Dr Vijay Yadav
Vijay's laboratory uses mouse genetic, genomic, and proteomic approaches to investigate how molecules originating from within, and outside the bone regulate bone remodelling.
Vijay graduated from University of Lucknow with a BSc in Biology in 1997 and went on to complete his MSc in Biochemistry in 1999. He earned his PhD in Molecular Reproductive Physiology from the Indian Institute of Science, Bangalore in 2005.
During his doctoral work, Vijay used rodent, bovine and primate model organisms to explore how pituitary hormones regulate ovarian function during female reproductive cycles. During the course of these studies, he became interested in osteoporosis, a disease that predominantly affects females after ovarian failure. This research led him to his postdoctoral work, trying to identify novel endocrine interactions that regulate bone cell functions, with Gerard Karsenty at Columbia University. During the last few years, Vijay's work has illustrated novel endocrine interactions in the brain and gut that regulate bone mass.
In 2010, Vijay joined the Wellcome Trust Sanger Institute as a Faculty member in the Mouse and Zebrafish Genetics programme.
Selected Publications
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Signaling through the M(3) muscarinic receptor favors bone mass accrual by decreasing sympathetic activity.
Cell metabolism 2010;11;3;231-8
PUBMED: 20197056; PMC: 2832931; DOI: 10.1016/j.cmet.2010.01.005
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Pharmacological inhibition of gut-derived serotonin synthesis is a potential bone anabolic treatment for osteoporosis.
Nature medicine 2010;16;3;308-12
PUBMED: 20139991; PMC: 2836724; DOI: 10.1038/nm.2098
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A serotonin-dependent mechanism explains the leptin regulation of bone mass, appetite, and energy expenditure.
Cell 2009;138;5;976-89
PUBMED: 19737523; PMC: 2768582; DOI: 10.1016/j.cell.2009.06.051
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Dissociation of the neuronal regulation of bone mass and energy metabolism by leptin in vivo.
Proceedings of the National Academy of Sciences of the United States of America 2008;105;51;20529-33
PUBMED: 19074282; PMC: 2629309; DOI: 10.1073/pnas.0808701106
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Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum.
Cell 2008;135;5;825-37
PUBMED: 19041748; PMC: 2614332; DOI: 10.1016/j.cell.2008.09.059
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Dynamic changes in mitogen-activated protein kinase (MAPK) activities in the corpus luteum of the bonnet monkey (Macaca radiata) during development, induced luteolysis, and simulated early pregnancy: a role for p38 MAPK in the regulation of luteal function.
Endocrinology 2006;147;4;2018-27
PUBMED: 16410301; DOI: 10.1210/en.2005-1372
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Prostaglandin F2alpha-mediated activation of apoptotic signaling cascades in the corpus luteum during apoptosis: involvement of caspase-activated DNase.
The Journal of biological chemistry 2005;280;11;10357-67
PUBMED: 15623530; DOI: 10.1074/jbc.M409596200
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Identification of novel genes regulated by LH in the primate corpus luteum: insight into their regulation during the late luteal phase.
Molecular human reproduction 2004;10;9;629-39
PUBMED: 15235106; DOI: 10.1093/molehr/gah089
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Cloning of a buffalo (Bubalus bubalis) prostaglandin F(2alpha) receptor: changes in its expression and concentration in the buffalo cow corpus luteum.
Reproduction (Cambridge, England) 2004;127;6;705-15
PUBMED: 15175507; DOI: 10.1530/rep.1.00107
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Apoptosis during spontaneous and prostaglandin F(2alpha)-induced luteal regression in the buffalo cow (Bubalus bubalis): involvement of mitogen-activated protein kinases.
Biology of reproduction 2002;67;3;752-9
PUBMED: 12193381

