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.
Wu L, Zhao Z, Shin YJ, Yin Y, Raju A, Vaiyapuri TS, Idzham K, Son M, Lee Y, Sa JK, Chua JYH, Unal B, Zhai Y, Fan W, Huang L, Hu H, Gunaratne J, Nam DH, Jiang T, Tergaonkar V. (2024). Tumour microenvironment programming by an RNA-RNA-binding protein complex creates a druggable vulnerability in IDH-wild-type glioblastoma.; Nature Cell Biology
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A*STAR, IMCB
Institute of Molecular and Cell Biology
61 Biopolis Dr, Singapore 138673
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inquiry@tergaonkar-lab.com