Overview

Also Known As: C3H Heston, C3, C3H

C3H/HeJ mice, commonly called C3H, 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 in Tlr4 occurred in C3H/HeJ at the lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4^Lps-d) making C3H/HeJ mice more resistant to endotoxin. C3H/HeJ mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica. The C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6b^rd1), causing blindness by weaning age.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

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Research Applications

Cardiovascular Research
Cancer Research
Research Tools
Sensorineural Research
Immunology, Inflammation and Autoimmunity Research
Neurobiology Research
Mouse/Human Gene Homologs

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Base Price

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$25.33 Domestic price for male 3-week

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Details

Important Note

This strain does not carry mouse mammary tumor virus (MMTV). This strain is homozygous for retinal degeneration allele Pde6b^rd1, the defective lipopolysaccharide response allele Tlr4^Lps-d, and for a chromosomal inversion on Chromosome 6. A sighted alternative is Stock No. 003648, C3Sn.BLiA-Pde6b⁺/DnJ.

Detailed 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 (Pde6b^rd1), which causes blindness by weaning age, but lack the nob5 allele of Gpr179 (Chang, 2015). 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, Tlr4^Lps-d) making C3H/HeJ mice endotoxin resistant. C3H/HeJ (Tlr4^Lps-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. The spontaneous mutation, spike wave discharge 1 (Gria4^spkw1), is present in C3H/HeJ, but not C3HeB/FeJ. Mice homozygous for this mutation exhibit a modest incidence of absence seizures. This strain is also homozygous for a hypomorphic allele in Pcnx2, which is caused by an IAP insertion and which dampens the severity of the absence seizure phenotype caused by Gria4^spkw1 (Frankel et al., 2014).

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, Tlr4^lps) making C3H/HeJ mice endotoxin resistant while the other three C3H strains are endotoxin sensitive.

Selected References

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):311-3PubMed: 16309882 MGI: J:105810
Chang B. 2015. Survey of the nob5 mutation in C3H substrains. Mol Vis 21:1101-5PubMed: 26396487 MGI: J:224435
Frankel WN; Mahaffey CL; McGarr TC; Beyer BJ; Letts VA. 2014. Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy. PLoS Genet 10(7):e1004454PubMed: 25010494 MGI: J:228536
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):141-8PubMed: 4322934 MGI: 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):917-23PubMed: 2997536 MGI: J:24864
Dragani TA; Manenti G; Gariboldi M; Degregorio L; Pierotti MA. 1995. Genetics of liver tumor susceptibility in mice. Toxicol Lett 82-3:613-619PubMed: 8597117 MGI: J:31816
Cheers C; McKenzie IF. 1978. Resistance and susceptibility of mice to bacterial infection: genetics of listeriosis. Infect Immun 19(3):755-62PubMed: 305895 MGI: J:5965
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):902-11PubMed: 15081119 MGI: J:89298

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Genetics

Hrh1^Bphs-r

Allele Symbol: Hrh1^Bphs-r

Allele Name	B pertussis induced histamine sensitization, resistant
Allele Type	Spontaneous
Allele Synonym(s)	B pertussis induced histamine sensitization, resistant; Hrh1^Bphs-r
Gene Symbol and Name	Hrh1, histamine receptor H1
Gene Synonym(s)	Bphs; Bphs; H1-R; Hir; hisH1; Bordetella pertussis induced histamine sensitization; HH1R; H1R; Hisr
Strain of Origin	C3H/HeJ or CBA/J
Chromosome	6
General Note	Mice homozygous for this allele do not die from hypotensive and hypovolemic shock induced by vasoactive amine challenge after pertussis toxin sensitization (J:77938).
Molecular Note	This allele confers resistance to Bordetella pertussis induced histamine sensitization and occurs in strains C3H/HeJ and CBA/J. These strains carry three concordant amino acid changes in the predicted protein sequence (L263P, M313V and S331P) that are in the third intracellular loop and are postulated to be associated with signal transduction function.

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Allele Name	defective lipopolysaccharide response
Allele Type	Spontaneous
Allele Synonym(s)	Tlr4^Lps-d; defective lipopolysaccharide response
Gene Symbol and Name	Tlr4, toll-like receptor 4
Gene Synonym(s)	ARMD10; Rasl2-8; Rasl2-8; CD284; lipopolysaccharide response; Lps; lipopolysaccharide response; Lps; TLR-4; RAS-like, family 2, locus 8; TOLL
Strain of Origin	C3H/HeJ
Chromosome	4
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 Tlr4^lps-n allele; others, including Tlr4^Lps-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.

