About   Help   FAQ
Inbred Strains of Mice: C3H

C3H

Inbr: F130 to F170 depending on substrain. Agouti. Genet: +, rd. Developed by Strong 1920 from a cross of Bagg albino with DBA male (see CBA) with selection for a high incidence of mammary tumours. Now among the most widely used of all mouse strains. Most substrains have a good reproductive performance. Unfostered substrains (which are now relatively rare since 'SPF' animals have become popular) have a high incidence of mammary tumours (usually > 90% at one year) caused by a virus which is passed from mother to offspring through the milk. Fostering of the young or transfer of fertilised ova to a mammary tumour virus-free strain eliminates the virus, and substantially reduces the incidence of mammary tumours. Note that all `SPF' stock will be free of this virus.

The unfostered substrains are widely used in cancer research for the sake of their mammary tumours. Fostered stock are widely used as a general-purpose strain which is readily available and well known. The strain should be used with care in behavioural studies, since it carries the rd (retinal degeneration) gene and is blind after about 6 weeks.

Some substrain differences are large, and can not be accounted for solely on the basis of mutation, and must be ascribed either to substantial residual heterozygosity or genetic contamination (McLaren and Tait, 1969), though C3H/HeJ is known to differ from C3H/He as a result of a mutation at the lps (lipopolysaccharide) locus.

The following major substrains are recognised:

C3H/Bi

Strong to Bittner 1931, to Kirschbaum 1952. Has 83% mammary tumours in unfostered breeders. Low leukaemia.

C3H/Fg

Origin not known, but has a very high incidence of lymphatic leukaemia (over 90%) (Fuchs, 1962).

C3H/He

This substrain was passed to Heston in 1941,and is now the most widely distributed of all. Non-fostered substrains have more than 90% mammary tumours by about 11 months. Fostered substrains have a high incidence of hepatomas (Festing and Blackmore, 1971).

C3H/HeJ

Heston, to Jackson Laboratory in 1947, and now widely distributed. Has poor immune response to endotoxic lipopolysaccharide due to a B-cell deficit (Rosenstreich and Glode, 1975; Coutinho, 1976).

C3HeB/De

A substrain developed by transfer of fertilised ova to strain C57BL by Deringer. This substrain lacks the mammary tumour virus and therefore has a lower incidence of mammary tumours (4% in virgin females and 55% in breeding females and 74% in force-bred females) (Deringer, 1959a).

C3HeB/FeJLe-a/a

Inbr. N10F12 (1993). The a allele transferred from C57BL/6J. Now used to create a B6C3Fe-a/a non-agouti hybrid as a coat colour marker for stocks maintained by ovarian transfer.

C3HeB/Fe (syn: TC3H)

Developed by Fekete in 1948 by transfer of fertilized ova of C3H/HeJ to C57BL/6. Lacks mammary tumour virus.

C3H/He-mg

`Mahogany' coat colour mutation occurred spontaneously in C3H/He stock held at Laboratory Animals Centre, Carshalton, in 1967. The strain has been propagated because authenticity can be guaranteed by the colour of the coat.

C3H/He-Avy

Congenic line developed by backcrossing the Avy to the C3H background. Has an exceptionally high mammary tumour incidence, virtually 100% at 7-8 months. The fostered substrain C3H-Avy fB has a 90% incidence of mammary tumours transmitted by either parent (Vlahakis et al., 1970., 1970).

C3H.PRI-Flvr (formerly C3H.RV ) and C3H.M.Dom-Flvr

Congenic line resistant to flavivirus (arbovirus) infection, developed by Groschel and Koprowski (1965) by backcrossing the resistance gene from PRI to C3H, and by Shallam by backcrossing the resistance gene from wild M.m. domesticus to C3H.


Behaviour

Low intrastrain aggression (10/14) (Southwick and Clark, 1966). Long latency to emerge from home-cage (6/7), low rearing (7/7), long latency to cross barrier in open-field (6/7), low hole-in-the-wall entries (6/7) and low Y-maze exploration (7/7) (McClearn et al., 1970., 1970). Low open-field activity (13/13) (Bruell, 1964). Low open-field defaecation (5/5) (Bruell, 1969). High food drive (3/15) (Thompson, 1953), but poor performance in food-seeking task (5/6) (Henderson, 1970). Short time of immobility in a forced swimming test (9/9) (Nikulina et al 1991).

Low shock-avoidance learning (8/9) (Bovet et al., 1966., 1966, 1969). Good short- term but poor long-term memory in contrast with DBA/2 (Bovet et al., 1969., 1969). Good T-maze learning (1/6) (Stasik, 1970). Poor water-escape learning (6/6) (Festing, 1973b). Low radial-arm maze learning (3/3) (Ammassari-Teule et al, 1993). High social grooming score during aggressive encounters (3/14) (Southwick and Clark, 1968).

Carries the retinal degeneration gene and is capable of pattern discrimination up to 40 days, and brightness discrimination to at least 100 days (Nagy and Misanin, 1970).

Life-span and spontaneous disease

Almost 100% of mammary tumours in females of unfostered substrains (Heston, 1963). Mammary adenocarcinomas in unfostered substrains less than 1% in males, 95% in breeding and 88% in virgin females. Lymphatic leukaemia zero incidence (Hoag, 1963). Mammary tumours 100% at 6.8 months in C3H-Avy , 90% in C3H- Avy fC57BL at 15.3 months. Mammary tumours 40% at 18.8 months in C3HfC57BL, but 99% at 7.2 months in unfostered C3H (Heston and Vlahakis, 1971). Mammary tumours 37% at 2 years in fostered substrain (Bentvelzen et al., 1970., 1970). Median latent period to develop mammary tumours in unfostered substrains ranged from 276 to 566 days, depending on breeding status and environmental stress (Riley, 1975). A high proportion of the mammary tumours are of the acinar type (2/7) (Tengbergen, 1970). Incidence of mammary tumours reduced by bromocriptine and interferon Stravoravdi et al, 1993).

Hepatomas 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females (Heston, 1963). Hepatomas have eosinophilic cytoplasmic inclusion bodies (Liebelt et al., 1971., 1971). Good model of genetic predisposition to hepatocellular tumours, susceptibility being associated with six chromosomal regions (Dragani et al, 1995). Point mutations in H-ras do not generally play a major or initiating role in spontaneous hepatocarcinogenesis in this strain (Enomoto et al, 1993).

Lung adenomas 2-10% in fostered A substrain, leukaemia 6-30% (Muhlbock and Tengbergen, 1971). Occasional Harderian gland tumours (Heston, 1963). Rare "lipomatous" hamartomas or choristomas have been noted (Adkison et al 1991).

Life-span in SPF fostered conditions intermediate in both sexes (11/17 = 590 days in males, 12/17 = 676 days in females). Liver tumours 9-23%, lung tumours 2-10% and mammary tumours 21-36%. Heart defects 13-26% and cystic ovaries 13-26% (Festing and Blackmore, 1971). Tail lesions similar in appearance to bit wounds were found in grouped C3H/HeJ by Les (1972). Develop dystrophic cardiac calcification which may be related to disturbed myocyte calcium metabolism (Brunnert, 1997).

Can be made obese by a suitable diet (Fenton and Dowling, 1953). Resistant to the development of aortic cartilaginous metaplasia (contrast C57BL/6) (Qiao et al, 1995). Resistant to diet-induced aortic fatty streak lesions which correlates with a high level of paroxinase mRNA (contrast C57BL/6) (Shih et al, 1996).

C3HeB/FeJ

Primary lung tumours 8% in males, 4% in breeding females and 10% in Virgin females. Lymphatic leukaemia zero. Mammary adenocarcinomas zero in males, 12% in breeding females, 2% in virgin females (Hoag, 1963). Ovarian tumours 47% in Virgin and 37% in breeding females, 29% in force-bred females (Heston, 1963). Hepatomas 91% in breeding males, 58% in Virgin and 30% in breeding females (Murphy, 1966). Life-span above average in both sexes (16/22 = 652 days in males, 17/22 = 657 days in females). High gross tumour incidence in males (5/22) (Storer, 1966).

