion covers 20% of Chromosome 6 between D6Mit124 (~30.3 cM) and D6Mit150 (~51.0 cM), but results in no reported phenotype. Results from screening other C3H substrains and cryopreserved stock from C3H/HeJ suggest that the mutation arose after 1952. See JAX Notes, Fall 2003, No. 491. The spontaneous mutation, spike wave discharge 1 (spkw1), is present in C3H/HeJ, but not C3HeB/FeJ. Mice homozygous for this mutation exhibit a modest incidence of absence seizures.

Development
The C3H parent strain was developed by LC Strong in 1920 from a cross of a Bagg albino female with a DBA male followed by selection for high incidence of mammary tumors. This high incidence resulted from exogenous mouse mammary tumor virus (MMTV) transmitted through the mother's milk. The Jackson Laboratory maintains four C3H substrains, C3H/HeJ (Stock No. 000659), C3H/HeOuJ (Stock No. 000635), C3HeB/FeJ (Stock No. 000658) and C3H/HeSnJ (Stock No. 000661) that are now free of exogenous MMTV. C3H/HeJ and C3H/HeOuJ mice previously carried MMTV but were rederived in 1999 during planned efforts to increase the overall health status of the mice and the virus was not reintroduced. C3H/HeJ and C3H/HeOuJ substrains were separated in 1952 and are genetically very similar. However, a spontaneous mutation occurred in C3H/HeJ sometime between 1960 and 1968 at lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4lps) making C3H/HeJ mice endotoxin resistant while the other three C3H strains are endotoxin sensitive.

Related Strains

C3H Strains
005972   C3H/HeJBirLtJ
001824   C3H/HeJSxJ
000635   C3H/HeOuJ
000474   C3H/HeSn
000661   C3H/HeSnJ
000658   C3HeB/FeJ
001908   C3HfB/BiJ
View C3H Strains     (7 strains)

Strains carrying   Ahrb-2 allele
000645   A/HeJ
000646   A/J
000130   B6.C-H17c/(HW14)ByJ
000370   B6.C-H38c/(HW119)ByJ
001026   BALB/cByJ
000653   BUB/BnJ
000656   CBA/J
000657   CE/J
000352   CXB2/ByJ
000353   CXB3/ByJ
000354   CXB4/ByJ
000355   CXB5/ByJ
000357   CXB7/ByJ
000673   HRS/J
000679   P/J
000930   PERA/EiJ
000644   SEA/GnJ
000280   SF/CamEiJ
View Strains carrying   Ahrb-2     (18 strains)

Strains carrying   Pde6brd1 allele
004202   B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J
000002   B6.C3-Pde6brd1 Hps4le/J
001022   B6C3FeF1/J a/a
000652   BDP/J
000653   BUB/BnJ
002439   C3.129P2(B6)-B2mtm1Unc/J
005494   C3.129S1(B6)-Grm1rcw/J
000509   C3.Cg-Lystbg-2J/J
000480   C3.MRL-Faslpr/J
001957   C3A Pde6brd1.O20/A-Prph2Rd2/J
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
003968   C3Bir.129P2(B6)-Il10tm1Cgn/LtJ
006435   C3Fe.SW-Soaa/MonJ
001904   C3H-Atcayji-hes/J
000511   C3H/HeJ-Ap3d1mh-2J/J
000784   C3H/HeJ-Faslgld/J
002433   C3H/HeJ-Sptbn4qv-lnd2J/J
005972   C3H/HeJBirLtJ
001824   C3H/HeJSxJ
000635   C3H/HeOuJ
000474   C3H/HeSn
001431   C3H/HeSn-ocd/J
000661   C3H/HeSnJ
002333   C3H/HeSnJ-gri/J
001576   C3He-Atp7btx-J/J
000658   C3HeB/FeJ
002588   C3HeB/FeJ-Eya1bor/J
001533   C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J
001908   C3HfB/BiJ
001502   C3Sn.B6-Epha4rb/EiGrsrJ
002235   C3Sn.C3-Ctnna2cdf/J
001547   C3Sn.Cg-Cm/J
001906   C3fBAnl.Cg-Catb/AnlJ
000656   CBA/J
000813   CBA/J-Atp7aMo-pew/J
000660   DA/HuSnJ
000023   FL/1ReJ
000025   FL/4ReJ
003024   FVB.129P2(B6)-Fmr1tm1Cgr/J
002539   FVB.129P2-Abcb4tm1Bor/J
002935   FVB.129S2(B6)-Ccnd1tm1Wbg/J
002953   FVB.Cg-Tg(MMTVTGFA)254Rjc/J
003170   FVB.Cg-Tg(Myh6-tTA)6Smbf/J
003078   FVB.Cg-Tg(WapIgf1)39Dlr/J
003487   FVB.Cg-Tg(XGFAP-lacZ)3Mes/J
003257   FVB/N-Tg(GFAPGFP)14Mes/J
002856   FVB/N-Tg(TIE2-lacZ)182Sato/J
002384   FVB/N-Tg(UcpDta)1Kz/J
001800   FVB/NJ
001491   FVB/NMob
000804   HPG/BmJ
000734   MOLD/RkJ
000550   MOLF/EiJ
002423   NON/ShiLtJ
000679   P/J
000680   PL/J
000268   RSV/LeJ
000269   SB/LeJ
010968   SB;C3Sn-Lrp4mdig-2J/GrsrJ
005651   SJL.AK-Thy1a/TseJ
000686   SJL/J
000688   ST/bJ
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
002648   STOCK a/a Cln6nclf/J
000279   STOCK gr +/+ Ap3d1mh/J
005965   STOCK Tg(Pomc1-cre)16Lowl/J
004770   SW.B6-Soab/J
002023   SWR.M-Emv21 Emv22/J
000689   SWR/J
000939   SWR/J-Clcn1adr-mto/J
000692   WB/ReJ KitW/J
100410   WBB6F1/J-KitW/KitW-v/J
000693   WC/ReJ KitlSl/J
View Strains carrying   Pde6brd1     (73 strains)