In(6)1J

Allele Symbol: In(6)1J

Allele Name	inversion, Chr 6, Jackson 1
Allele Type	Spontaneous
Allele Synonym(s)	inversion, Chr 6, Jackson 1; In(6)1J
Gene Symbol and Name	In(6)1J, inversion, Chr 6, Jackson 1
Gene Synonym(s)
Strain of Origin	C3H/HeJ
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.

Pcnx2^C3H/HeJ

Allele Symbol: Pcnx2^C3H/HeJ

Allele Name	C3H/HeJ
Allele Type	Spontaneous (Hypomorph)
Allele Synonym(s)	C3H/HeJ; Pcnx2^C3H/HeJ
Gene Symbol and Name	Pcnx2, pecanex homolog 2
Gene Synonym(s)	E330039K12Rik; E330039K12Rik; AU067631; Pcnxl2; RGD1305883; RIKEN cDNA E330039K12 gene; pecanex-like 2 (Drosophila); expressed sequence AU067631; PCNXL2; Pcnxl2
Strain of Origin	C3H/HeJ
Chromosome	8
Molecular Note	This IAP insertion in intron 19 causes diminished expression of this gene by RT-PCR in C3H/HeJ and is not found in C3HeB/FeJ, C3H/HeOuJ, or C3H/HeSnJ.

Mx1^s1

Allele Symbol: Mx1^s1

Allele Name	myxovirus susceptibility 1
Allele Type	Spontaneous
Allele Synonym(s)	Mx1^s1; myxovirus susceptibility 1
Gene Symbol and Name	Mx1, MX dynamin-like GTPase 1
Gene Synonym(s)	Mx; Mx-1; Mx; Mx-1; AI893580; myxovirus (influenza) resistance 1 polypeptide; expressed sequence AI893580; IFI-78K; MxA; MX; IFI78; MXB
Strain of Origin	multiple strains
Chromosome	16
General Note	The Mx genes determine resistance to the lethal effects of various myxoviruses including neurotropic avian influenza A virus injected intracerebrally, pneumotropic strains injected intranasally, and a hepatotropic strain injected intraperitoneally (J:5645, J:13136). Resistance is not dependent on presence of the thymus and is not abolished by immunosuppression or by inhibitors of macrophage function (J:5735, J:5478, J:5645). Resistance is specific for the orthomyxoviruses (J:6265). It is dependent on the presence of interferon-alpha and -beta but not -gamma (J:7365). The resistance allele at the Mx1 locus, under induction by alpha/beta interferon, produces the 75 kDa protein MX-1, which confers resistance to the influenza virus, in the nuclei of cells carrying the allele. Susceptibility alleles do not produce the protein (J:8273). The protein is located in the nucleus (J:7703) and produces its antiviral effect by preventing synthesis of viral mRNA in the nucleus (J:7992). Nuclear localization is necessary for anti-influenza virus activity (J:1417), but mutations induced in Mx1 showed that nuclear position was not sufficient for the effect; mutations in several domains can cause its loss (J:11840). The MX-1 protein is a GTPase containing a GTP binding domain (J:1417) and this binding core is also necessary (J:21243). Resistance is expressed by macrophages and other cells in vitro (J:6649, J:5940) but could not be transferred to susceptible animals by transfer of macrophages from resistant mice (J:6149). Resistance to infection with two tick-borne viruses, Thogoto virus (J:8273) and Dhori virus (J:27760), is also conferred by Mx1^r. The Mx1^r allele occurs only in strains A2G, SL/NiA, and T9, the latter being a strain derived from an influenza-resistant wild stock, and CAST/Ei, derived from Mus musculus castaneus. Most inbred strains, including C57BL/6J, C3H/HeJ, and BALB/cJ, carry an influenza susceptible Mx1^s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1^r allele. This large deletion apparently renders the protein incapable of providing resistance to influenza. The CBA/J, CE/J, I/LnJ, and PERA/Ei strains, also susceptible to the virus, have another form of the Mx1^s2 allele in which there is a nonsense mutation (J:9452). Interferon is induced by viral infection and in turn induces the Mx protein (J:7703). Although some interferon-induced genes respond directly to virus invasion as well as indirectly through induction by virus-induced interferon, this primary response is very weak for the MX-1 protein in response to either influenza or Newcastle disease viruses (J:1892).
Molecular Note	Many inbred mouse strains have an exon 9 to 11 deletion, resulting in a null allele and susceptibility to myxoviruses, including: A/J, ABP/Le, AKR/J, AU/SsJ, BALB/cJ, BDP/J, BUB/BnJ, C3H/HeJ, C57BL/6J, C57BL/10J, C57BL/KsJ, C57L/J, C58/J, DA/HuSn, DBA/2J, FSB/GnEi, FVB/NJ, LIS/A, LP/J, MA/MyJ, MAS/A, NZB/BINJ, P/J, PL/J, RIIIS/J, RF/J, SEA/GnJ, SEC1/ReJ, SJL/J, ST/bJ, TS1/A, TW1/A. YBR/Ei, 020/A, 129/J, SF/CamEi and SK/CamEi.