Normal physiology and biochemistry

Low blood pressure (15/17) (Mullink et al., 1975). Low serum calcium in Fg substrain (5/6) but He substrain has high level at 4 months (1/6) (Barrett et al., 1975., 1975). High serum cholesterol (1/5) (Bruell et al., 1962., 1962). High plasma cholesterol (11/11) and triglycerides (10/11). High erythrocyte catalase (5/18) (Hoffman and Rechcigl, 1971). Low serum haptoglobin level (10/11) (Peacock et al, 1967 , 1967). Low peripheral nerve conduction velocity (6/6) (Hegmann, 1972). Low percentage of time spent sleeping (5/6) with low percentage of slow-wave sleep (5/6) and small diurnal variation (5/6) (Valatx and Bugat, 1974). High brain glutamic acid decarboxylase (GABA) in He-mg substrain (2/10) (Gaitonde and Festing, 1976). High brain aromatic L-amino acid decarboxylase (1/5) in C3H/2 substrain (Pryor et al., 1966., 1966). Low metabolic rate (5/6) (Pennycuik, 1967). High liver tyrosine aminotransferase level in fasted mice (1/10) (Blake, 1970). Low adrenal corticosteroid production (4/4) (Nandi et al., 1967., 1967). High peptidyl proline hydroxylase activity in tumour tissue and mammary gland fat pad (1/5) (Cutroneo et al., 1973., 1973). Slow cell turnover as judged by rate of clearance of DNA- bound radioactivity (14/17) (Heiniger et al., 1972., 1972). Harderian gland has a high porphyrin content (2/16) (Margolis, 1971). Low hepatic ammonia-lyase activity (5/6 and 6/6 in two substrains) (Hanford et al., 1974., 1974). Low spermatozoal beta-glucuronidase activity (9/9) (Erickson, 1976). Low basal level of renal glutathione S-transferase (4/4) but high basal level of renal glutathione reductase (1/4) (Misra et al 1991). Low hepatic nicotinamide N-methyltransferase levels (10/10) (Scheller et al, 1996). Maintain normal auditory sensitivity beyond one year of age in both HeJ and HeSnJ substrains, but by 30 months there was little hearing function due to sensorineural degeneration (Trune et al, 1996).

High level of alpha-fetoprotein in plasma at 7 days (2/6) (Adinolfi et al 1990). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). Loci on chromosomes 1, 3, 5 and 11 are associated with variation in high density lipoprotein levels with coordinate expression of cholesterol-7-alpha hydroxylase in a cross involving atherosclerosis susceptible C57BL/6 mice (Machleder et al, 1997).

Hepatic iodothyonine deiodinase activity was only 18% of that found in C57BL/6 mice (Schoenmakers et al, 1993). Decreased levels of deiodinase mRNA and hyperthyroxinemia associated with a 21-base pair insert in the promoter region of the type 1 deiodinase gene (Maia et al, 1995). Resistant to severe hypercapnia with hypoxia assessed by elevated minute ventilation rate (8/8) (Tankersley et al, 1994). Has a slow and deep breathing pattern phenotype (contrast C57BL/6) (Tankersley et al, 1997). High intra-ocular pressure (1/4) (John et al, 1997).

C3HeB/FeJ

Low systolic blood pressure (19/19) (Schlager and Weibust, 1967). Low plasma cholinesterase activity in females (18/22) (Angel et al, 1967). High N'- methylnicotinamide oxidase activity (1/7) (Huff and Chaykin, 1967).


Anatomy

Low total leukocyte count (18/18), low erythrocyte count (16/18), low haematocrit (18/18), low haemoglobin (17/18) (Russell et al., 1951., 1951). Small thymus/body weight ratio (5/6) (Belyaev et al., 1970., 1970), small thymus/body weight ratio (6/8 to 8/8, depending on age) (Albert et al., 1965., 1965). Large pituitary (1/6) (Sinha et al., 1975., 1975). Adrenal gland X zone large (1/8), with high incidence of vacuolisation (2/6) (Delost and Chirvan-Nia, 1958). Low percentage of mice have accessory spleens (9/9) (Hummel et al., 1966., 1966). Many Peyer's patches (2/7) (Hummel et al., 1966., 1966). Plasma volume low (4/4) at 5.97 ml/100 g and red cell volume low (4/4) at 4.64ml/100g body weight in He substrain (Kano and Mizuma, 197.4). Intermediate proportion of sperm-head abnormalities (2/5, 13%) in C3H/HeJ (Styrna et al 1991). High retinal ganglion cell number (24/24) in HeJ (Williams et al, 1996). High bone density of femur (1/11) (Beamer et al, 1996).

Megakaryocytes have a higher average ploidy than all other mouse strains tested. This is due to multiple additive alleles (McDonald and Jackson, 1994).

C3HeB/FeJ

Large brain weight (15/18 male, 17/18 female) (Storer, 1967). Small brain/body weight ratio (19/20) (Roderick et al., 1973., 1973).


Drugs

Susceptible to skin ulceration to DMBA (cf. 13/22) (Thomas et al., 1973., 1973). Sensitive to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). Susceptible to induction of subcutaneous tumours by 3-methylcholanthrene (1/14 to 4/14, depending on substrain) (Kouri et al., 1973., 1973). Susceptible to tumour induction by 3-methylcholanthrene in fostered and unfostered substrains (1/8 to 2/8) (Whitmire and Salerno, 1972), (2/12) (Whitmire et al., 1971., 1971). Susceptible to induction of liver (1/6) but resistant to pulmonary (5/6) tumours by neonatally administered DMBA (Flaks, 1968). High susceptibility to tumour induction by 3,4-benzpyrene (1/6) (Liebelt et al., 1970., 1970). High susceptibility to induction of mammary tumours by urethane (2/7) (Bentvelzen et al., 1970., 1970). High incidence of gastric tumours after administration of methylcholanthrene by gavage (2/5) (Akamatsu and Barton, 1974). Susceptible to fibrosarcoma induction by methylcholanthrene (2/15 male, 1/15 female) (Strong, 1952). Highly susceptible to the induction of hepatocellular tumours by various carcinogens, with the volume of hepatic lesions being >100-fold greater than in more resistant strains. Susceptibility is linked to at least six chromosomal regions (Dragani et al, 1995). C3HxMSM F1 hybrids treated with N-methyl-N-nitrosourea (MNU) develop squamous cell carcinomas of the forestomach with about 20% and 15% having mutations in H-ras and p53, respectively (Masui et al, 1997).

Phenobarbitone in the diet to give an intake of 85mg/kg per day resulted in 70% of animals developing basophilic nodules by 91 weeks of age (contrast 4% in C57BL/6), but no increase in liver carcinomas (Evans et al, 1992). However, there was a two-fold greater level of DNA synthesis in C3H mice relative to C57BL/6 mice after partial hepatactomy, though partial hepatectomy is a tumour promoter in C57BL/6 but not in C3H mice (Bennett et al, 1995).

