of Mice: 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:
Strong to Bittner 1931, to Kirschbaum 1952. Has 83% mammary tumours in
unfostered breeders. Low leukaemia.
Origin not known, but has a very high incidence of lymphatic leukaemia
(over 90%) (Fuchs, 1962
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
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
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,
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.
`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
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 )
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.
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)
), 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,
). 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,
). A high proportion of the mammary tumours are of the acinar
type (2/7) (Tengbergen, 1970
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
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).
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
High serum cholesterol (1/5) (Bruell et al.,
., 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
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,
). 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
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).
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).
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
). 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
). 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,
Large brain weight (15/18 male, 17/18 female) (Storer,
1967). Small brain/body weight ratio (19/20) (Roderick et al., 1973., 1973).
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
to induction of subcutaneous tumours by 3-methylcholanthrene (1/14 to
4/14, depending on substrain) (Kouri et al.,
., 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)
). 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
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,
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,
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
lipopolysaccharide (Di Pauli, 1972
). Responder to
synthetic polypeptide Glu57
(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)
). 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). Refractory to sensitising effects of HSF from Bordetella
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).
Resistant to infection by Salmonella typhimurium
strain C5 (5/7)
(Plant and Glynn, 1974
), Susceptible to
et al., 1972
., 1972). Experimental Mycoplasma pulmonis
results in acute pneumonia with severe hemorrhage, edema and often death
(Faulkner et al, 1995
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,
). 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).
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
to LCM virus infection (1/5) (Oldstone and
). Resistant to induction of diabetes mellitus by encephalomyocarditis
virus (cf. 7/14) (Boucher et al., 1975
1975). Susceptible to lethal infection with Rickettsia akari
Kaplan, in contrast with seven other substrains of C3H and 24 other strains
(Anderson and Osterman 1980a
mammary tumor proviral loci have been identified by Lee and Eicher (1990
). High immunological response to Salmonella
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).
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.,
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
High reproductive performance (1/8). Litter size 6.4 + 0.2, sterility
4% (Nagasawa et al., 1973., 1973).
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).
Recommended host for transplantable hepatoma H4 (Kaliss, 1972). High incidence
of spontaneous `deviants' (5/21) (Schlager
and Dickie, 1967).
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.
D. L. and Sundberg J. P. (1991) "Lipomatous" hamartomas and choristomas
in inbred laboratory mice. Vet. Pathol. 28, 305-312.
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.
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,
G. W. and Osterman J. V. (1980a) Host defenses in experimental rickettsialpox:
genetics of natural resistance to infection. Infect. Immun. 28,
R., Mahin D. T., Farris R. D., and Woodward K. T. (1967) Heritability
of plasma cholinesterase activity in inbred mouse strains. Science
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.
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.
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.
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,
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.
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.
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.
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.
P. S., Jordan T. W., and Mackay I. R. (1990) Mouse strain differences
in susceptibility to sporidesmin-induced biliary tract injury. Liver
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.
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-Nitti F., and Oliverio A. (1966) Effects of nicotine on avoidance
conditioning of inbred strains of mice. Psychopharmacologia 10,
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.
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.
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
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.
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.
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.
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,
K. (1959a) Necrotizing arteritis in strain BL/De mice. Lab. Invest.
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.
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.
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,
Erickson R. P.
(1976) Strain variation in spermatazoal -glucuronidase in mice. Genet.
Res. 28, 139-145.
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
Fahey J. L. (1965) Differences
in the electrophoretic mobility of antibody from inbred strains of mice.
J. Immunol. 94, 819-823.
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.
P. F. and Dowling M. T. (1953) Studies on obesity. I. Nutritional obesity
in mice. J. Nutrit. 49, 319-331.
G., Yunis E. J., and Good R. A. (1973) Reproductive deficiency of NZB
male mice. Possibility of a viral basis. Lab. Invest. 29,
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
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.
M. G., Abrams G. D., and Murphy W. H. (1972) Lethal toxicity of Mycoplasma
fermentens in mice. J. Infect. Dis. 125, 153-160.
S., Currie J. A., and Tully J. G. (1965) Factors affecting formation of
incomplete Vi antibody in mice. J. Bacteriol. 90, 635-642.
M. K. and Festing M. F. W. (1976) Brain glutamic acid decarboxylase and
open field activity in ten inbred strains of mice. Brain Res.
D. L. and Silvers W. K. (1971) Genetic basis of male skin rejection in
mice. Transplant. 12, 412-414.
C., Azar C. A., and Maren T. H. (1973) Strain differences in susceptibility
to the teratogenic effect of acetazolamide in mice. Teratology
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.
W. C., Nep R. L., and Arfin S. M. (1974) Genetic variation in histidine
ammonia-lyase activity in the mouse. Biochem. Biophys. Res. Comm.