Strains carrying   Tlr4Lps-d allele
002930   C.C3-Tlr4Lps-d/J
005973   C3Bir.129P2(B6)-Il10C3Bir/LtJ
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
003968   C3Bir.129P2(B6)-Il10tm1Cgn/LtJ
005972   C3H/HeJBirLtJ
View Strains carrying   Tlr4Lps-d     (5 strains)

Strains carrying other alleles of Ahr
000690   129P3/J
000648   AKR/J
002920   B6(D2N).Spretus-Ahrb-3/J
002831   B6.129-Ahrtm1Bra/J
000136   B6.C-H34c/(HW22)ByJ
008599   B6.Cg-Cyp1a2/Cyp1a1tm2Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ
002921   B6.D2N-Ahrd/J
002727   B6;129-Ahrtm1Bra/J
000652   BDP/J
000663   C57BL/6By
001139   C57BL/6ByJ
000664   C57BL/6J
000662   C57BLKS/J
000667   C57BR/cdJ
000668   C57L/J
000669   C58/J
000926   CAROLI/EiJ
000928   CAST/EiJ
000351   CXB1/ByJ
000356   CXB6/ByJ
002937   D2.B6-Ahrb-1/J
000671   DBA/2J
000674   I/LnJ
000675   LG/J
000676   LP/J
000677   MA/MyJ
000550   MOLF/EiJ
000684   NZB/BlNJ
000726   RBF/DnJ
000682   RF/J
000686   SJL/J
001146   SPRET/EiJ
000688   ST/bJ
006203   STOCK Ahrtm3.1Bra/J
000689   SWR/J
000693   WC/ReJ KitlSl/J
000933   YBR/EiJ
View Strains carrying other alleles of Ahr     (37 strains)

Strains carrying other alleles of Gria4
012618   B6.129(Cg)-Gria4tm2.1Rlh/J
012619   B6.129-Gria4tm1Rlh/J
View Strains carrying other alleles of Gria4     (2 strains)

View Strains carrying other alleles of Pde6b     (13 strains)

Strains carrying other alleles of Tlr4
024872   B6(Cg)-Tlr4tm1.1Karp/J
007227   B6.B10ScN-Tlr4lps-del/JthJ
000029   BXD29-Tlr4lps-2J/J
003752   C57BL/10ScNJ
View Strains carrying other alleles of Tlr4     (4 strains)

Additional Web Information

C3H strains free of exogenous MMTV
JAX® NOTES, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX® NOTES, Fall 2003; 491. Chromosomal Inversion Discovered in C3H/HeJ Mice.
JAX® NOTES, January 1988; 432. Arthritis Models in the Mouse.
JAX® NOTES, July 1987; 430. LPS Responsiveness of C3H Substrains.
JAX® NOTES, July 1987; 430. Mammary Tumor Incidence in C3H/HeJ and C3H/OuJ.
JAX® NOTES, Spring 1995; 461. Neoplastic and Hyperplastic Lesions in the C3H/HeJ Mouse Strain.
JAX® NOTES, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX® NOTES, Spring 2005; 497. Update of Chromosome 6 Inversion in JAX® Mice Strain C3H/HeJ.
JAX® NOTES, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX® NOTES, Summer 2005; 498. Toll-like Receptor JAX® Mice for Immunological Research.
JAX® NOTES, Winter 2006; 504. JAX® Mice: the Gold Standard Just Got Better.
JAX® NOTES, Winter 2006; 504. Reliable New Sperm Cryopreservation Service Developed at The Jackson Laboratory.
Mouse Phenome Database / SNP Facility
Sequence data is available from the Mouse Genomes Project at the Wellcome Trust Sanger Institute

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data

Body Weight Information - JAX® Mice Strain C3H/HeJ (000659)

(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)
Mouse Phenome Database
Festing Inbred Strain Characteristics: C3H
JAX® Physiological Data Summary [pdf]
JAX® Physiological Data Protocol [pdf]
View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Retinitis Pigmentosa 40; RP40
Toll-Like Receptor 4; TLR4
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Macular Degeneration, Age-Related, 10; ARMD10   (TLR4)
Night Blindness, Congenital Stationary, Autosomal Dominant 2; CSNBAD2   (PDE6B)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ahrb-2/Ahrb-2

        C3H/He
  • mortality/aging
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • mice are susceptible to DMBA induced lethality   (MGI Ref ID J:26440)
  • homeostasis/metabolism phenotype
  • increased physiological sensitivity to xenobiotic
    • mice are susceptible to the pathological effects of DMBA and exhibit lethality, weight loss, peritonitis, decreased spleen weight, and decreased thymus weight   (MGI Ref ID J:26440)
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • mice are susceptible to DMBA induced lethality   (MGI Ref ID J:26440)

Gria4spkw1/Gria4spkw1

        C3H/HeJ
  • behavior/neurological phenotype
  • absence seizures
    • mice show higher spike wave discharge incidence than C3HeB/FeJ or C57BL/6 mice   (MGI Ref ID J:135814)
  • nervous system phenotype
  • absence seizures
    • mice show higher spike wave discharge incidence than C3HeB/FeJ or C57BL/6 mice   (MGI Ref ID J:135814)

In(6)1J/In(6)1J

        C3H/HeJ
  • normal phenotype
  • no abnormal phenotype detected
    • no phenotype is known to be associated with this chromosomal inversion   (MGI Ref ID J:87486)

Pde6brd1/Pde6brd1

        C3H/HeJ
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • despite the absence of rods, mice exhibit normal photopotentiation (defined as a 50% augmentation in pupillary light response (PLR) compared to pre-bright light PLR during a one minute dim blue light exposure after bright light exposure)   (MGI Ref ID J:123259)
    • abnormal retinal outer nuclear layer morphology
      • nearly complete absence of outer nuclear layer   (MGI Ref ID J:66580)
    • absent photoreceptor outer segment   (MGI Ref ID J:66580)
    • retinal degeneration
      • entire outer retina is destroyed, however the inner retina remains intact   (MGI Ref ID J:66580)
  • nervous system phenotype
  • absent photoreceptor outer segment   (MGI Ref ID J:66580)