Insensitive to histamine (9/9) (Brown, 1965). Airways of C3H/HeJ hyporeactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). Resistant to teratogenic effect of acetazolamide (5/6) (Green et al., 1973., 1973). Pentobarbital i.p. induces hepatic epoxide hydrase (cf. 4/7) (Oesch et al., 1973., 1973). Sensitive to X-irradiation (25/27) (Roderick, 1963). Long survival on Warfarin (12/12) (Lush and Arnold, 1975). Sensitive to hyperbaric oxygen (2/18) (Hill et al., 1968., 1968). Sensitive uterine response to oestrogens (5/5) (Chai and Dickie, 1966). Short hexobarbital sleeping time (3/9) (Vesell, 1968). Long survival in 90% oxygen (1/10) and highly susceptible to pulmonary hyaline-membrane formation (1/10) (Lieberman and Kellog, 1967). Resistant to the induction of pulmonary fibrosis by bleomycin (contrast C57BL/6) (Haston et al, 1996), and irradiation though the sensitivity of lung fibroblasts to irradiation in-vitro does not correlate with in-vivo sensitivity (Dileto and Travis, 1996). Sensitive to chloroform toxicity (cf. 4/9) (Deringer et al., 1953., 1953). Susceptible to toxic effects of isoniazid (10/10) (Taylor, 1976b). High ED50 to behavioural effects of nicotine (17/19) (Marks et al 1989). Low self-selection of nicotine (5/6) which is inversely correlated with sensitivity to nicotine-induced seizures (Robinson et al, 1996).

Low bronchial reactivity (5/6) to methacholine and serotonin (Konno et al 1993). No increase in renal lipid peroxidation following treatment with nickel (4/4) (Misra et al 1991). Susceptible to biliary tract injury following oral dosing with 500 micrograms of the fungal toxin sporidesmin (2/4) (Bhathal et al 1990). Low histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser ( c.f. 5/8) (Toda et al 1989). High histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Cadmium highly hepatotoxic (1/5) (Shaikh et al, 1993). Resistant (cf 3/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995, Kleeberger et al, 1993). Susceptible to weight loss induced by cocaine, but this is attenuated by anisomycin (cf SJL, CBA) (Shimosato et al, 1994). Estrogen does not induce an increase in VLDL and LDL-cholesterol (like BALB/c, contrast C57BL/6 and C57L)) (Srivastava, 1995).

C3HeB/FeJ

Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas et al., 1973., 1973). Sensitive to X-irradiation (23/27) (Roderick, 1963). Good ovulatory response (94%) to 3 I.U. PMS (1/6), but poor response (33%) to 7 I.U. PMS. Response facilitated by exposure to males (Zarrow et al., 1971., 1971). Susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995).


Immunology

Sensitive to amyloid induction (2/10) but low level of spontaneous amyloid formation (Ram et al., 1969., 1969). Low lymphocyte phytohaemagglutinin response (38/43) (Heiniger et al., 1975., 1975). Good immune response to small doses of bovine gamma globulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to Cholera A and B antigens (8/8) (Cerny et al., 1971., 1971). Good splenic PFC immune response to pneumococcal polysaccharide (2/9) (Amsbaugh et al., 1972., 1972). Females fail to reject male skin grafts after 100 days (contrast nine strains) (Gasser and Silvers, 1971). Poor immune response to ovomucoid and ovalbumin (cf. 2/12) (Vaz et al., 1971., 1971). Poor primary immune response to bovine serum albumin (5/6) (James and Milne, 1972). Good immune response to Salmonella anatum (1/5) and S. senftenberg (2/5) lipopolysaccharide (Di Pauli, 1972). Responder to synthetic polypeptide Glu57, Lys38, Ala5 (cf. 3/7) (Pinchuk and Maurer, 1965). Good immune response to Vi antigen (2/5) (Gaines et al., 1965., 1965). Precipitating and skin-sensitising antibodies have slow electrophoretic mobility (2/6) (Fahey, 1965). High antibody affinity to HSA (3/9) (Petty et al., 1972., 1972). Erythrocytes have high agglutinability (cf. 14/25) (Rubinstein et al., 1974., 1974). Low immune response to ferritin in He substrain (15/16) (Young et al., 1976., 1976). Non- discriminator between `H' and `L' sheep erythrocytes (cf. 6/18) (McCarthy and Dutton, 1975). High anti-DNP antibody concentration (2/7) (Paul et al., 1970., 1970). Antibodies to lipoid A antigen do not cross-react with sheep red blood cells (contrast eight strains). Strain also resistant to toxic effect of Salmonella lipopolysaccharide (1/8) (Rank et al., 1969., 1969). Refractory to sensitising effects of HSF from Bordetella pertussis to histamine (contrast sixteen strains) (Bergman and Munoz, 1968).

Low level of "leakiness" when the scid mutation is maintained on this genetic background (contrast CB17) (Nonoyama et al, 1993).

Good immune response to Pro-Gly-Pro-ovalbumin (1/7) and (Pro-Gly- Pro)n (2/7) (Fuchs et al., 1974., 1974). High susceptibility (3/12) to IgE-mediated passive cutaneous anaphylaxis (De Souza et al., 1974., 1974). Good immune response to Salmonella strasbourg lipopolysaccharide (1/7) (Di Pauli, 1972). Low PHA- stimulated lymphocyte blastogenic response in Ent substrain (6/6) (Hellman and Fowler, 1972). Erythrocytes of C3HeB/FeJ have a high agglutinability (cf. 14/25) (Rubinstein et al., 1974., 1974). He substrain resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). He and HeN substrains are susceptible (2/12) to experimental autoimmune orchitis induced by two or three sc injections with viable syngeneic testicular germ cells without any adjuvants, but C3H/BiKi is resistant (12/12) (Tokunaga et al 1993). High immune response to ganglio-series gangliosides in C3H/HeN (c.f. 2/10), but low response in C3H/HeJ (c.f. 4/10) (Kawashima et al 1992). Anti-BPO IgE monoclonal antibody did not produce potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 5/8) (Harada et al 1991). Carries a strain-specific allele at the alpha globin locus (Sato et al, 1996).

High natural killer cell response to the immunostimulent 7-allyl-8-oxoguanosine (1/6) (Pope et al, 1994).


Infection

Resistant to infection by Salmonella typhimurium strain C5 (5/7) (Plant and Glynn, 1974), Susceptible to Mycoplasma fermentens (1/6) (Gabridge et al., 1972., 1972). Experimental Mycoplasma pulmonis infection results in acute pneumonia with severe hemorrhage, edema and often death (Faulkner et al, 1995). Susceptible to mammary tumour virus, which is carried in an active form in unfostered substrains (Murray and Little, 1967). Susceptible to oncogenic effect of polyoma virus given at birth (Law, 1966a). Susceptible to measles virus induced encephalitis, which correlates with a high cytotoxic T-lymphocyte response (like C57BL/6, contrast BALB/c) (Niewiesk et al, 1993).

Susceptible to Mycobacterium marinum (2/9)(Shepard and Habas, 1967). Susceptible to infection by Mycobacterium marinum (1/6) (Yamamoto et al 1991). Susceptible to infection by Entamoeba histolytica (1/4) (Neal and Harris, 1975). Resistant to mouse hepatitis virus (Bang and Warwick, 1960). 100% transmission of murine leukaemia virus (Scripps) through three successive generations (cf. 2/5) (Jenson et al., 1976., 1976). Highly susceptible to measles virus (cf. 3/6) (Rager-Zisman et al., 1976., 1976). The BiDa substrain is susceptible (9/9) to tumorigenesis following infection with polyoma virus in contrast with C57BL/6 (Freund et al 1992) and C57BR/cd due to a single dominant gene Pyvs for susceptibility, which may be identical to Mtv-7 (Lukacher et al, 1995). Highly susceptible to tumour induction by polyoma virus (1/9) (Freund et al, 1992). Following administration of murine cytomegalovirus, C3H mice exhibited minimal carditis after neonatal or adult infection. However neonatal infection appears to accelerate age-related cardiopathy, which is severe in retired breeders of this strain. (contrast BALB/c and C57BL/10) (Price et al 1991). Highly susceptible to Lyme borreliosis (Borrelia burgdorferi) when inoculated at 3 weeks of age (1/5) and as adults. Mice inoculated at age 3 weeks also developed polyarthritis, but severity was reduced when inoculated as adults. Carditis was also common (Barthold et al 1990), and mice were susceptible to the development of arthritis (contrast BALB/c) (Matyniak and Reiner, 1995). Resistant to intra-vaginally innoculated Neisseria gonorrhoeae (c.f. 5/5) (Johnson et al 1989). Resistant (3/10) to infection with Ehrlichia risticii (Williams and Timoney, 1994). Susceptibile to infection by Helicobacter felis with moderate to severe chronic active gastritis in the body of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996).