C. T., Judge F. J., and Whitney R. A. (1973) Catalog of NIH rodents.
National Institutes of Health. DHEW publication (NIH) 74-606, Bethesda.
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
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,
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.
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.
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.
D. (1970) Genetic influences on the behaviour of mice can be obscured
by laboratory rearing. J. Comp. Physiol. Psychol. 72,
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,
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.
Hoag W. G. (1963) Spontaneous
cancer in mice. Ann. NY Acad. Sci. 108, 805-831.
H. A. and Rechcigl M. Jr. (1971) Erythrocyte catalase in inbred mice.
Enzyme 12, 219-225.
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.
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.
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.
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.
A. P., Tuffrey M., and Taylor-Robinson D. (1989) Resistance of mice to
genital infection with Neisseria gonorrhoeae. J. Med. Microbiol.
I., Nakamura O., and Tai T. (1992) Antibody responses to ganglio-series
gangliosides in different strains of inbred mice. Molecular Immunology
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
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
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,
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.
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.
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.
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.
J. and Kellog F. (1967) Hyaline-membrane formation and pulmonary plasminogen-activator
activity in various strains of mice. Pediatrics 39, 75-81.
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.
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.
J., Stitzel J. A., and Collins A. C. (1989) Genetic influences on nicotine
responses. Pharmacol. Biochem. Behav. 33, 667-678.
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,
J. E. and Reiner S. L. (1995) T helper phenotype and genetic susceptibility
in experimental lyme disease. Journal Of Experimental Medicine
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.
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.
A. and Tait A. (1969) Cytoplasmic isocitrate dehydrogenase variation within
the C3H inbred strain. Genet. Res. 14, 93.
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.
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.
W. S. and Little C. C. (1967) Genetic studies of carcinogenesis in mice.
J. Natl. Cancer Inst. 38, 639-656.
H., Miyamoto M., and Fujimoto M. (1973) Reproductivity in inbred strains
of mice and project for their efficient production. Exp. Animals (Japan)
Nagy Z. M.
and Misanin J. R. (1970) Visual perception in the retinal degenerate C3H
mouse. J. Comp. Physiol. Psychol. 72, 306-310.
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.
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.
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.
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.
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.
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.
S., Smith F. O., Bernstein I. D., and Ochs H. D. (1993) Strain-dependent
leakiness of mice with severe combined immune deficiency. J. Immunol.
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,
M. B. A. and Dixon F. J. (1968) Susceptibility of different mouse strains
to lymphocytic choriomeningitis virus. J. Immunol. 100,
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.
A. C., Gelderman A. H., Ragland R. H., and Hoffman H. A. (1967) Haptoglobin
levels in serum of various strains of mice. Science 158,
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.
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.
and Glynn A. A. (1974) Natural resistance to Salmonella infection, delayed
hypersensitivity and Ir genes in different strains of mice. Nature
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.
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.
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.
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.
S. F., Marks M. J., and Collins A. C. (1996) Inbred mouse strains vary
in oral self-selection of nicotine. Psychopharmacology 124,
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.
D. L. and Glode L. M. (1975) Differences in cell nitrogen responsiveness
between closely related strains of mice. J. Immunol. 115,
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.
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.
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.
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
G. and Dickie M. M. (1967) Spontaneous mutations and mutation rates in
the house mouse. Genetics 57, 319-330.
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.
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.
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.
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,
K., Saito T., and Marley R. J. (1994) Genotype-specific blockade of cocaine-induced
weight loss by the protein synthesis inhibitor, anisomycin. Life Sciences
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.
C. H. and Clark L. H. (1966) Aggressive behaviour and exploratory activity
in fourteen mouse strains. Am. Zool. 6, 559.
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.
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.
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,
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.
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,
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.
Y. and Esaki K. (1971) Strain differences in mortality of anaphylactic
shock in mice-challenging by intravenous injection. Exp. Animals (Japan)
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.
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.
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,
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.
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.
R., Kempton J. B., and Mitchell C. (1996) Auditory function in the C3H/HeJ
and C3H/HeSnJ mouse strains. Hearing Research 96, 41-45.
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.
J. L. and Bugat R. (1974) Facteurs gènètiques dans le determinisme
du cycle veille-sommeil chez la souris. Brain Res. 69,
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.
Vesell E. S. (1968)
Factors altering the responsiveness of mice to hexobarbital. Pharmacology
G., Heston W. E., and Smith G. H. (1970) Strain C3H-AvyfB mice: ninety
percent incidence of mammary tumours transmitted by either parent. Science
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.
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.
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.
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
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
Y., Saito H., Setogawa T., and Tomioka H. (1991) Sex differences in host
resistance to Mycobacterium marinum infection in mice. Infect. Immun.
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,
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,
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
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,