Ahr^b-2

Allele Symbol: Ahr^b-2

Allele Name	b-2 variant
Allele Type	Not Applicable
Allele Synonym(s)	b-2 variant; Ahr^b-2
Gene Symbol and Name	Ahr, aryl-hydrocarbon receptor
Gene Synonym(s)	bHLHe76; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; Ahh; dioxin receptor; In; Ah; Ahre; inflammatory reactivity
Strain of Origin	BALB/cBy
Chromosome	12
General Note	C57BL/6 carries the responsive Ahr^b allele; DBA/2 carries nonresponsive Ahr^d. Heterozygotes (Ahr^b/Ahr^d) 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 Ahr^b-1; Ahr^b-2 is carried by BALB/cBy, A, and C3H; and Ahr^b-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 Ahr^b-1 and Ahr^d 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/cBy allele. 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).

Cd5^a

Allele Symbol: Cd5^a

Allele Name	a variant
Allele Type	Spontaneous (Not Applicable)
Allele Synonym(s)	Cd5^a; a variant
Gene Symbol and Name	Cd5, CD5 antigen
Gene Synonym(s)	Ly-12; lymphocyte antigen 1; T1; T-lymphocyte antigen 1; LEU1; Ly-1; Lyt-1; lymphocyte antigen 12; Ly-12; Lyt-1; Ly-A; Ly-1
Strain of Origin	multiple strains
Chromosome	19
Molecular Note	Sequence analysis of C3H/HeJ showed that this polymorphic variant has point mutations relative to the b variant that result in valine instead of isoleucine at amino acid 9, leucine instead of glutamine at amino acid 52, and isoleucine instead of phenylalanine at amino acid 71, all within the amino terminal scavenger receptor cysteine-rich D1 domain, in addition to 7 silent point mutations. This allele is found in many inbred strains including CBA/J, C3H and DBA substrains.

Gria4^spkw1

Allele Symbol: Gria4^spkw1

Allele Name	spike wave discharge 1
Allele Type	QTL
Allele Synonym(s)	Gria4^spkw1; spike wave discharge 1
Gene Symbol and Name	Gria4, glutamate receptor, ionotropic, AMPA4 (alpha 4)
Gene Synonym(s)	Gluralpha4; spkw1; Glur-4; Glur4; spkw1; GluA4; Glur-4; GluR-D; GLUR4C; GLURD; GLUR4; glutamate receptor 4; spike wave 1; GluR4; Glur4; NEDSGA
Strain of Origin	C3H/HeJ
Chromosome	9
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	This mutation was originally identified as a QTL allele conferring increased incidence of spike wave discharges in the brains of C3H/HeJ mice as compared to C57BL/6J. 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 C3H/HeJ cerebella are reduced compared with controls.

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Allele Name	retinal degeneration 1
Allele Type	Spontaneous
Allele Synonym(s)	retinal degeneration 1; Pde6b^rd1
Gene Symbol and Name	Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Gene Synonym(s)	rd; rd1; Pdeb; r; rd; rd10; nmf137; r; retinal degeneration; retinal degeneration 1; retinal degeneration 10; CSNB3; CSNBAD2; rd1; rd-1; rd10; PDEB; RP40; phosphodiesterase, cGMP, rod receptor, beta polypeptide; Pdeb; GMP-PDEbeta
Strain of Origin	various
Chromosome	5
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.

