作者: Randall J. Roper , John S. Griffith , C. Richard Lyttle , R. W. Doerge , Andrew W. McNabb
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摘要: The steroid hormone estradiol (E2) elicits a spectrum of systemic and uterotropic responses in vivo. For example, E2 treatment ovariectomized adult sexually immature rodents leads to uterine leukocytic infiltration, cell proliferation, organ growth. E2-regulated growth is also associated with variety normal pathological phenotypes. Historically, the response has been used as key model understand molecular biochemical mechanisms underlying E2-dependent In this study, genome exclusion mapping identified two quantitative trait loci (QTL) mouse, Est2 Est3 on chromosomes 5 11, respectively, that control phenotypic variation wet weight. Both QTL are linked genes, suggesting they may represent within conserved gene complexes play fundamental roles mediating effects E2. Interaction multiple analyses using leukocyte weight suggest Est4, chromosome 10, encode an interacting factor influences both responses. Our results show can be genetically controlled genetic basis underlie observed many