Tlr4Lps-d/Tlr4Lps-d

        involves: C3H/HeJ
  • immune system phenotype
  • abnormal T-helper 2 physiology
    • Th2 responses elevated after induction of autoimmune arthritis   (MGI Ref ID J:96356)
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • abnormal tumor necrosis factor level
    • diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
    • macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage   (MGI Ref ID J:124334)
  • increased susceptibility to bacterial infection
    • low responsiveness of spleen cells to lipopolysaccharides   (MGI Ref ID J:5721)
    • increased sensitivity to gram (-) infection   (MGI Ref ID J:51522)
    • significantly shortened survival after infection with Klebsiella pneumoniae   (MGI Ref ID J:87807)
    • increased K. pneumoniae levels in the lung   (MGI Ref ID J:87807)
  • increased susceptibility to induced arthritis
    • reduced susceptibility to arthritis induced by type II collagen   (MGI Ref ID J:96356)
  • behavior/neurological phenotype
  • hyporesponsive to tactile stimuli
    • reduced mechanical allodynia after nerve injury   (MGI Ref ID J:97819)
  • increased thermal nociceptive threshold
    • attenuated response to heat   (MGI Ref ID J:97819)
  • skeleton phenotype
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • increased susceptibility to induced arthritis
    • reduced susceptibility to arthritis induced by type II collagen   (MGI Ref ID J:96356)
  • muscle phenotype
  • *normal* muscle phenotype
    • MCP-1 (monocyte chemoattractant protein-1) release from isolated mouse aorta smooth muscle cells (MAoSMC) by stimulation with dsRNA is normal relative to controls   (MGI Ref ID J:116310)
  • integument phenotype
  • hyporesponsive to tactile stimuli
    • reduced mechanical allodynia after nerve injury   (MGI Ref ID J:97819)
  • increased thermal nociceptive threshold
    • attenuated response to heat   (MGI Ref ID J:97819)
  • nervous system phenotype
  • abnormal glial cell apoptosis
    • isolated microglia exposed to LPS are resistant to apoptosis   (MGI Ref ID J:99051)
  • homeostasis/metabolism phenotype
  • abnormal circulating enzyme level
    • myeloperoxidase levels are reduced after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
    • increased HO-1 expression   (MGI Ref ID J:114368)
    • decreased circulating alanine transaminase level
      • serum levels decreased after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
  • abnormal tumor necrosis factor level
    • diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion   (MGI Ref ID J:114368)
    • macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage   (MGI Ref ID J:124334)
  • hematopoietic system phenotype
  • abnormal T-helper 2 physiology
    • Th2 responses elevated after induction of autoimmune arthritis   (MGI Ref ID J:96356)
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • cellular phenotype
  • abnormal glial cell apoptosis
    • isolated microglia exposed to LPS are resistant to apoptosis   (MGI Ref ID J:99051)
  • abnormal osteoclast differentiation
    • lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls   (MGI Ref ID J:131353)
    • antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL   (MGI Ref ID J:131353)
  • hearing/vestibular/ear phenotype
  • *normal* hearing/vestibular/ear phenotype
    • cisplatin and lipopolysaccharide treatment does not lead to significant increases in auditory brainstem response as is observed in controls   (MGI Ref ID J:168789)