C3H/HeJ

Substrain (which carries the lps mutation) resistant to LCM virus (76% survival) prior to 1970, but has now become susceptible (3% survival) (Oldstone and Dixon, 1973). Resistant to LCM virus infection (1/5) (Oldstone and Dixon, 1968). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher et al., 1975., 1975). Susceptible to lethal infection with Rickettsia akari strain Kaplan, in contrast with seven other substrains of C3H and 24 other strains (Anderson and Osterman 1980a,b). Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). High immunological response to Salmonella typhi porins (1/4) (Gonzales et al, 1995). Resistant to infection with Mycobacterium paratuberculosis (contrast BALB/c) (Tanaka et al, 1994).

Susceptible, with high amylase response to the fungus Paracoccidioides brasiliensis (cf 6/12) (Xidieh et al, 1994). Resistant to Leishmania major (contrast BALB/c) (Laskay et al, 1995, Scott et al, 1996). Lipopolysaccharide mutant (lps) and non-mutant mice are equally susceptible to Escherichia coli (Hopkins et al, 1996).

C3HeB/FeJ

Highly susceptible to mammary tumour virus, but believed to be free of the virus (Murray and Little, 1967). Low susceptibility to BALB/Tennant leukaemia virus (11/12) (Tennant, 1965). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher et al., 1975., 1975).


Reproduction

Breeding performance intermediate/good (5/25 He substrain, 10/25 He-mg sub-line). Colony output 1.1 to 1.4 young/female/week. Litter size at weaning 5.9 (8/25) (Festing, 1976a). Good reproductive performance (2/8), litter size 6.4, sterility 10% (Nagasawa et al., 1973., 1973). Large litter size (1/6 to 3/6), high proportion of females produce four or more litters (1/6) and high proportion of fertile matings (1/6) (Fernandes et al., 1973., 1973). Good breeding performance, 2.0 to 2.2 young per female per month (9/24 to 7/24) in fostered and unfostered substrains, respectively (Hansen et al., 1973., 1973). C3H/HeJ has shorter and less regular oestrus cycles than C57BL/6J (Nelson et al 1992). Early opening of vagina and first cornification (1/3 compared with C57BL/6 and DBA/2), but late onset of cyclicity (3/3) (Nelson et al 1990)

C3HeB/FeJ

High reproductive performance (1/8). Litter size 6.4 + 0.2, sterility 4% (Nagasawa et al., 1973., 1973).


Miscellaneous

Recommended host for the following transplantable tumours: lymphosarcoma 6C3HED and mammary adenocarcinomas C3HBA and H2712 (Kaliss, 1972). Recommended host for sarcoma BP8 used as a model for screening potential anticancer drugs (E.O.R.T.C. Screening Group, 1972). High mortality after neonatal thymectomy (6/6) (Law, 1966a).

High rate of spontaneous mutations (1/21) and total deviants (4/21) (Schlager and Dickie, 1967).

C3HeB/FeJ

Recommended host for transplantable hepatoma H4 (Kaliss, 1972). High incidence of spontaneous `deviants' (5/21) (Schlager and Dickie, 1967).


Adinolfi M., Beck S. E., Seller M. J., Fedor T., and McLaren A. (1990) Alpha-fetoprotein levels in different strains of mice during development. Exp. Clin. Immunogenet. 7, 123-128.

Adkison D. L. and Sundberg J. P. (1991) "Lipomatous" hamartomas and choristomas in inbred laboratory mice. Vet. Pathol. 28, 305-312.

Albert S., Wolf P. L., Pryjma I., and Moore W. (1965) Thymus development in high and low-leukemic mice. J. Reticuloendothel. Soc. 2, 218-237.

Ammassari-Teule M., Hoffman H. J., and Rossi-Arnaud C. (1993) Learning in inbred mice: strain-specific abilities across three radial maze problems. Behav. Genet. 23, 405-412.

Amsbaugh D. F., Hansen C. T., Prescott B., Stashak P. W., Barthold D. R., and Baker P. J. (1972) Genetic control of the antibody response to type III pneumococcal polysaccharide in mice. I. Evidence that an X-linked gene plays a decisive role in determining responsiveness. J. Exp. Med. 136, 931-949.

Anderson G. W. and Osterman J. V. (1980a) Host defenses in experimental rickettsialpox: genetics of natural resistance to infection. Infect. Immun. 28, 132-136.

Angel C. R., Mahin D. T., Farris R. D., and Woodward K. T. (1967) Heritability of plasma cholinesterase activity in inbred mouse strains. Science 156, 529-530.

Bang F. B. and Warwick A. (1960) Mouse macrophages as host cells for the mouse hepatitis virus and the genetic basis of their susceptibility. Proc. Natl. Acad. Sci. USA 46, 1065-1071.

Barrett C. P., Donati E. J., Volz J. E., and Smith E. B. (1975) Variations in serum calcium between strains of inbred mice. Lab. Animal Sci. 25, 638-640.

Barthold S. W., Beck D. S., Hansen G. M., Terwilliger G. A., and Moody K. D. (1990) Lyme borreliosis in selected strains and ages of laboratory mice. J. Infect. Dis. 162, 133-138.

Beamer W. G., Donahue L. R., Rosen C. J., and Baylink D. J. (1996) Genetic-variability in adult bone-density among inbred strains of mice. Bone 18, 397-403.

Belyaev D. K., Gruntenko E. V., and Videlets I. Y. (1970) Genetic differentiation of the thymus in mice of different strains with respect to malignant growth communication. II. Differences in the weight of the thymus in various strains of mice. Sov. Genet. 6, 47-51.

Bennett L. M., Farnham P. J., and Drinkwater N. R. (1995) Strain-dependent differences in DNA synthesis and gene expression in the regenerating livers of C57BL/6J and C3H/HeJ mice. Molecular Carcinogenesis 14, 46-52.

Bentvelzen P., Daams J. H., Hageman P., and Calafat J. (1970) Genetic transmission of viruses that incite mammary tumors in mice. Proc. Natl. Acad. Sci. USA 67, 377-384.

Bergman R. K. and Munoz J. (1968) Action of the histamine sensitizing factor from Bordetella pertussis on inbred and random bred strains of mice. Int. Arch. Allergy 34, 331-338.

Bhathal P. S., Jordan T. W., and Mackay I. R. (1990) Mouse strain differences in susceptibility to sporidesmin-induced biliary tract injury. Liver 10, 193-204.

Blake R. L. (1970) Regulation of liver tyrosine amino transferase activity in inbred strains and mutant mice. I. Strain variance in fasting enzyme levels. Int. J. Biochem. 1, 361-370.

Boucher D. W., Hayashi K., Rosenthal J., and Notkins A. L. (1975) Virus-induced diabetes mellitus. III. Influence of sex and strain of host. J. Infect. Dis. 131, 462-466.

Bovet D., Bovet-Nitti F., and Oliverio A. (1966) Effects of nicotine on avoidance conditioning of inbred strains of mice. Psychopharmacologia 10, 1-5.

Bovet D., Bovet-Nitti F., and Oliverio A. (1969) Genetic aspects of learning and memory in mice. Science 163, 139-149.

Brown A. M. (1965) Pharmacogenetics of the mouse. Lab. Anim. Care 15, 111-118.

Bruell J. H., Daroczy A. F., and Hellerstein H. K. (1962) Strain and sex differences in serum cholesterol levels in mice. Science 135, 1071-1072.