Disease/Phenotype

Disease Terms

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

Research Areas By Genotype

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

Cardiovascular Research
- Diet-Induced Atherosclerosis
  - Relatively Resistant
Cancer Research
- Increased Tumor Incidence
  - Hepatomas
  - Mammary Gland Tumors: late onset
  - Mammary Gland Tumors
Research Tools
- General Purpose
- Infectious Disease
  - Anthrax
Sensorineural Research
- Retinal Degeneration
  - Homozygous for Pde6b^rd1
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - Tlr deficiency
Neurobiology Research
- Epilepsy

Genotype: Tlr4^Lps-d related

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

Genotype: Pde6b^rd1 related

Sensorineural Research
- Retinal Degeneration
Mouse/Human Gene Homologs
- retinitis pigmentosa, autosomal recessive

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: In(6)1J/In(6)1J
C3H/HeJ

normal phenotype

no abnormal phenotype detected
- Normal - no phenotype is known to be associated with this chromosomal inversion

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
involves: C3H/HeJ

behavior/neurological phenotype

hyporesponsive to tactile stimuli
- reduced mechanical allodynia after nerve injury

increased thermal nociceptive threshold
- attenuated response to heat

immune system phenotype

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

abnormal T-helper 2 physiology
- Th2 responses elevated after induction of autoimmune arthritis

abnormal tumor necrosis factor level
- diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion
- macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage

increased susceptibility to bacterial infection
- increased K. pneumoniae levels in the lung
- increased sensitivity to gram (-) infection
- low responsiveness of spleen cells to lipopolysaccharides
- significantly shortened survival after infection with Klebsiella pneumoniae

increased susceptibility to induced arthritis
- reduced susceptibility to arthritis induced by type II collagen

integument phenotype

hyporesponsive to tactile stimuli
- reduced mechanical allodynia after nerve injury

increased thermal nociceptive threshold
- attenuated response to heat

mammalian phenotype

hearing/vestibular/ear phenotype
- Normal - cisplatin and lipopolysaccharide treatment does not lead to significant increases in auditory brainstem response as is observed in controls

muscle phenotype
- Normal - MCP-1 (monocyte chemoattractant protein-1) release from isolated mouse aorta smooth muscle cells (MAoSMC) by stimulation with dsRNA is normal relative to controls

nervous system phenotype

abnormal glial cell apoptosis
- isolated microglia exposed to LPS are resistant to apoptosis

skeleton phenotype

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

increased susceptibility to induced arthritis
- reduced susceptibility to arthritis induced by type II collagen

cellular phenotype

abnormal glial cell apoptosis
- isolated microglia exposed to LPS are resistant to apoptosis

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

hematopoietic system phenotype

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

abnormal T-helper 2 physiology
- Th2 responses elevated after induction of autoimmune arthritis

homeostasis/metabolism phenotype

abnormal circulating enzyme level
- increased HO-1 expression
- myeloperoxidase levels are reduced after 90 minutes of liver ischemia followed by 6 hours of reperfusion

abnormal tumor necrosis factor level
- diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion
- macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage

decreased circulating alanine transaminase level
- serum levels decreased after 90 minutes of liver ischemia followed by 6 hours of reperfusion

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C3H/HeJ-Tlr4

adipose tissue phenotype

decreased epididymal fat pad weight
- reduced 40% compared to controls when on a high fat diet
- weight similar to controls on a normal diet

decreased fat cell size
- adipocyte size reduced 30% relative to controls on a high fat diet
- reduced aggregation of macrophage around dying adipocytes than in controls

decreased percent body fat/body weight
- 70% less body fat

cellular phenotype

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal muscle cell glucose uptake
- insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

decreased neuron apoptosis
- neurons are resistant to apoptosis caused by glucose deficiency

skeleton phenotype

decreased susceptibility to bone fracture
- bones resistant to fracture

increased bone mass
- increased bone area of the tibia

increased bone mineral content
- greater mineral content

increased bone mineral density
- density continues to increase over time
- significantly increased bone mineral density at 20 weeks

digestive/alimentary phenotype

rectal hemorrhage
- recover from bleeding after 10 days of treatment when 50% of controls are dead
- rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls

growth/size/body region phenotype

decreased body size
- always smaller than controls

decreased body weight
- food intake comparable to controls
- lower body weight than controls after 8 weeks on a high fat diet
- weights are 15% lower than controls after 8 months on a high fat diet

decreased susceptibility to weight loss
- reduced weight loss following infection with Vac-GFL

hematopoietic system phenotype

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal phagocyte morphology
- Normal - however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells
- phagocytes fail to respond to LPS stimulation

abnormal spleen weight
- spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls

homeostasis/metabolism phenotype

abnormal circulating glucose level
- faster disappearance of glucose in response to insulin when on a high fat diet

abnormal circulating leptin level
- increase in blood leptin on a high fat diet is 36% less than in controls

