National Institutes of Health (USA) - 1996 (F169)
Colour and related genotype:
Agouti mouse, A/A - MHC: HaplotypeH2k
Description of our model and application areas
The C3H strain was developed by STRONG in 1920 from a cross of BAGG ALBINO female with DBA male. It was selected for a high incidence of mammary tumours. This sensitivity to mammary tumours is due to an exogenous virus transmitted by the mother’s milk (the Mouse Mammary Tumour Virus – MMTV). In 1930, STRONG sent a colony to ANDERVONT who in turn sent one to HESTON (at generation F35). HESTON stock was then transferred to the NIH in 1951 (generation F51). C3H/HeN mice are used in a wide range of studies. They are homozygous for the Pde6brd1 allele and have an early onset severe retinal degeneration that causes blindness at weaning age.
This strain has a high incidence of hepatoma. Even if MMTV is not present, virgin and breeding females can develop mammary tumours. Despite an atherogenic diet, C3H/HeN mice do not develop aortic atherosclerosis, in contrast to the C57BL/6J. There is a genetically mediated difference between the C3H/HeN and the C3H/HeJ regarding their response to bacterial endotoxin (LPS). This response is linked to the TL4 protein (Toll-like receptor 4; previously lps). C3H/HeN are Tlr4lps-n (toll-like receptor 4; normal LPS response), previously LPSn. This strain will have a normal response to an LPS challenge, it is said to be endotoxin-sensitive. Per contra, the C3H/HeJ strain is Tlr4lps-d, previously LPSn and said to be endotoxin-resistant.
Important: This strain no longer carries MMTV (Mouse Mammary
Main application and research fields
The growth curve represents an average which reflects the weight variation of the strain measured between 21 and 84 days for males and females.
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