Bruell J. H. (1964) Inheritance of behavioural and physiological characters of mice and the problem of heterosis. Am. Zool. 4, 125-138.

Bruell J. H. (1969) Genetics and adaptive significance of emotional defecation in mice. Ann. NY Acad. Sci. 159, 825-830.

Brunnert S. R. (1997) Morphologic response of myocardium to freeze-thaw injury in mouse strains with dystrophic cardiac calcification. Lab. Animal Sci. 47, 11-18.

Cerny J., McAlack R. F., Sajid M. A., and Friedman H. (1971) Genetic differences in the immunocyte response of mice to separate determinants on one bacterial antigen. Nature New Biol. 230, 247-248.

Chai C. K. and Dickie M. M. (1966) Endocrine variations, in Biology of the laboratory mouse, 2nd. ed. (Green E. L., ed), pp. 387-403. McGraw-Hill, New York.

Coutinho A. (1976) Genetic control of B-cell responses. II. Identification of the spleen B-cell defect in C3H/HeJ mice. Scand.J. Immunol. 5, 129-140.

Cutroneo K. R., Guzman N. A., and Liebelt A. G. (1973) Elevation of peptidylproline hydroxylase activity and collagen synthesis in spontaneous primary mammary cancers of inbred mice. Cancer Res. 32, 2828-2833.

De Souza C. M., Maia L. C. S., and Vaz N. M. (1974) Susceptibility to cutaneous anaphylaxis in inbred strains of mice. J. Immunol. 112, 1369-1372.

Delost P. and Chirvan-Nia P. (1958) Differences raciales dans l'involution de la zone x multi surrenalienne chez la souris adulte vierge. C. R. Soc. Biol. 152, 453-455.

Deringer M. K., Dunn T. B., and Heston W. E. (1953) Results of exposure of strain C3H mice to chloroform. Proc. Soc. Exp. Biol. Med. 83, 474-479.

Deringer M. K. (1959a) Necrotizing arteritis in strain BL/De mice. Lab. Invest. 8, 1461-1465.

Di Pauli R. (1972) Genetics of the immune response. I. Differences in the specificity of antibodies to lipopolysaccharides among different strains of mice. J. Immunol. 109, 394-400.

Dileto C. L. and Travis E. L. (1996) Fibroblast radiosensitivity in-vitro and lung fibrosis in-vivo -comparison between a fibrosis-prone and fibrosis-resistant mouse strain. Radiation Res. 146, 61-67.

Enomoto T., Weghorst C. M., Ward J. M., Anderson L. M., Perantoni A. O., and Rice J. M. (1993) Low frequency of H-ras activation in naturally occurring hepatocellular tumors of C3H/HeNCr mice. Carcinogenesis 14, 1939-1944.

Erickson R. P. (1976) Strain variation in spermatazoal -glucuronidase in mice. Genet. Res. 28, 139-145.

Evans J. G., Collins M. A., Lake B. G., and Butler W. H. (1992) The histology and development of hepatic nodules and carcinoma in C3H/He and C57BL/6 mice following chronic phenobarbitone administration. Toxicologic Pathology 20, 585-594.

Fahey J. L. (1965) Differences in the electrophoretic mobility of antibody from inbred strains of mice. J. Immunol. 94, 819-823.

Faulkner C. B., Davidson M. K., Davis J. K., Schoeb T. R., Simecka J. W., and Lindsey J. R. (1995) Acute Mycoplasma pulmonis infection associated with coagulopathy in C3H/HeN mice. Lab. Animal Sci. 45, 368-372.

Fenton P. F. and Dowling M. T. (1953) Studies on obesity. I. Nutritional obesity in mice. J. Nutrit. 49, 319-331.

Fernandes G., Yunis E. J., and Good R. A. (1973) Reproductive deficiency of NZB male mice. Possibility of a viral basis. Lab. Invest. 29, 278-281.

Festing M. F. W. and Blackmore D. K. (1971) Life span of specified-pathogen-free (MRC category 4) mice and rats. Lab. Anim. 5, 179-192.

Flaks A. (1968) The susceptibility of various strains of neonatal mice to the carcinogenic effects of 9, 1 0-dimethyl- 1, 2-benzanthracene. Eur. J. Cancer 4, 579-585.

Fuchs S., Mozes E., Maoz A., and Sela M. (1974) Thymus independence of a collagen-like synthetic polypeptide and of collagen, and the need for thymus and bone marrow-cell cooperation in the immune response to gelatin. J. Exp. Med. 139, 148-158.

Fuchs P. C. (1962) Attempts to alter incidence of leukemia, and mammary cancer in C3H/Fg mice. Anat. Rev. 142, 233.

Gabridge M. G., Abrams G. D., and Murphy W. H. (1972) Lethal toxicity of Mycoplasma fermentens in mice. J. Infect. Dis. 125, 153-160.

Gaines S., Currie J. A., and Tully J. G. (1965) Factors affecting formation of incomplete Vi antibody in mice. J. Bacteriol. 90, 635-642.

Gaitonde M. K. and Festing M. F. W. (1976) Brain glutamic acid decarboxylase and open field activity in ten inbred strains of mice. Brain Res. 103, 617-621.

Gasser D. L. and Silvers W. K. (1971) Genetic basis of male skin rejection in mice. Transplant. 12, 412-414.

Green M. C., Azar C. A., and Maren T. H. (1973) Strain differences in susceptibility to the teratogenic effect of acetazolamide in mice. Teratology 8, 143-145.

Groschel D. and Koprowski H. (1965) Development of a virus-resistant inbred mouse strain for the study of innate resistance to arbo B virus. Arch. Ges. Virusforsch. 17, 379-391.

Hanford W. C., Nep R. L., and Arfin S. M. (1974) Genetic variation in histidine ammonia-lyase activity in the mouse. Biochem. Biophys. Res. Comm. 61, 1434-1437.

Hansen C. T., Judge F. J., and Whitney R. A. (1973) Catalog of NIH rodents. National Institutes of Health. DHEW publication (NIH) 74-606, Bethesda.

Harada M., Nagata M., Takeuchi M., Ohara T., Makino S., and Watanabe A. (1991) Age-dependent difference in susceptibility to IgE antibody- and IgG1 antibody-mediated passive anaphylactic shock in the mouse. Immunological Investigations 20, 515-523.

Haston C. K., Amos C. I., King T. M., and Travis E. L. (1996) Inheritance of susceptibility to bleomycin-induced pulmonary fibrosis in the mouse. Cancer Res. 56, 2596-2601.

Hegmann J. P. (1972) Physiological function and behavioural genetics. I. Genetic variance for peripheral nerve conduction velocity in mice. Behav. Genet. 2, 55-67.

Heiniger H. J., Chen H. W., Meier H., Taylor B. A., and Commerford L. S. (1972) Studies on the genetic control of cell proliferation. 1. Clearance of DNA-bound radioactivity in 19 inbred strains and hybrid mice. Life Sci. 11, 87-98.

Heiniger H. J., Taylor B. A., Hards E. J., and Meier H. (1975) Heritability of the phytohaemagglutinin responsiveness of lymphocytes and its relationship to leukemogenesis. Cancer Res. 35, 825-831.

Hellman A. and Fowler A. K. (1972) Studies of the blastogenic response of murine lymphocyte. III. Specific viral transformation. Proc. Soc. Exp. Biol. Med. 141, 106-109.

Henderson N. D. (1970) Genetic influences on the behaviour of mice can be obscured by laboratory rearing. J. Comp. Physiol. Psychol. 72, 505-511.

Heston W. E. and Vlahakis G. (1971) Mammary tumours, plaques and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumour virus. Int. J. Cancer 7, 141-148.

Heston W. E. (1963) Genetics of neoplasia, in Methodology in mammalian genetics (Burdette W. J., ed), pp. 247-268. Holden-Day, San Francisco.