Tlr4Lps-d/Tlr4Lps-d

        C3H/HeJ-Tlr4Lps-d
  • mortality/aging
  • decreased sensitivity to induced morbidity/mortality
    • bacterial lipoteichoic acid exposure after priming by IFNgamma and sensitization with D-galactosamine induces lethal shock in Tlr4-deficient mutants, while Tlr2- and Tlr2/4-doubly deficient mice are protected   (MGI Ref ID J:121930)
    • systemic challenge with Myr3-CSK4 (a synthetic lipopeptide) after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected   (MGI Ref ID J:121930)
    • heat-inactivated E. coli exposure results in fatal toxemia as in wild type mice heat-inactivated E. coli exposure results in fatal toxemia as in wild-type mice   (MGI Ref ID J:121930)
  • increased susceptibility to viral infection induced morbidity/mortality
    • 10 days after intranasal infection with 5 x 105 pfu Vac-GFL 70% of mice succumb unlike wild-type controls that all survive   (MGI Ref ID J:162716)
  • growth/size/body phenotype
  • decreased body size
    • always smaller than controls   (MGI Ref ID J:118467)
    • decreased body weight
      • lower body weight than controls after 8 weeks on a high fat diet   (MGI Ref ID J:126488)
      • weights are 15% lower than controls after 8 months on a high fat diet   (MGI Ref ID J:126488)
      • food intake comparable to controls   (MGI Ref ID J:126488)
  • decreased percent body fat
    • 70% less body fat   (MGI Ref ID J:118467)
  • decreased susceptibility to weight loss
    • reduced weight loss following infection with Vac-GFL   (MGI Ref ID J:162716)
  • immune system phenotype
  • abnormal cytokine level
    • keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
    • macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
    • abnormal interleukin level
      • Il-6 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • il6 levels increase less on a high fat diet than in controls   (MGI Ref ID J:96680)
      • increased circulating interleukin-6 level
        • increased levels after 7 days of dextran sodium sulfate treatment   (MGI Ref ID J:37271)
    • abnormal tumor necrosis factor level
      • TNF alpha levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • less increase in TNF alpha on a high fat diet than in controls   (MGI Ref ID J:96680)
  • abnormal macrophage chemotaxis
    • robust macrophage response at the site of spinal injury   (MGI Ref ID J:122597)
  • abnormal microglial cell physiology
    • resistant to lipopolysaccharide induced apoptosis   (MGI Ref ID J:99051)
  • abnormal phagocyte morphology
    • phagocytes fail to respond to LPS stimulation   (MGI Ref ID J:125179)
    • however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells   (MGI Ref ID J:125179)
  • abnormal spleen weight
    • spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls   (MGI Ref ID J:37271)
  • altered susceptibility to infection
    • following intranasal infection with 1x104 pfu Vac-GFL (a recombinant vaccinia virus that expresses a reporter protein) weight loss is reduced at 1 - 3 and 7 - 8 days after infection but the decrease in body temperature is more severe at 4 - 7 days afteinfection and viral replication is increased   (MGI Ref ID J:162716)
    • increased susceptibility to viral infection induced morbidity/mortality
      • 10 days after intranasal infection with 5 x 105 pfu Vac-GFL 70% of mice succumb unlike wild-type controls that all survive   (MGI Ref ID J:162716)
  • liver inflammation
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • lung inflammation
    • no increase in white blood cells or neutrophiles in bronchoalveolar fluid   (MGI Ref ID J:96680)
    • white blood cells and neutrophiles are not detected by myeloperoxidase assay   (MGI Ref ID J:96680)
  • hematopoietic system phenotype
  • *normal* hematopoietic system phenotype
    • B cell apoptosis in Peyer's patch is not observed after bile duct ligation (BDL)   (MGI Ref ID J:135830)
    • abnormal macrophage chemotaxis
      • robust macrophage response at the site of spinal injury   (MGI Ref ID J:122597)
    • abnormal microglial cell physiology
      • resistant to lipopolysaccharide induced apoptosis   (MGI Ref ID J:99051)
    • abnormal phagocyte morphology
      • phagocytes fail to respond to LPS stimulation   (MGI Ref ID J:125179)
      • however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells   (MGI Ref ID J:125179)
    • abnormal spleen weight
      • spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls   (MGI Ref ID J:37271)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • after BDL, serum alanine transaminase levels are not different from controls   (MGI Ref ID J:135830)
    • abnormal circulating leptin level
      • increase in blood leptin on a high fat diet is 36% less than in controls   (MGI Ref ID J:126488)
    • abnormal cytokine level
      • keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
      • abnormal interleukin level
        • Il-6 levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
        • il6 levels increase less on a high fat diet than in controls   (MGI Ref ID J:96680)
        • increased circulating interleukin-6 level
          • increased levels after 7 days of dextran sodium sulfate treatment   (MGI Ref ID J:37271)
      • abnormal tumor necrosis factor level
        • TNF alpha levels in lungs are unaffected by lipopolysaccharide   (MGI Ref ID J:96680)
        • less increase in TNF alpha on a high fat diet than in controls   (MGI Ref ID J:96680)
    • abnormal gas homeostasis   (MGI Ref ID J:126488)
      • decreased respiratory quotient
        • lower respiratory exchange ratio   (MGI Ref ID J:126488)
      • increased oxygen consumption
        • oxygen consumption is higher after 8 weeks on a high fat diet than controls   (MGI Ref ID J:126488)
    • abnormal glucose homeostasis   (MGI Ref ID J:126488)
      • abnormal circulating glucose level
        • faster disappearance of glucose in response to insulin when on a high fat diet   (MGI Ref ID J:126488)
      • decreased circulating insulin level
        • lower blood insulin levels when on a high fat diet   (MGI Ref ID J:126488)
      • improved glucose tolerance
        • lower blood glucose in a glucose tolerance test when on a high fat diet   (MGI Ref ID J:126488)
    • abnormal lipid level   (MGI Ref ID J:126488)
      • abnormal fatty acid level
        • less elevated than for controls on a high fat diet   (MGI Ref ID J:126488)
      • decreased liver triglyceride level
        • less increase in hepatic triglycerides on a high fat diet than in controls   (MGI Ref ID J:126488)
    • decreased body temperature
      • more severe reduction in body temperature following infection with Vac-GFL   (MGI Ref ID J:162716)
    • decreased susceptibility to ischemic brain injury
      • reduced brain edema after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • less inflammation after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • less nerve cell swelling after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • reduced neurological impairment after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
      • decreased cerebral infarction size
        • infarctions due to cerebral ischemia/reperfusion are smaller in size   (MGI Ref ID J:117223)
        • damage due to middle cerebral artery occlusion is considerably reduced   (MGI Ref ID J:124100)
    • increased adiponectin level
      • levels remain elevated on a high fat diet   (MGI Ref ID J:126488)
    • pulmonary edema
      • resistant to lipopolysaccharide induced lung interstitial edema   (MGI Ref ID J:96680)
      • less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation   (MGI Ref ID J:96680)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL   (MGI Ref ID J:135830)
  • abnormal liver physiology
    • liver protected from ischemia/reperfusion injury   (MGI Ref ID J:98036)
    • decreased hepatocyte apoptosis
      • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
    • liver inflammation
      • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • decreased liver triglyceride level
    • less increase in hepatic triglycerides on a high fat diet than in controls   (MGI Ref ID J:126488)
  • focal hepatic necrosis   (MGI Ref ID J:135830)
  • adipose tissue phenotype
  • decreased epididymal fat pad weight
    • reduced 40% compared to controls when on a high fat diet   (MGI Ref ID J:126488)
    • weight similar to controls on a normal diet   (MGI Ref ID J:126488)
  • decreased fat cell size
    • adipocyte size reduced 30% relative to controls on a high fat diet   (MGI Ref ID J:126488)
    • reduced aggregation of macrophage around dying adipocytes than in controls   (MGI Ref ID J:126488)
  • decreased percent body fat
    • 70% less body fat   (MGI Ref ID J:118467)
  • cardiovascular system phenotype
  • rectal hemorrhage
    • rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls   (MGI Ref ID J:37271)
    • recover from bleeding after 10 days of treatment when 50% of controls are dead   (MGI Ref ID J:37271)
  • digestive/alimentary phenotype
  • rectal hemorrhage
    • rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls   (MGI Ref ID J:37271)
    • recover from bleeding after 10 days of treatment when 50% of controls are dead   (MGI Ref ID J:37271)
  • respiratory system phenotype
  • abnormal respiratory system morphology   (MGI Ref ID J:114985)
    • abnormal pulmonary alveolus morphology
      • destruction of normal alveolar structures   (MGI Ref ID J:114985)
    • dilated pulmonary alveolar ducts
      • enlarged air spaces distal to the terminal bronchioles   (MGI Ref ID J:114985)
    • enlarged lung
      • significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months   (MGI Ref ID J:114985)
  • abnormal respiratory system physiology   (MGI Ref ID J:96680)
    • lung inflammation
      • no increase in white blood cells or neutrophiles in bronchoalveolar fluid   (MGI Ref ID J:96680)
      • white blood cells and neutrophiles are not detected by myeloperoxidase assay   (MGI Ref ID J:96680)
    • pulmonary edema
      • resistant to lipopolysaccharide induced lung interstitial edema   (MGI Ref ID J:96680)
      • less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation   (MGI Ref ID J:96680)
  • nervous system phenotype
  • abnormal microglial cell physiology
    • resistant to lipopolysaccharide induced apoptosis   (MGI Ref ID J:99051)
  • abnormal nervous system morphology   (MGI Ref ID J:124100)
    • abnormal myelin sheath morphology
      • increased myelin destruction at site of spinal cord injury   (MGI Ref ID J:122597)
      • no clear delineation between injured and spared tissues   (MGI Ref ID J:122597)
  • decreased neuron apoptosis
    • neurons are resistant to apoptosis caused by glucose deficiency   (MGI Ref ID J:124100)
  • decreased susceptibility to ischemic brain injury
    • reduced brain edema after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • less inflammation after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • less nerve cell swelling after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • reduced neurological impairment after cerebral ischemia/reperfusion   (MGI Ref ID J:117223)
    • decreased cerebral infarction size
      • infarctions due to cerebral ischemia/reperfusion are smaller in size   (MGI Ref ID J:117223)
      • damage due to middle cerebral artery occlusion is considerably reduced   (MGI Ref ID J:124100)
  • behavior/neurological phenotype
  • abnormal locomotor behavior
    • locomotor recovery impaired as measured 4-6 weeks after spinal cord injury   (MGI Ref ID J:122597)
  • abnormal motor coordination/ balance
    • impaired recovery of fore-limb-hindlimb coordination as measured 4-6 weeks after spinal cord injury   (MGI Ref ID J:122597)
  • skeleton phenotype
  • decreased susceptibility to bone fracture
    • bones resistant to fracture   (MGI Ref ID J:118467)
  • increased bone mass
    • increased bone area of the tibia   (MGI Ref ID J:118467)
  • increased bone mineral content
    • greater mineral content   (MGI Ref ID J:118467)
  • increased bone mineral density
    • significantly increased bone mineral density at 20 weeks   (MGI Ref ID J:118467)
    • density continues to increase over time   (MGI Ref ID J:118467)
  • muscle phenotype
  • abnormal muscle cell glucose uptake
    • insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids   (MGI Ref ID J:126488)
  • cellular phenotype
  • abnormal macrophage chemotaxis
    • robust macrophage response at the site of spinal injury   (MGI Ref ID J:122597)
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
  • decreased neuron apoptosis
    • neurons are resistant to apoptosis caused by glucose deficiency   (MGI Ref ID J:124100)
View Research Applications

