University of Delhi, India, 1988
Genetic approaches to study the physiology of the mouse reproductive axis
Our laboratory studies development and regulation of the reproductive axis using both gain-of-function (transgenic) and loss-of-function (gene knockout) approaches. These unique genetic models mimic many of the human diseases and thus enable us to experimentally tract them both in time and space. Specific projects include unraveling signaling pathways in the hypothalamic medical preoptic area that contributes to male sexual behavior, understanding human pituitary null cell adenoma, mechanisms of secretion of pituitary gonadotropins, and delineating mechanisms of gonadotropin regulation of testis and ovarian development and function. These studies are clinically relevant and have significant impact in understanding the physiology and pathology of the mammalian reproductive axis including abnormal reproductive tract development, infertility, and cancer of the pituitary and gonads.
Iqbal J, Sun L, Kumar TR, Blair HC and Zaidi M (2006). FSH Stimulates TNF production from immune cells: A novel mechanism for hypogonadal bone loss. Proceedings of The National Academy of Sciences (USA), 103: 14925-14930.
Shariff AJ*, Kumar TR*, Eklund, J and Boime I (2006). Single chain triple domain gonadotropin analogs with disulfide bond mutations in the alpha subunit elicit dual FSH and LH activities in vivo. Molecular Endocrinology, 20: 1437-1446. * equal contribution
Sun L, Peng Y, Sharrow AC, Iqbal J, Zhang Z, Papachristou DJ, Zaidi S, Zhu LL, Yaroslavskiy BB, Zhou H, Zallone A, Sairam MR, Kumar TR, et al., (2006). FSH directly regulates bone mass: implications for understanding the pathogenesis of the osteoporosis due to hypogonadism. Cell, 125: 247-260.
Kumar TR, Schuff KG, Nusser KD and Low MJ (2006). Gonadotroph-specific expression of the human follicle-stimulating hormone B gene in transgenic mice. Molecular and Cellular Endocrinology, 247:103-115.
Ma X, Reyna A, Mani SK, Matzuk MM and Kumar TR (2005). Impaired male sexual behavior and reduced NOS activity in the medial pre-optic area in activin receptor II knockout mice. Biology of Reproduction, 73:1182-1190.
Ma X, Dong YL, Matzuk MM and Kumar TR (2004). Targeted mutagenesis of LH b leads to hypogonadism, defects in steroidogenesis and infertility. Proceedings of National Academy of Sciences (USA), 101: 17294-17299.
Garcia-Campayo V, Boime I, Xiaoping Ma, Iken DD and Kumar TR (2004). A tetradomain single chain glycoprotein analog elicits multiple hormone activities in vivo. Biology of Reproduction, 72: 301-308.
Matzuk MM, Hadsell, LA, De Mayo F and Kumar TR (2003). Overexpression of human chorionic gonadotropin in transgenic mice causes multiple reproductive defects. Biology of Reproduction, 338-346.
Kumar TR (2001). Neuroendocrine cell-specific immortalization using transgenic approaches. In: "Transgenics in Endocrinology", Ed: Matzuk MM, Brown CE and Kumar TR, Humana Press, Totowa, NJ, pp: 425-466.
Kumar TR, Graham KE, Asa SL and Low MJ (1998). Simian Virus 40-T Antigen induced gonadotroph adenomas: a model of human null-cell adenomas. Endocrinology, 139: 3342-3351.
Kumar TR, Lu H, Wang Y, and Matzuk MM (1997). Follicle Stimulating hormone is required for ovarian follicle maturation but not male fertility. Nature Genetics,15: 201-204.
Matzuk MM, Kumar TR and Bradley, A (1995). Different phenotypes for mice deficient in either activins or activin receptor type II. Nature, 374: 356-360.
Matzuk MM, Kumar TR, Vassali A, Bickenbach JR, Roop DR, Jaenisch R and Bradley A (1995). Functional analysis of activins in mammalian development. Nature 374:354-356.
Funding: NICHD, NIDDK, Diagnostic Systems Labs, TX.