Hill G. B., Osterhout S., and O'Fallon W. M. (1968) Variation in response to hyperbaric oxygen among inbred strains of mice. Proc. Soc. Exp. Biol. Med. 129, 687-689.

Hoag W. G. (1963) Spontaneous cancer in mice. Ann. NY Acad. Sci. 108, 805-831.

Hoffman H. A. and Rechcigl M. Jr. (1971) Erythrocyte catalase in inbred mice. Enzyme 12, 219-225.

Hopkins W. J., GendronFitzpatrick A., McCarthy D. O., Haine J. E., and Uehling D. T. (1996) Lipopolysaccharide-responder and nonresponder C3H mouse strains are equally susceptible to an induced Escherichia coli urinary tract infection. Infect. Immun. 64, 1369-1372.

Huff S. D. and Chaykin S. (1967) Genetic and androgenic control of N- methylnicotinamide oxidase activity in mice. J. Biol. Chem. 242, 1265-1270.

Hummel K. P., Richardson F. L., and Fekete E. (1966) Anatomy, in Biology of the Laboratory Mouse, 2nd. ed. (Green E. L., ed), pp. 247-307. McGraw-Hill, New York.

James K. and Milne I. (1972) The effect of anti-lymphocytic antibody on the humoral immune response in different strains of mice. I. The response to bovine serum albumin. Immunol. 23, 897-909.

Jenson A. B., Groff D. E., McConahey P. J., and Dixon F. J. (1976) Transmission of murine leukemia virus (Scripps) from parent to progeny mice as determined by P30 antigenemia. Cancer Res. 36, 1228-1232.

John S. W. M., Hagaman J. R., MacTaggart T. E., Peng L., and Smithes O. (1997) Intraocular pressure in inbred mouse strains. Investigative Ophthalmology & Visual Science 38, 249-253.

Johnson A. P., Tuffrey M., and Taylor-Robinson D. (1989) Resistance of mice to genital infection with Neisseria gonorrhoeae. J. Med. Microbiol. 30, 33-36.

Kawashima I., Nakamura O., and Tai T. (1992) Antibody responses to ganglio-series gangliosides in different strains of inbred mice. Molecular Immunology 29, 625-632.

Kleeberger S. R., Levitt R. C., and Zhang L. Y. (1993) Susceptibility to ozone-induced inflammation. I. Genetic control of the response to subacute exposure. American Journal of Physiology - Lung Cellular and Molecular Physiology 264, L15-L20.

Konno S., Adachi M., Matsuura T., Sunouchi K., Hoshino H., Okazawa A., Kobayashi H., and Takahashi T. (1993) Bronchial reactivity to methacholine and serotonin in six inbred mouse strains. [Japanese]. Japanese Journal of Allergology 42, 42-47.

Kouri R. E., Salerno R. A., and Whitmire C. E. (1973) Relationships between arylhydrocarbon hydroxylase inducibility and sensitivity to chemically induced subcutaneous sarcomas in various strains of mice. J. Natl. Cancer Inst. 50, 363-368.

Laskay T., Diefenbach A., Rollinghoff M., and Solbach V. (1995) Early parasite containment is decisive for resistance to Leishmania major infection. Eur. J. Immunol. 25, 2220-2227.

Law L. W. (1966a) Studies of thymic function with emphasis on the role of the thymus in oncogenesis. Cancer Res. 26, 551-574.

Lee B. K. and Eicher E. M. (1990) Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets [published erratum appears in J Virol 1991 Mar;65(3):1666]. J. Virol. 64, 4568-4572.

Les E. P. (1972) A disease related to cage population density: tail lesions of C3H/HeJ mice. Lab. Animal Sci. 22, 56-60.

Levine B. B. and Vaz N. M. (1970) Effect of combinations of inbred strain, antigen and antigen dose on immune responsiveness and reagin production in the mouse. Int. Arch. Allergy 39, 156-171.

Liebelt R. A., Suzuki S., Liebelt A. G., and Lane M. (1970) Virus-like particles in chemically induced sarcomas in high- and low-leukemia strains of mice. Cancer Res. 30, 2438-2448.

Liebelt A. G., Liebelt R. A., and Dmochowski L. (1971) Cytoplasmic inclusion bodies in primary and transplanted hepatomas of mice of different strains. J. Natl. Cancer Inst. 47, 413-427.

Lieberman J. and Kellog F. (1967) Hyaline-membrane formation and pulmonary plasminogen-activator activity in various strains of mice. Pediatrics 39, 75-81.

Lukacher A. E., Ma Y., Carroll J. P., AbromsonLeeman S. R., Laning J. C., Dorf M. E., and Benjamin T. L. (1995) Susceptibility to tumors induced by polyoma virus is conferred by an endogenous mouse mammary tumor virus superantigen. Journal Of Experimental Medicine 181, 1683-1692.

Lush I. E. and Arnold C. J. (1975) High coumarin 7-hydroxylase activity does not protect mice against Warfarin. Heredity 35, 279-281.

Machleder D., Ivandic B., Welch C., Castellani L., Reue K., and Lusis A. J. (1997) Complex genetic control of HDL levels in mice in response to an atherogenic diet - Coordinate regulation of HDL levels and bile acid metabolism. J. Clin. Invest. 99, 1406-1419.

Maia A. L., Berry M. J., Sabbag R., Harney J. W., and Larsen P. R. (1995) Structural and functional differences in the dio1 gene in mice with inherited type 1 deiodinase deficiency. Molec. Endocrinol. 9, 969-980.

Margolis F. L. (1971) Regulation of porphyrin biosynthesis in the Harderian gland of inbred mouse strains. Arch. Biochem. Biophys. 145, 373-381.

Marks M. J., Stitzel J. A., and Collins A. C. (1989) Genetic influences on nicotine responses. Pharmacol. Biochem. Behav. 33, 667-678.

Masui T., Tezuka N., Nakanishi H., Inada K. I., Miyashita N., and Tatematsu M. (1997) Induction of invasive squamous cell carcinomas in the forestomach of (C3H x MSM)F1, MSM, and C3H mice by N-methyl-N-nitrosourea and mutational analysis of the H-ras and p53 genes. Cancer Lett. 111, 97-104.

Matyniak J. E. and Reiner S. L. (1995) T helper phenotype and genetic susceptibility in experimental lyme disease. Journal Of Experimental Medicine 181, 1251-1254.

McCarthy M. M. and Dutton R. W. (1975) The humoral response of mouse spleen cells to two types of sheep erythrocytes. J. Immunol. 115, 1316-1321.

McClearn G. E., Wilson J. R., and Meredith W. (1970) The use of isogenic and heterogenic mouse stocks in behavioral research, in Contribution to behavior genetic analysis. The mouse as a prototype (Lindzey G. and Thiessen D. D., eds), pp. 3-32. Appleton-Century-Crofts, New York.

McLaren A. and Tait A. (1969) Cytoplasmic isocitrate dehydrogenase variation within the C3H inbred strain. Genet. Res. 14, 93.

Misra M., Rodriguez R. E., North S. L., and Kasprzak K. S. (1991) Nickel-induced renal lipid peroxidation in different strains of mice: concurrence with nickel effect on antioxidant defense systems [published erratum appears in Toxicol Lett 1992 60:239]. Toxicol. Lett. 58, 121-133.

Muhlbock O. and Tengbergen W. P. Jr. (1971) Instability of characteristics in inbred strains of mice, in Defining the laboratory animal (Schneider H. A., ed), pp. 230-249. Proc. IV ICLAS Symposium, .

Murphy E. D. (1966) Characteristic tumors, in Biology of the laboratory mouse, 2nd. ed. (Green E. L., ed), pp. 521-562. McGraw-Hill, New York.

Murray W. S. and Little C. C. (1967) Genetic studies of carcinogenesis in mice. J. Natl. Cancer Inst. 38, 639-656.