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

Cancer Research
Increased Tumor Incidence
      Hepatomas
      Mammary Gland Tumors
      Mammary Gland Tumors: late onset

Cardiovascular Research
Diet-Induced Atherosclerosis
      Relatively Resistant

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
      Tlr deficiency

Neurobiology Research
Epilepsy

Research Tools
General Purpose
Infectious Disease
      Anthrax

Sensorineural Research
Retinal Degeneration
      Homozygous for Pde6brd1

Pde6brd1 related

Sensorineural Research
Retinal Degeneration

Tlr4Lps-d related

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
      Tlr deficiency
Immunodeficiency
      Tlr deficiency
Inflammation
      Tlr deficiency

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ahrb-2
Allele Name b-2 variant
Allele Type Not Applicable
Common Name(s) Ahb-2; Ahh;
Strain of OriginBALB/cBy
Gene Symbol and Name Ahr, aryl-hydrocarbon receptor
Chromosome 12
Gene Common Name(s) Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity;
General Note C57BL/6 carries the responsive Ahrb allele; DBA/2 carries nonresponsive Ahrd. Heterozygotes (Ahrb/Ahrd) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahrb-1; Ahrb-2 is carried by BALB/cBy, A, and C3H; and Ahrb-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahrb-1 and Ahrd have been determined (J:17460).

Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains

Molecular Note This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cByallele. This change would extend translation of the BALB/cBy mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa, vs 95 kDa for the C57BL/6J allele). [MGI Ref ID J:15153] [MGI Ref ID J:22144]
 
Allele Symbol Gria4spkw1
Allele Name spike wave discharge 1
Allele Type QTL
Strain of OriginC3H/HeJ
Gene Symbol and Name Gria4, glutamate receptor, ionotropic, AMPA4 (alpha 4)
Chromosome 9
Gene Common Name(s) GLUR4; GLUR4C; GLURD; GluA4; GluR-D; Glur-4; Glur4; Gluralpha4; glutamate receptor 4; spike wave 1; spkw1;
General Note This allele interacts with spkw2. Animals with the highest incidence of spike wave discharges are homozygous for C3H/HeJ-derived alleles at spkw1 and heterozygous for C57BL/6J and C3H/HeJ alleles at spkw2.
Molecular Note Genomic PCR and sequencing showed a full-length intracisternal A-particle (IAP) proviral insertion in the last intron of Gria4 in C3H/HeJ mice. qRT-PCR showed a 10-fold difference in C3H/HeJ and C3HeB/FeJ substrains in transcripts detected between exons flanking the IAP-containing intron, and a neglible difference between upstream exon transcript levels in these substrains. Gria4 protein levels in HeJ cerebella are reduced compared with controls. [MGI Ref ID J:135814]
 
