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It is the most widely used "genetic background" for genetically modified mice for use as models of human disease. They are the most widely used and best-selling mouse strain due to the availability of congenic strains, easy breeding, and robustness. [1] The median lifespan of C57BL/6 mice is 27–29 months and the maximum lifespan is about 36 ...
MHC-based sexual selection is known to involve olfactory mechanisms in such vertebrate taxa as fish, mice, humans, primates, birds, and reptiles. [1] At its simplest level, humans have long been acquainted with the sense of olfaction for its use in determining the pleasantness or the unpleasantness of one's resources, food, etc.
In humans, the MHC gene cluster is divided into three regions: classes I, II, and III. The A, B and C genes belong to MHC class I, whereas the six D genes belong to class II. MHC alleles are expressed in codominant fashion. [60] This means the alleles (variants) inherited from both parents are expressed equally:
Despite superficial differences, especially in size and weight, the mouse brain and its function can serve as a powerful animal model for study of human brain diseases or mental disorders (see e.g. Reeler, Chakragati mouse). This is because the genes responsible for building and operating both mouse and human brain are 90% identical. [4]
Unlike most laboratory mouse strains, the C57BL/6 drinks alcoholic beverages voluntarily. It is more susceptible than average to morphine addiction, atherosclerosis, and age-related hearing loss. [11] When compared directly to BALB/c mice, C57BL/6 mice also express both a robust response to social rewards [43] [44] and empathy. [45]
The discovery of the MHC and role of histocompatibility in transplantation was a combined effort of many scientists in the 20th century. A genetic basis for transplantation rejection was proposed in a 1914 Nature paper by C.C. Little and Ernest Tyyzer, which showed that tumors transplanted between genetically identical mice grew normally, but tumors transplanted between non-identical mice were ...
Peptides that fail to bind MHC class I molecules in the lumen of the endoplasmic reticulum (ER) are removed from the ER via the sec61 channel into the cytosol, [16] [17] where they might undergo further trimming in size, and might be translocated by TAP back into ER for binding to a MHC class I molecule.
Non-classical MHC class I genes are very often located on the same chromosome (mice chromosome 17, human chromosome 6) and interspaced within the same loci as the classical MHC genes. MR1 is located on another chromosome, the detailed gene analysis revealed that MR1 is a paralog originated by duplication of MHC locus on chromosome 17 (mice).