abnormal cytokine level
- keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide
- macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide

abnormal fatty acid level
- less elevated than for controls on a high fat diet

abnormal gas homeostasis

abnormal glucose homeostasis

abnormal interleukin level
- Il-6 levels in lungs are unaffected by lipopolysaccharide
- il6 levels increase less on a high fat diet than in controls

abnormal lipid level

abnormal tumor necrosis factor level
- less increase in TNF alpha on a high fat diet than in controls
- TNF alpha levels in lungs are unaffected by lipopolysaccharide

decreased body temperature
- more severe reduction in body temperature following infection with Vac-GFL

decreased cerebral infarction size
- damage due to middle cerebral artery occlusion is considerably reduced
- infarctions due to cerebral ischemia/reperfusion are smaller in size

decreased circulating insulin level
- lower blood insulin levels when on a high fat diet

decreased liver triglyceride level
- less increase in hepatic triglycerides on a high fat diet than in controls

decreased respiratory quotient
- lower respiratory exchange ratio

decreased susceptibility to ischemic brain injury
- less inflammation after cerebral ischemia/reperfusion
- less nerve cell swelling after cerebral ischemia/reperfusion
- reduced brain edema after cerebral ischemia/reperfusion
- reduced neurological impairment after cerebral ischemia/reperfusion

improved glucose tolerance
- lower blood glucose in a glucose tolerance test when on a high fat diet

increased adiponectin level
- levels remain elevated on a high fat diet

increased circulating interleukin-6 level
- increased levels after 7 days of dextran sodium sulfate treatment

increased oxygen consumption
- oxygen consumption is higher after 8 weeks on a high fat diet than controls

pulmonary edema
- less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation
- resistant to lipopolysaccharide induced lung interstitial edema

immune system phenotype

abnormal cytokine level
- keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide
- macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide

abnormal interleukin level
- Il-6 levels in lungs are unaffected by lipopolysaccharide
- il6 levels increase less on a high fat diet than in controls

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal phagocyte morphology
- Normal - however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells
- phagocytes fail to respond to LPS stimulation

abnormal spleen weight
- spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls

abnormal tumor necrosis factor level
- less increase in TNF alpha on a high fat diet than in controls
- TNF alpha levels in lungs are unaffected by lipopolysaccharide

altered susceptibility to infection
- days afteinfection and viral replication is increased
- 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

increased circulating interleukin-6 level
- increased levels after 7 days of dextran sodium sulfate treatment

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

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

lung inflammation
- no increase in white blood cells or neutrophiles in bronchoalveolar fluid
- white blood cells and neutrophiles are not detected by myeloperoxidase assay

behavior/neurological phenotype

abnormal locomotor behavior
- locomotor recovery impaired as measured 4-6 weeks after spinal cord injury

abnormal motor coordination/balance
- impaired recovery of fore-limb-hindlimb coordination as measured 4-6 weeks after spinal cord injury

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

abnormal liver physiology
- liver protected from ischemia/reperfusion injury

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

decreased liver triglyceride level
- less increase in hepatic triglycerides on a high fat diet than in controls

focal hepatic necrosis

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

mammalian phenotype

hematopoietic system phenotype
- Normal - B cell apoptosis in Peyer's patch is not observed after bile duct ligation (BDL)

homeostasis/metabolism phenotype
- Normal - after BDL, serum alanine transaminase levels are not different from controls

cardiovascular system phenotype

rectal hemorrhage
- recover from bleeding after 10 days of treatment when 50% of controls are dead
- rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls

mortality/aging

decreased sensitivity to induced morbidity/mortality
- Normal - 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
- heat-inactivated E. coli exposure results in fatal toxemia as in wild type mice
- Normal - heat-inactivated E. coli exposure results in fatal toxemia as in wild-type mice
- systemic challenge with Myr₃-CSK₄ (a synthetic lipopeptide) after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected

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

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

nervous system phenotype

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal myelin sheath morphology
- increased myelin destruction at site of spinal cord injury
- no clear delineation between injured and spared tissues

abnormal nervous system morphology

decreased cerebral infarction size
- damage due to middle cerebral artery occlusion is considerably reduced
- infarctions due to cerebral ischemia/reperfusion are smaller in size

decreased neuron apoptosis
- neurons are resistant to apoptosis caused by glucose deficiency

decreased susceptibility to ischemic brain injury
- less inflammation after cerebral ischemia/reperfusion
- less nerve cell swelling after cerebral ischemia/reperfusion
- reduced brain edema after cerebral ischemia/reperfusion
- reduced neurological impairment after cerebral ischemia/reperfusion

respiratory system phenotype

abnormal pulmonary alveolus morphology
- destruction of normal alveolar structures

abnormal respiratory system morphology

abnormal respiratory system physiology

dilated pulmonary alveolar ducts
- enlarged air spaces distal to the terminal bronchioles

enlarged lung
- significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months

lung inflammation
- no increase in white blood cells or neutrophiles in bronchoalveolar fluid
- white blood cells and neutrophiles are not detected by myeloperoxidase assay

pulmonary edema
- less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation
- resistant to lipopolysaccharide induced lung interstitial edema

Genotype: Pde6b^rd1/Pde6b^rd1
C3H/HeJ

mammalian phenotype

vision/eye phenotype
- Normal - 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)

nervous system phenotype

absent photoreceptor outer segment

vision/eye phenotype

abnormal retinal outer nuclear layer morphology
- nearly complete absence of outer nuclear layer

absent photoreceptor outer segment

retinal degeneration
- entire outer retina is destroyed, however the inner retina remains intact

Genotype: Ahr^b-2/Ahr^b-2
C3H/He

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

increased sensitivity to xenobiotic induced morbidity/mortality
- mice are susceptible to DMBA induced lethality

mortality/aging

increased sensitivity to xenobiotic induced morbidity/mortality
- mice are susceptible to DMBA induced lethality

Genotype: Gria4^spkw1/Gria4^spkw1
C3H/HeJ

behavior/neurological phenotype

absence seizures
- mice show higher spike wave discharge incidence than C3HeB/FeJ or C57BL/6 mice

nervous system phenotype

absence seizures
- mice show higher spike wave discharge incidence than C3HeB/FeJ or C57BL/6 mice

Phenotype Information

References

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):311-3PubMed: 16309882 MGI: J:105810
Chang B. 2015. Survey of the nob5 mutation in C3H substrains. Mol Vis 21:1101-5PubMed: 26396487 MGI: J:224435
Frankel WN; Mahaffey CL; McGarr TC; Beyer BJ; Letts VA. 2014. Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy. PLoS Genet 10(7):e1004454PubMed: 25010494 MGI: J:228536
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):141-8PubMed: 4322934 MGI: 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):917-23PubMed: 2997536 MGI: J:24864
Dragani TA; Manenti G; Gariboldi M; Degregorio L; Pierotti MA. 1995. Genetics of liver tumor susceptibility in mice. Toxicol Lett 82-3:613-619PubMed: 8597117 MGI: J:31816
Cheers C; McKenzie IF. 1978. Resistance and susceptibility of mice to bacterial infection: genetics of listeriosis. Infect Immun 19(3):755-62PubMed: 305895 MGI: J:5965
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):902-11PubMed: 15081119 MGI: J:89298