Allele Symbol In(6)1J
Allele Name inversion, Chr 6, Jackson 1
Allele Type Spontaneous
Strain of OriginC3H/HeJ
Gene Symbol and Name In(6)1J, inversion, Chr 6, Jackson 1
Chromosome 6
General Note C3H/HeJ and C3H/HeJBir carry this inversion; C3H/HeSnJ and C3HeB/FeJ do not. Examination of recombination distances in Recombinant Inbred (RI) strain sets developed using C3H/HeJ as a progenitor suggest none of these harbor the inversion. Mouse strains carrying spontaneous mutations that arose on the C3H/HeJ background after 1965-1970 could carry the inversion and are expected to if the mutation arose after the early 1970s.
Molecular Note The In(6)1J inversion covers approximately 20% of Chr 6 in C3H/HeJ mice. Therefore, linkage crosses using C3H/HeJ will show no recombination in this region of Chr 6. Genetic analyses of congenic construction crosses suggested that the suppressed region lies between D6Mit124 (cytological band 6C3) and D6Mit150 (cytological band 6F1). FISH analyses using flanking BACs detected a paracentric chromosomal region between ~73 Mb and ~116 Mb. [MGI Ref ID J:105810] [MGI Ref ID J:87486]
 
Allele Symbol Pde6brd1
Allele Name retinal degeneration 1
Allele Type Spontaneous
Common Name(s) Pdebrd1; rd; rd-1; rd1; rodless retina;
Strain of Originvarious
Gene Symbol and Name Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Chromosome 5
Gene Common Name(s) CSNB3; CSNBAD2; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10;
General Note The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
Molecular Note Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361]
 
Allele Symbol Tlr4Lps-d
Allele Name defective lipopolysaccharide response
Allele Type Spontaneous
Common Name(s) TLR4-M; TLR4-Mu; TLR4lps-def; TLR4d; Tlr4-; Tlr4d; TlrLps-d; lpsd; mutant TLR4;
Strain of OriginC3H/HeJ
Gene Symbol and Name Tlr4, toll-like receptor 4
Chromosome 4
Gene Common Name(s) ARMD10; CD284; Lps; RAS-like, family 2, locus 8; Rasl2-8; TLR-4; TOLL; lipopolysaccharide response;
General Note C3H/HeJ mice carry this allele. Various combinations of Lps-associated traits have been followed in crosses between C3H/HeJ and other C3H substrains, and the traits have in all cases segregated together (J:30692, J:5557, J:5593, J:5938). Some of the traits show dominance of the Tlr4lps-n allele; others, including Tlr4Lps-d, show codominance.

Genbank ID for this allele: AF095353

Molecular Note This allele corresponds to a mutation in the third exon of the gene. A C to A substitution at nucleotide position 2342 results in an amino acid substitution that replaces proline with histidine at position 712. [MGI Ref ID J:51522] [MGI Ref ID J:53519] [MGI Ref ID J:57938]

Genotyping

Genotyping Information

Inbred mouse strains are maintained through sibling (sister x brother) matings; no genotyping required.

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Akeson EC; Donahue LR; Beamer WG; Shultz KL; Ackert-Bicknell C; Rosen CJ; Corrigan J; Davisson MT. 2006. Chromosomal inversion discovered in C3H/HeJ mice. Genomics 87(2):311-3. [PubMed: 16309882]  [MGI Ref ID J:105810]

Dragani TA; Manenti G; Gariboldi M; Degregorio L; Pierotti MA. 1995. Genetics of liver tumor susceptibility in mice. Toxicol Lett 82-3:613-619. [PubMed: 8597117]  [MGI Ref ID J:31816]

Heston WE; Vlahakis G. 1971. Mammary tumors, plaques, and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumor virus. Int J Cancer 7(1):141-8. [PubMed: 4322934]  [MGI Ref ID J:24674]

Outzen HC; Corrow D; Shultz LD. 1985. Attenuation of exogenous murine mammary tumor virus virulence in the C3H/HeJ mouse substrain bearing the Lps mutation. J Natl Cancer Inst 75(5):917-23. [PubMed: 2997536]  [MGI Ref ID J:24864]

Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11. [PubMed: 15081119]  [MGI Ref ID J:89298]

Additional References

DiPetrillo K; Tsaih SW; Sheehan S; Johns C; Kelmenson P; Gavras H; Churchill GA; Paigen B. 2004. Genetic analysis of blood pressure in C3H/HeJ and SWR/J mice. Physiol Genomics 17(2):215-20. [PubMed: 14996992]  [MGI Ref ID J:89267]

Ewart SL; Kuperman D; Schadt E; Tankersley C; Grupe A; Shubitowski DM; Peltz G; Wills-Karp M. 2000. Quantitative trait loci controlling allergen-induced airway hyperresponsiveness in inbred mice. Am J Respir Cell Mol Biol 23(4):537-45. [PubMed: 11017920]  [MGI Ref ID J:66641]

Fortier AH; Slayter MV; Ziemba R; Meltzer MS; Nacy CA. 1991. Live vaccine strain of Francisella tularensis: infection and immunity in mice. Infect Immun 59(9):2922-8. [PubMed: 1879918]  [MGI Ref ID J:27016]

International Nomenclature Committee. 1952. COMMITTEE on Standardized Nomenclature for Inbred Strains of Mice Cancer Res 12(8):602-13. [PubMed: 14945054]  [MGI Ref ID J:166288]

Keane TM; Goodstadt L; Danecek P; White MA; Wong K; Yalcin B; Heger A; Agam A; Slater G; Goodson M; Furlotte NA; Eskin E; Nellaker C; Whitley H; Cleak J; Janowitz D; Hernandez-Pliego P; Edwards A; Belgard TG; Oliver PL; McIntyre RE; Bhomra A; Nicod J; Gan X; Yuan W; van der Weyden L; Steward CA; Bala S; Stalker J; Mott R; Durbin R; Jackson IJ; Czechanski A; Guerra-Assuncao JA; Donahue LR; Reinholdt LG; Payseur BA; Ponting CP; Birney E; Flint J; Adams DJ. 2011. Mouse genomic variation and its effect on phenotypes and gene regulation. Nature 477(7364):289-94. [PubMed: 21921910]  [MGI Ref ID J:177037]

McElwee KJ; Boggess D; King LE Jr; Sundberg JP. 1998. Experimental induction of alopecia areata-like hair loss in C3H/HeJ mice using full-thickness skin grafts. J Invest Dermatol 111(5):797-803. [PubMed: 9804341]  [MGI Ref ID J:111520]

McElwee KJ; Boggess D; Miller J; King LE Jr; Sundberg JP. 1999. Spontaneous alopecia areata-like hair loss in one congenic and seven inbred laboratory mouse strains J Investig Dermatol Symp Proc 4(3):202-6. [PubMed: 10674366]  [MGI Ref ID J:60482]