Nagasawa H., Miyamoto M., and Fujimoto M. (1973) Reproductivity in inbred strains of mice and project for their efficient production. Exp. Animals (Japan) 22, 119-126.

Nagy Z. M. and Misanin J. R. (1970) Visual perception in the retinal degenerate C3H mouse. J. Comp. Physiol. Psychol. 72, 306-310.

Nandi J., Bern H. A., Biglieri E. G., and Pieprzyk J. K. (1967) In vitro steroidogenesis by the adrenal glands of mice. Endocrinol. 80, 576-582.

Neal R. A. and Harris W. G. (1975) Attempts to infect inbred strains of rats and mice with Entamoeba histolytica. Trans. R. Soc. Trop. Med. Hyg. 69, 429-430.

Nelson J. F., Karelus K., Felicio L. S., and Johnson T. E. (1990) Genetic influences on the timing of puberty in mice. Biol. Reprod. 42, 649-655.

Nelson J. F., Karelus K., Felicio L. S., and Johnson T. E. (1992) Genetic influences on oestrous cyclicity in mice: evidence that cycle length and frequency are differentially regulated. J. Reprod. Fertil. 94, 261-268.

Niewiesk S., Brinckmann U., Bankamp B., Sirak S., Liebert U. G., and Ter Meulen V. (1993) Susceptibility to measles virus-induced encephalitis in mice correlates with impaired antigen presentation to cytotoxic T lymphocytes. Journal of Virology 67, 75-81.

Nikulina E. M., Skrinskaya J. A., and Popova N. K. (1991) Role of genotype and dopamine receptors in behaviour of inbred mice in a forced swimming test. Psychopharmacology 105, 525-529.

Nishina P. M., Wang J., Toyofuku W., Kuypers F. A., Ishida B. Y., and Paigen B. (1993) Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. Lipids 28, 599-605.

Nonoyama S., Smith F. O., Bernstein I. D., and Ochs H. D. (1993) Strain-dependent leakiness of mice with severe combined immune deficiency. J. Immunol. 150, 3817-3824.

Oesch F., Morris N., and Daly J. W. (1973) Genetic expression of the induction of epoxide hydrase and aryl hydrocarbon hydroxylase activities in the mouse by phenobarbital or 3-methylcholanthrene. Molec. Pharmacol. 9, 692-696.

Oldstone M. B. A. and Dixon F. J. (1968) Susceptibility of different mouse strains to lymphocytic choriomeningitis virus. J. Immunol. 100, 355-357.

Oldstone M. B. A. and Dixon F. J. (1973) Change in susceptibility of C3H/He mice to LCM virus infection. J. Immunol. 111, 1613-1615.

Paul W. E., Yoshida T., and Benacerraf B. (1970) Genetic control of the specificity of anti-DNP antibodies. II. Differences in the specificity of anti-DNP antibody produced by several inbred strains of mice. J. Immunol. 105, 314-321.

Peacock A. C., Gelderman A. H., Ragland R. H., and Hoffman H. A. (1967) Haptoglobin levels in serum of various strains of mice. Science 158, 1703-1704.

Pennycuik P. R. (1967) A comparison of the effects of a variety of factors on the metabolic rate of the mouse. Aust. J. Biol. Med. Sci. 45, 331-346.

Petty R. E., Steward M. W., and Soothill J. F. (1972) The heterogeneity of antibody affinity in inbred mice and its possible immunopathologic significance. Clin. Exp. Immunol. 12, 231-241.

Plant J. and Glynn A. A. (1974) Natural resistance to Salmonella infection, delayed hypersensitivity and Ir genes in different strains of mice. Nature 248, 345-347.

Pope B. L., Chourmouzis E., MacIntyre J. P., Lee S., and Goodman M. G. (1994) Murine strain variation in the natural killer cell and proliferative responses to the immunostimulatory compound 7-Allyl-8-oxoguanosine: Role of cytokines. Cell. Immunol. 159, 194-210.

Price P., Eddy K. S., Papadimitriou J. M., Faulkner D. L., and Shellam G. R. (1991) Genetic determination of cytomegalovirus-induced and age-related cardiopathy in inbred mice. Characterization of infiltrating cells. Am. J. Pathol. 138, 59-67.

Pryor G. T., Schlesinger K., and Calhoun W. H. (1966) Differences in brain enzymes among five inbred strains of mice. Life Sci. 5, 2105-2111.

Qiao J. H., Fishbein M. C., Demer L. L., and Lusis A. J. (1995) Genetic determination of cartilaginous metaplasia in mouse aorta. Arteriosclerosis, Thrombosis, and Vascular Biology 15, 2265-2272.

Rager-Zisman B., Ju G., and Udem S. (1976) Resistance and susceptibility of mice to infection with measles virus. Fed. Proc. 35, 391.

Ram J. S., Dehellis R. A., and Glenner G. G. (1969) Amyloid. VIII on strain variation in experimental murine amyloidosis. Proc. Soc. Exp. Biol. Med. 130, 462-464.

Rank W. R., Flugge U., and DiPauli R. (1969) Inheritance of the lipoid A- induced 19S-plaque-forming cell-response in mice. Evidence for three antigen-recognition mechanisms. Behringwirk- Mitt. 49, 222-229.

Riley V. (1975) Mouse mammary tumors: alteration of incidence as an apparent function of stress. Science 189, 465-467.

Robinson S. F., Marks M. J., and Collins A. C. (1996) Inbred mouse strains vary in oral self-selection of nicotine. Psychopharmacology 124, 332-339.

Roderick T. H., Wimer R. E., Wimer C. C., and Schwartzkroin P. A. (1973) Genetic and phenotypic variation in weight of brain and spinal cord between inbred strains of mice. Brain Res. 64, 345-353.

Roderick T. H. (1963) The response of twenty-seven inbred strains of mice to daily doses of whole-body X-irradiation. Radiation Res. 20, 631-639.

Rosenstreich D. L. and Glode L. M. (1975) Differences in cell nitrogen responsiveness between closely related strains of mice. J. Immunol. 115, 777-780.

Rubinstein P., Liu N., Strenn E. W., and Decary F. (1974) Electrophoretic mobility and agglutinability of red blood cells: a `new' polymorphism in mice. J. Exp. Med. 139, 313-322.

Russell E. S., Neufeld E. F., and Higgins C. T. (1951) Comparison of normal blood picture of young adults from 18 inbred strains of mice. Proc. Soc. Exp. Biol. Med. 78, 761-766.

Sakagami T., Dixon M., ORourke J., Howlett R., Alderuccio F., Vella J., Shimoyama T., and Lee A. (1996) Atrophic gastric changes in both Helicobacter felis and Helicobacter pylori infected mice are host dependent and separate from antral gastritis. Gut 39, 639-648.

Scheller T., Orgacka H., Szumlanski C. L., and Weinshilboum R. M. (1996) Mouse liver nicotinamide N-methyltransferase pharmacogenetics: Biochemical properties and variation in activity among inbred strains. Pharmacogenetics 6, 43-53.

Schlager G. and Dickie M. M. (1967) Spontaneous mutations and mutation rates in the house mouse. Genetics 57, 319-330.

Schoenmakers C. H. H., Pigmans I. G. A. J., Poland A., and Visser T. J. (1993) Impairment of the selenoenzyme type I iodothyronine deiodinase in C3H/He mice. Endocrinol. 132, 357-361.

Scott P., Eaton A., Gause W. C., Zhou X. D., and Hondowicz B. (1996) Early IL-4 production does not predict susceptibility to Leishmania major. Experimental Parasitology 84, 178-187.

Shaikh Z. A., Jordan S. A., and Tewari P. C. (1993) Cadmium disposition and metallothionein induction in mice: Strain-, sex-, age- and dose-dependent differences. Toxicology 80, 51-70.

Shepard C. C. and Habas J. A. (1967) Relation of infection to tissue temperature in mice infected with Mycobacterium marinum and Mycobacterium leprae. J. Bacteriol. 93, 790-796.

