Vinay TERGAONKAR

NFkB Signaling in Human Ailments
 

SUMMARY
Vinay Tergaonkar is a senior Principal Investigator and Research Director at the Cancer Signalling & Therapy (CST) Division at the Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR).

Vinay obtained his PhD in 2001. During his graduate studies he was awarded an international cancer society (UICC) fellowship for collaborative research at Tufts University, Boston, USA. He has been a Fellow (2001-2004) and a Special Fellow (2004-present) of the Leukemia and Lymphoma Society of America and conducted his postdoctoral studies at the Salk Institute for Biological Studies, La Jolla, California. He joined IMCB in late 2005 as Principal Investigator and became a Senior Principal Investigator in 2010 and Research Director in 2015. 

Vinay’s research interests are in cancer cell signalling & biology, genomics, non-coding RNAs, novel anti-cancer strategies, oncology drug development, small molecules, peptide/siRNA therapeutics, patient derived xenografts and orphan disease models.

Vinay has been invited to speak at various international venues and meetings such as the Barossa and Hunter valley meetings in Australia, Genes and Cancer meeting in UK, The Argentine Pharmacological society meeting in Buenos Aires, Aichi and Japanese Cancer Society meetings in Japan and the Keystone Symposia. 

In addition, Vinay serves on a number of Editorial Boards, including Science Advances, Molecular and Cellular Biology (American Society for Microbiology), and Biochemical Journal (Portland Press). 

RESEARCH

NFkB Signaling in Human Ailments
Inflammation involving the innate and adaptive immune systems is a normal response to infection. However, it is now known that when allowed to continue unchecked, chronic inflammation is a key underlying cause for the development of autoimmune disorders, neurodegenerative diseases, metabolic syndromes such as diabetes and cancer. Our lab studies a transcription factor called NFkB which is a master regulator of inflammation. Indeed deregulated activity of NFkB precedes and is causally linked to chronic inflammation and the development of several human ailments including metabolic syndromes and cancers. However, given that NFkB signaling is also essential for many housekeeping cellular and developmental events in normal human beings, simply blocking NFkB B to curb inflammation is not an option. Hence deciphering the regulation of NFkB signaling is crucial to understanding the mechanism and role of uncontrolled/unwanted NFkB activity seen in human ailments and in developing better and safer anti-inflammatory drug. We are focusing and our efforts to identify targets that will help develop drugs which will block NFkB /inflammation more selectively and not generically and hence may have less side effects.


PUBLICATIONS