Moeller GR; Terry L; Snyderman R. 1978. The inflammatory response and resistance to endotoxin in mice. J Immunol 120(1):116-23. [PubMed: 627714]  [MGI Ref ID J:5936]

Moy SS; Nadler JJ; Young NB; Perez A; Holloway LP; Barbaro RP; Barbaro JR; Wilson LM; Threadgill DW; Lauder JM; Magnuson TR; Crawley JN. 2007. Mouse behavioral tasks relevant to autism: phenotypes of 10 inbred strains. Behav Brain Res 176(1):4-20. [PubMed: 16971002]  [MGI Ref ID J:138682]

Paigen B; Ishida BY; Verstuyft J; Winters RB; Albee D. 1990. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis 10(2):316-23. [PubMed: 2317166]  [MGI Ref ID J:22615]

Roberts JE; Watters JW; Ballard JD; Dietrich WF. 1998. Ltx1, a mouse locus that influences the susceptibility of macrophages to cytolysis caused by intoxication with Bacillus anthracis lethal factor, maps to chromosome 11. Mol Microbiol 29(2):581-91. [PubMed: 9720874]  [MGI Ref ID J:49726]

Siebenhaar F; Sharov AA; Peters EM; Sharova TY; Syska W; Mardaryev AN; Freyschmidt-Paul P; Sundberg JP; Maurer M; Botchkarev VA. 2007. Substance P as an immunomodulatory neuropeptide in a mouse model for autoimmune hair loss (alopecia areata). J Invest Dermatol 127(6):1489-97. [PubMed: 17273166]  [MGI Ref ID J:122923]

Sultzer BM. 1968. Genetic control of leucocyte responses to endotoxin. Nature 219(160):1253-4. [PubMed: 4877918]  [MGI Ref ID J:5087]

Sundberg JP; Boggess D; Silva KA; McElwee KJ; King LE; Li R; Churchill G; Cox GA. 2003. Major locus on mouse chromosome 17 and minor locus on chromosome 9 are linked with alopecia areata in C3H/HeJ mice. J Invest Dermatol 120(5):771-5. [PubMed: 12713579]  [MGI Ref ID J:83350]

Sundberg JP; Cordy WR; King LE Jr. 1994. Alopecia areata in aging C3H/HeJ mice. J Invest Dermatol 102(6):847-56. [PubMed: 8006447]  [MGI Ref ID J:18877]

Welkos SL; Keener TJ; Gibbs PH. 1986. Differences in susceptibility of inbred mice to Bacillus anthracis. Infect Immun 51(3):795-800. [PubMed: 3081444]  [MGI Ref ID J:8197]

West DB; Boozer CN; Moody DL; Atkinson RL. 1992. Dietary obesity in nine inbred mouse strains. Am J Physiol 262(6 Pt 2):R1025-32. [PubMed: 1621856]  [MGI Ref ID J:1348]

Xie C; Sharma R; Wang H; Zhou XJ; Mohan C. 2004. Strain distribution pattern of susceptibility to immune-mediated nephritis. J Immunol 172(8):5047-55. [PubMed: 15067087]  [MGI Ref ID J:122988]

Ahrb-2 related

Nebert DW; Considine N; Owens IS. 1973. Genetic expression of aryl hydrocarbon hydroxylase induction. VI. Control of other aromatic hydrocarbon-inducible mono-oxygenase activities at or near the same genetic locus. Arch Biochem Biophys 157(1):148-59. [PubMed: 4716952]  [MGI Ref ID J:84313]

Nebert DW; Gielen JE. 1972. Genetic regulation of aryl hydrocarbon hydroxylase induction in the mouse. Fed Proc 31(4):1315-25. [PubMed: 4114109]  [MGI Ref ID J:5282]

Nebert DW; Jensen NM; Shinozuka H; Kunz HW; Gill TJ 3rd. 1982. The Ah phenotype. Survey of forty-eight rat strains and twenty inbred mouse strains. Genetics 100(1):79-87. [PubMed: 7095422]  [MGI Ref ID J:6809]

Nebert DW; Robinson JR; Niwa A; Kumaki K; Poland AP. 1975. Genetic expression of aryl hydrocarbon hydroxylase activity in the mouse. J Cell Physiol 85(2 Pt 2 Suppl 1):393-414. [PubMed: 1091656]  [MGI Ref ID J:84317]

Niwa A; Kumaki K; Nebert DW; Poland AP. 1975. Genetic expression of aryl hydrocarbon hydroxylase activity in the mouse. Distinction between the 'responsive' homozygote and heterozygote at the Ah locus. Arch Biochem Biophys 166(2):559-64. [PubMed: 1119809]  [MGI Ref ID J:84316]

Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12. [PubMed: 2169579]  [MGI Ref ID J:34840]

Poland A; Glover E; Taylor BA. 1987. The murine Ah locus: a new allele and mapping to chromosome 12. Mol Pharmacol 32(4):471-8. [PubMed: 2823093]  [MGI Ref ID J:8895]

Poland A; Palen D; Glover E. 1994. Analysis of the four alleles of the murine aryl hydrocarbon receptor. Mol Pharmacol 46(5):915-21. [PubMed: 7969080]  [MGI Ref ID J:22144]

Robinson JR; Considine N; Nebert DW. 1974. Genetic expression of aryl hydrocarbon hydroxylase induction. Evidence for the involvement of other genetic loci. J Biol Chem 249(18):5851-9. [PubMed: 4413562]  [MGI Ref ID J:84315]

Schmid FA; Pena RC; Robinson W; Tarnowski GS. 1967. Toxicity of intraperitoneal injections of 7, 12-dimethylbenz[a]anthracene in inbred mice. Cancer Res 27(3):558-62. [PubMed: 6021513]  [MGI Ref ID J:26440]

Schmidt JV; Carver LA; Bradfield CA. 1993. Molecular characterization of the murine Ahr gene. Organization, promoter analysis, and chromosomal assignment. J Biol Chem 268(29):22203-9. [PubMed: 8408082]  [MGI Ref ID J:15153]