Additional References

Bell TA; de la Casa-Esperon E; Doherty HE; Ideraabdullah F; Kim K; Wang Y; Lange LA; Wilhemsen K; Lange EM; Sapienza C; de Villena FP. 2006. The Paternal Gene of the DDK Syndrome Maps to the Schlafen Gene Cluster on Mouse Chromosome 11. Genetics 172(1):411-23PubMed: 16172501 MGI: J:105162
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):797-803PubMed: 9804341 MGI: J:111520
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):1489-97PubMed: 17273166 MGI: J:122923
Xie C; Sharma R; Wang H; Zhou XJ; Mohan C. 2004. Strain distribution pattern of susceptibility to immune-mediated nephritis. J Immunol 172(8):5047-55PubMed: 15067087 MGI: J:122988
West DB; Boozer CN; Moody DL; Atkinson RL. 1992. Dietary obesity in nine inbred mouse strains. Am J Physiol 262(6 Pt 2):R1025-32PubMed: 1621856 MGI: J:1348
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):4-20PubMed: 16971002 MGI: J:138682
International Nomenclature Committee. 1952. COMMITTEE on Standardized Nomenclature for Inbred Strains of Mice Cancer Res 12(8):602-13PubMed: 14945054 MGI: 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):289-94PubMed: 21921910 MGI: J:177037
Sundberg JP; Cordy WR; King LE Jr. 1994. Alopecia areata in aging C3H/HeJ mice. J Invest Dermatol 102(6):847-56PubMed: 8006447 MGI: J:18877
Hui ST; Parks BW; Org E; Norheim F; Che N; Pan C; Castellani LW; Charugundla S; Dirks DL; Psychogios N; Neuhaus I; Gerszten RE; Kirchgessner T; Gargalovic PS; Lusis AJ. 2015. The genetic architecture of NAFLD among inbred strains of mice. Elife 4:e05607PubMed: 26067236 MGI: J:223755
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):316-23PubMed: 2317166 MGI: J:22615
Belknap JK; Noordewier B; Lame M. 1989. Genetic dissociation of multiple morphine effects among C57BL/6J, DBA/2J and C3H/HeJ inbred mouse strains. Physiol Behav 46(1):69-74PubMed: 2813556 MGI: J:24259
Sundberg JP; Awgulewitsch A; Pruett ND; Potter CS; Silva KA; Stearns TM; Sundberg BA; Munoz MW; Cuasnicu PS; King LE Jr; Rice RH. 2014. Crisp1 and alopecia areata in C3H/HeJ mice. Exp Mol Pathol 97(3):525-8PubMed: 25446841 MGI: J:244188
Wall EH; Case LK; Hewitt SC; Nguyen-Vu T; Candelaria NR; Teuscher C; Lin CY. 2014. Genetic control of ductal morphology, estrogen-induced ductal growth, and gene expression in female mouse mammary gland. Endocrinology 155(8):3025-35PubMed: 24708240 MGI: J:244714
Sundberg JP; Pratt CH; Silva KA; Kennedy VE; Stearns TM; Sundberg BA; King LE; HogenEsch H. 2016. Dermal lymphatic dilation in a mouse model of alopecia areata. Exp Mol Pathol 100(2):332-6PubMed: 26960166 MGI: J:262269
Rendina-Ruedy E; Hembree KD; Sasaki A; Davis MR; Lightfoot SA; Clarke SL; Lucas EA; Smith BJ. 2015. A Comparative Study of the Metabolic and Skeletal Response of C57BL/6J and C57BL/6N Mice in a Diet-Induced Model of Type 2 Diabetes. J Nutr Metab 2015:758080PubMed: 26146567 MGI: J:266370
Gubner NR; Wilhelm CJ; Phillips TJ; Mitchell SH. 2010. Strain differences in behavioral inhibition in a Go/No-go task demonstrated using 15 inbred mouse strains. Alcohol Clin Exp Res 34(8):1353-62PubMed: 20491731 MGI: J:266371
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):2922-8PubMed: 1879918 MGI: J:27016
Zhang LY; Levitt RC; Kleeberger SR. 1995. Differential susceptibility to ozone-induced airways hyperreactivity in inbred strains of mice. Exp Lung Res 21(4):503-18PubMed: 7588439 MGI: J:31117
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):581-91PubMed: 9720874 MGI: J:49726
Sultzer BM. 1968. Genetic control of leucocyte responses to endotoxin. Nature 219(160):1253-4PubMed: 4877918 MGI: J:5087
Moeller GR; Terry L; Snyderman R. 1978. The inflammatory response and resistance to endotoxin in mice. J Immunol 120(1):116-23PubMed: 627714 MGI: J:5936
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):202-6PubMed: 10674366 MGI: J:60482
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):537-45PubMed: 11017920 MGI: J:66641
Glant TT; Bardos T; Vermes C; Chandrasekaran R; Valdez JC; Otto JM; Gerard D; Velins S; Lovasz G; Zhang J; Mikecz K; Finnegan A. 2001. Variations in susceptibility to proteoglycan-induced arthritis and spondylitis among C3H substrains of mice: evidence of genetically acquired resistance to autoimmune disease. Arthritis Rheum 44(3):682-92PubMed: 11263784 MGI: J:71295
Bouwknecht JA; Paylor R. 2002. Behavioral and physiological mouse assays for anxiety: a survey in nine mouse strains. Behav Brain Res 136(2):489-501PubMed: 12429412 MGI: J:80397
Welkos SL; Keener TJ; Gibbs PH. 1986. Differences in susceptibility of inbred mice to Bacillus anthracis. Infect Immun 51(3):795-800PubMed: 3081444 MGI: J:8197
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):771-5PubMed: 12713579 MGI: J:83350
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):215-20PubMed: 14996992 MGI: J:89267

