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Murine Inhibin α-Subunit Haploinsufficiency Causes Transient Abnormalities in Prepubertal Testis Development Followed by Adult Testicular Decline.
Endocrinology
June 2015
Priority Research Centres for Reproductive Science (C.I., A.B., J.M., S.E.) and Chemical Biology (C.I.), School of Environmental and Life Sciences, Faculty of Science and Information Technology, University of Newcastle, Callaghan, New South Wales 2308, Australia; Departments of Anatomy and Developmental Biology (H.G., Q.L., K.L.L.) and Biochemistry and Molecular Biology (S.C.M., K.L.L.) and Monash Micro Imaging (A.J.F.), Monash University, Clayton, Victoria 3800, Australia; and Faculty of Medicine, Nursing, and Health Sciences (J.C.G.D.), Department of Medicine, Monash Medical Centre, and Monash Institute of Medical Research-Prince Henry's Institute of Medical Research (M.P.H.), Clayton, Victoria 3168, Australia.
Activin production and signaling must be strictly regulated for normal testis development and function. Inhibins are potent activin inhibitors; mice lacking the inhibin-α gene (Inha-/- mice) cannot make inhibin and consequently have highly elevated activin and FSH serum concentrations and excessive activin signaling, resulting in somatic gonadal tumors and infertility. Dose-dependent effects of activin in testicular biology have been widely reported; hence, we hypothesized that male mice lacking one copy of the Inha gene would produce less inhibin and have an abnormal reproductive phenotype.
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