Smith AG; Clothier B; Robinson S; Scullion MJ; Carthew P; Edwards R; Luo J; Lim CK; Toledano M. 1998. Interaction between iron metabolism and 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice with variants of the Ahr gene: a hepatic oxidative mechanism. Mol Pharmacol 53(1):52-61. [PubMed: 9443932]  [MGI Ref ID J:45850]

Thomas PE; Hutton JJ; Taylor BA. 1973. Genetic relationship between aryl hydrocarbon hydroxylase inducibility and chemical carcinogen induced skin ulceration in mice. Genetics 74(4):655-9. [PubMed: 4750810]  [MGI Ref ID J:5387]

Gria4spkw1 related

Beyer B; Deleuze C; Letts VA; Mahaffey CL; Boumil RM; Lew TA; Huguenard JR; Frankel WN. 2008. Absence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4. Hum Mol Genet 17(12):1738-49. [PubMed: 18316356]  [MGI Ref ID J:135814]

Frankel WN; Beyer B; Maxwell CR; Pretel S; Letts VA; Siegel SJ. 2005. Development of a new genetic model for absence epilepsy: spike-wave seizures in C3H/He and backcross mice. J Neurosci 25(13):3452-8. [PubMed: 15800200]  [MGI Ref ID J:98638]

Pde6brd1 related

Acosta ML; Fletcher EL; Azizoglu S; Foster LE; Farber DB; Kalloniatis M. 2005. Early markers of retinal degeneration in rd/rd mice. Mol Vis 11:717-28. [PubMed: 16163270]  [MGI Ref ID J:103970]

Aftab U; Jiang C; Tucker B; Kim JY; Klassen H; Miljan E; Sinden J; Young M. 2009. Growth kinetics and transplantation of human retinal progenitor cells. Exp Eye Res 89(3):301-10. [PubMed: 19524569]  [MGI Ref ID J:151412]

Ahuja S; Ahuja-Jensen P; Johnson LE; Caffe AR; Abrahamson M; Ekstrom PA; van Veen T. 2008. rd1 Mouse retina shows an imbalance in the activity of cysteine protease cathepsins and their endogenous inhibitor cystatin C. Invest Ophthalmol Vis Sci 49(3):1089-96. [PubMed: 18326735]  [MGI Ref ID J:133024]

Ahuja-Jensen P; Johnsen-Soriano S; Ahuja S; Bosch-Morell F; Sancho-Tello M; Romero FJ; Abrahamson M; van Veen T. 2007. Low glutathione peroxidase in rd1 mouse retina increases oxidative stress and proteases. Neuroreport 18(8):797-801. [PubMed: 17471069]  [MGI Ref ID J:122802]

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Zanotti G; Casiraghi M; Abano JB; Tatreau JR; Sevala M; Berlin H; Smyth S; Funkhouser WK; Burridge K; Randell SH; Egan TM. 2009. Novel critical role of Toll-like receptor 4 in lung ischemia-reperfusion injury and edema. Am J Physiol Lung Cell Mol Physiol 297(1):L52-63. [PubMed: 19376887]  [MGI Ref ID J:151006]

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Zhang X; Shan P; Jiang G; Cohn L; Lee PJ. 2006. Toll-like receptor 4 deficiency causes pulmonary emphysema. J Clin Invest 116(11):3050-9. [PubMed: 17053835]  [MGI Ref ID J:114985]

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In(6)1J related

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           MP14
Room Number           MP24
Room Number           RB09

Colony Maintenance

Mating SystemSibling x Sibling         (Female x Male)   01-MAR-06
Breeding Considerations This strain is an exceptional breeder.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Weeks of AgePrice per mouse (US dollars $)Gender
3 weeks $24.00Female  
$21.05Male  
4 weeks $24.00Female  
$21.45Male  
5 weeks $24.00Female  
$21.45Male  
6 weeks $26.50Female  
$24.00Male  
7 weeks $29.10Female  
$26.65Male  
8 weeks $29.10Female  
$26.65Male  
9 weeks $29.10Female  
$26.65Male  
10 weeks $33.70Female  
$32.45Male  
11 weeks $33.70Female  
$32.45Male  
12 weeks $33.70Female  
$32.45Male  
13 weeks $36.35Female  
$34.90Male  
14 weeks $36.35Female  
$37.70Male  
15 weeks $36.35Female  
$40.40Male  

Standard Supply

Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.

Supply Notes


JAX® Cells, Tissues & Products

Select the cell line of interest to go to the cell line data sheet
C3H/HeJ AC386/GrsrJ mES cells
C3H/HeJ-PB151.24 mES cells
C3H/HeJ-PRX-C3H #2 mES cells
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)Gender
3 weeks $31.20Female  
$27.40Male  
4 weeks $31.20Female  
$27.90Male  
5 weeks $31.20Female  
$27.90Male  
6 weeks $34.50Female  
$31.20Male  
7 weeks $37.90Female  
$34.70Male  
8 weeks $37.90Female  
$34.70Male  
9 weeks $37.90Female  
$34.70Male  
10 weeks $43.90Female  
$42.20Male  
11 weeks $43.90Female  
$42.20Male  
12 weeks $43.90Female  
$42.20Male  
13 weeks $47.30Female  
$45.40Male  
14 weeks $47.30Female  
$49.10Male  
15 weeks $47.30Female  
$52.60Male  

Standard Supply

Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.

Supply Notes

  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.

JAX® Cells, Tissues & Products

Select the cell line of interest to go to the cell line data sheet
C3H/HeJ AC386/GrsrJ mES cells
C3H/HeJ-PB151.24 mES cells
C3H/HeJ-PRX-C3H #2 mES cells
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.

Important Note

This strain does not carry mouse mammary tumor virus (MMTV). See JAX® NOTES, May 2000, No. 480. This strain is homozygous for retinal degeneration allele Pde6brd1, the defective lipopolysaccharide response allele Tlr4Lps-d, and for a chromosomal inversion on Chromosome 6. A sighted alternative is Stock No. 003648, C3Sn.BLiA-Pde6b+/DnJ.

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
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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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