Additional - Hrh1^Bphs-r related

Additional - Ahr^b-2 related

Additional - Cd5^a related

Additional - Gria4^spkw1 related

Additional - Mx1^s1 related

Additional - Pcnx2^C3H/HeJ related

Additional - Pde6b^rd1 related

Additional - Tlr4^Lps-d related

Additional - In(6)1J related

Technical Support

Contact Technical Support

Genotyping Protocols
- End Point Analysis: Tlr4^Lps-d-Alternate 2
- Genotyping resources and troubleshooting
Inbred mouse strains are maintained through sibling (sister x brother) matings; no genotyping required.
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a good breeder.
- Additional Breeding and Husbandry Support
Mating System
- Sibling x Sibling
Appearance
- agouti
  Related Genotype: A/A
Citation
When using the C3H mouse strain in a publication, please include JAX stock #000659 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MP14 (Maximum)

RB09 (Maximum)

MP24 (High)

Pricing & Availability

Readily Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Inbred, 1 pair minimum will be supplied

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.

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.

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.

Terms Of Use

Terms of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

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"). "PRODUCT(S)" means biological materials supplied by JACKSON, and their derivatives. "SERVICES" means projects conducted by JACKSON for other parties that may include but are not limited to the use of MICE or PRODUCTS. "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 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, PRODUCTS or SERVICES 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.

Credit for PRODUCTS or SERVICES

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Animal Care and Use for SERVICES

Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody.

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.

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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.

Also Known As: C3H Heston, C3, C3H

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Selected References

Hrh1Bphs-r

Allele Symbol: Hrh1Bphs-r

Tlr4Lps-d

Allele Symbol: Tlr4Lps-d

In(6)1J

Allele Symbol: In(6)1J

Pcnx2C3H/HeJ

Allele Symbol: Pcnx2C3H/HeJ

Mx1s1

Allele Symbol: Mx1s1

Ahrb-2

Allele Symbol: Ahrb-2

Cd5a

Allele Symbol: Cd5a

Gria4spkw1

Allele Symbol: Gria4spkw1

Pde6brd1

Allele Symbol: Pde6brd1

Disease Terms

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).

Research Areas By Genotype

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

Genotype: Tlr4Lps-d related

Genotype: Pde6brd1 related

Mammalian Phenotype Terms by Genotype

Genotype: In(6)1J/In(6)1JC3H/HeJ

normal phenotype

Genotype: Tlr4Lps-d/Tlr4Lps-dinvolves: C3H/HeJ

behavior/neurological phenotype

immune system phenotype

integument phenotype

mammalian phenotype

nervous system phenotype

skeleton phenotype

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Tlr4Lps-d/Tlr4Lps-dC3H/HeJ-Tlr4

adipose tissue phenotype

cellular phenotype

skeleton phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

behavior/neurological phenotype

liver/biliary system phenotype

mammalian phenotype

cardiovascular system phenotype

mortality/aging

muscle phenotype

nervous system phenotype

respiratory system phenotype

Genotype: Pde6brd1/Pde6brd1C3H/HeJ

mammalian phenotype

nervous system phenotype

vision/eye phenotype

Genotype: Ahrb-2/Ahrb-2C3H/He

homeostasis/metabolism phenotype

mortality/aging

Genotype: Gria4spkw1/Gria4spkw1C3H/HeJ

behavior/neurological phenotype

nervous system phenotype

Phenotype Information

References

Additional References

Additional - Hrh1Bphs-r related

Additional - Ahrb-2 related

Additional - Cd5a related

Additional - Gria4spkw1 related

Additional - Mx1s1 related

Hrh1^Bphs-r

Allele Symbol: Hrh1^Bphs-r

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Pcnx2^C3H/HeJ

Allele Symbol: Pcnx2^C3H/HeJ

Mx1^s1

Allele Symbol: Mx1^s1

Ahr^b-2

Allele Symbol: Ahr^b-2

Cd5^a

Allele Symbol: Cd5^a

Gria4^spkw1

Allele Symbol: Gria4^spkw1

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Genotype: Tlr4^Lps-d related

Genotype: Pde6b^rd1 related

Genotype: In(6)1J/In(6)1J
C3H/HeJ

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
involves: C3H/HeJ

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C3H/HeJ-Tlr4

Genotype: Pde6b^rd1/Pde6b^rd1
C3H/HeJ

Genotype: Ahr^b-2/Ahr^b-2
C3H/He

Genotype: Gria4^spkw1/Gria4^spkw1
C3H/HeJ

Additional - Hrh1^Bphs-r related

Additional - Ahr^b-2 related

Additional - Cd5^a related

Additional - Gria4^spkw1 related

Additional - Mx1^s1 related

Additional - Pcnx2^C3H/HeJ related

Additional - Pde6b^rd1 related

Additional - Tlr4^Lps-d related