Shih D. M., Gu L., Hama S., Xia Y. R., Navab M., Fogelman A. M., and Lusis A. J. (1996) Genetic-dietary regulation of serum paraoxonase expression and its role in atherogenesis in a mouse model. J. Clin. Invest. 97, 1630-1639.

Shimosato K., Saito T., and Marley R. J. (1994) Genotype-specific blockade of cocaine-induced weight loss by the protein synthesis inhibitor, anisomycin. Life Sciences 55, PL293-PL299.

Sinha Y. M., Salocks C. B., and Vanderlaan W. P. (1975) Prolactin and growth hormone levels in different inbred strains of mice: patterns in association with estrous cycle, time of day and perphenazine stimulation. Endocrinol. 97, 1112-1122.

Southwick C. H. and Clark L. H. (1966) Aggressive behaviour and exploratory activity in fourteen mouse strains. Am. Zool. 6, 559.

Southwick C. H. and Clark L. H. (1968) Interstrain differences in aggressive behaviour and exploratory activity of inbred mice. Commun. Behav. Biol. Part A 1, 49-59.

Srivastava R. A. K. (1995) Increased apoB100 mRNA in inbred strains of mice by estrogen is caused by decreased RNA editing protein mRNA. Biochemical and Biophysical Research Communications 212, 381-387.

Stasik J. H. (1970) Inheritance of T-maze learning in mice. J. Comp. Physiol. Psychol. 71, 251-257.

Storer J. B. (1966) Longevity and gross pathology at death in 22 inbred strains of mice. J. Gerontol. 21, 404-409.

Storer J. B. (1967) Relation of lifespan to brain weight, body weight and metabolic rate among inbred mouse strains. Exp. Gerontol. 2, 173-182.

Strong L. C. (1952) Differences in response among mice of fifteen inbred strains to the subcutaneous injection of methylcholanthrene. Yale J. Biol. Med. 25, 34-43.

Styrna J., Imai H. T., and Moriwaki K. (1991) An increased level of sperm abnormalities in mice with a partial deletion of the Y chromosome. Genet. Res. 57, 195-199.

Takahashi M., Kleeberger S. R., and Croxton T. L. (1995) Genetic control of susceptibility to ozone-induced changes in mouse tracheal electrophysiology. American Journal of Physiology - Lung Cellular and Molecular Physiology 269, L6-L10.

Tanaka S., Sato M., Taniguchi T., and Yokomizo Y. (1994) Histopathological and morphometrical comparison of granulomatous lesions in BALB/c and C3H/HeJ mice inoculated with Mycobacterium paratuberculosis. J. Comp. Pathol. 110, 381-388.

Tanioka Y. and Esaki K. (1971) Strain differences in mortality of anaphylactic shock in mice-challenging by intravenous injection. Exp. Animals (Japan) 20, 127-130.

Tankersley C. G., Fitzgerald R. S., and Kleeberger S. R. (1994) Differential control of ventilation among inbred strains of mice. American Journal of Physiology - Regulatory Integrative and Comparative Physiology 267, R1371-R1377.

Tankersley C. G., Fitzgerald R. S., Levitt R. C., Mitzner W. A., Ewart S. L., and Kleeberger S. R. (1997) Genetic control of differential baseline breathing pattern. J. Appl. Physiol. 82, 874-881.

Tengbergen W. J. P. R. van E. (1970) Morphological classification of mammary tumours in the mouse. Path. Eur. 5, 260-272.

Tennant J. R. (1965) Susceptibility and resistance to viral leukemogenesis in the mouse. I. Biological definition of the virus. J. Natl. Cancer Inst. 34, 625-632.

Thomas P. E., Hutton J. J., and Taylor B. A. (1973) Genetic relationship between aryl hydrocarbon hydroxylase inducibility and chemical carcinogen induced skin ulceration in mice. Genetics 74, 655-659.

Thompson W. R. (1953) The inheritance of behaviour: behavioural differences in fifteen mouse strains. Can. J. Psychol. 7, 145-155.

Toda S., Kimura M., and Tohya K. (1989) Strain differences in histamine release from mouse peritoneal mast cells induced by compound 48/80 or A23187. Jikken Dobutsu - Experimental Animals 38, 135-137.

Tokunaga Y., Hiramine C., Itoh M., Mukasa A., and Hojo K. (1993) Genetic susceptibility to the induction of murine experimental autoimmune orchitis (EAO) without adjuvant. I. Comparison of pathology, delayed type hypersensitivity, and antibody. Clin. Immunol. Immunopathol. 66, 239-247.

Trune D. R., Kempton J. B., and Mitchell C. (1996) Auditory function in the C3H/HeJ and C3H/HeSnJ mouse strains. Hearing Research 96, 41-45.

Tsubura A., Senzaki H., Oyaizu T., Fujita Y., and Morii S. (1993) Strain differences in neoplastic response to DMBA-induced uterine vascular tumors in mice. International Journal of Oncology 2, 927-930.

Valatx J. L. and Bugat R. (1974) Facteurs gènètiques dans le determinisme du cycle veille-sommeil chez la souris. Brain Res. 69, 315-330.

Vaz N. M., Phillips-Quagliata J. M., Levine B. B., and Vaz E. M. (1971) H-2 linked genetic control of immune responsiveness to ovalbumin and ovomucoid. J. Exp. Med. 134, 1335-1348.

Vesell E. S. (1968) Factors altering the responsiveness of mice to hexobarbital. Pharmacology 1, 81-97.

Vlahakis G., Heston W. E., and Smith G. H. (1970) Strain C3H-AvyfB mice: ninety percent incidence of mammary tumours transmitted by either parent. Science 170, 185-187.

Whitmire C. E., Salerno R. A., Rabstein L. S., Heubner R. J., and Turner H. C. (1971) RNA tumour-virus antigen expression in chemically induced tumours. Virus-genome specified common antigens detected by complement fixation in mouse tumours induced by 3-methylcholanthrene. J. Natl. Cancer Inst. 47, 1255-1265.

Whitmire C. E. and Salerno R. A. (1972) RNA tumour virus antigen and tumour induction by various doses of 3-methylcholanthrene in various strains of mice treated as weanlings. Cancer Res. 32, 1129-1132.

Williams N. M. and Timoney P. J. (1994) Variation in susceptibility of ten mouse strains to infection with a strain of Ehrlichia risticii. J. Comp. Pathol. 110, 137-143.

Williams R. W., Strom R. C., Rice D. S., and Goldowitz D. (1996) Genetic and environmental-control of variation in retinal ganglion-cell number in mice. Journal of Neuroscience 16, 7193-7205.

Xidieh C. F., Singer-Vermes L. M., Calich V. L. G., and Burger E. (1994) Plasma amylase levels as a marker of disease severity in an isogenic murine model of paracoccidioidomycosis. Journal of Medical and Veterinary Mycology 32, 37-45.

Yamamoto Y., Saito H., Setogawa T., and Tomioka H. (1991) Sex differences in host resistance to Mycobacterium marinum infection in mice. Infect. Immun. 59, 4089-4096.

Young C. R., Deacon N. J., Ebringer A., and Davis D. A. L. (1976) Genetic control of the immune response to ferritin in mice. J. Immunogenet. 3, 199-205.

Zarrow M. X., Christenson C. M., and Eleftheriou B. C. (1971) Strain differences in the ovulatory response of immature mice to PMS and to the pheromonal facilitation of PMS-induced ovulation. Biol. Reprod. 4, 52-56.

Zhang L. Y., Levitt R. C., and Kleeberger S. R. (1995) Differential susceptibility to ozone-induced airways hyperreactivity in inbred strains of mice. Experimental Lung Research 21, 503-518.


INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
11/16/2021
MGI 6.17
The Jackson Laboratory