A role for IkappaB kinase 2 in bipolar spindle assembly.
Irelan JT, Murphy TJ, DeJesus PD, Teo H, Xu D, Gomez-Ferreria MA, Zhou Y, Miraglia LJ, Rines DR, Verma IM, Sharp DJ, Tergaonkar V, Chanda SK
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):16940-5
A probability-based approach for the analysis of large-scale RNAi screens.
König R, Chiang CY, Tu BP, Yan SF, DeJesus PD, Romero A, Bergauer T, Orth A, Krueger U, Zhou Y, Chanda SK
Nat Methods. 2007 Oct;4(10):847-9
Systematic identification of cellular signals reactivating Kaposi sarcoma-associated herpesvirus.
Yu F, Harada JN, Brown HJ, Deng H, Song MJ, Wu TT, Kato-Stankiewicz J, Nelson CG, Vieira J, Tamanoi F, Chanda SK, Sun R
PLoS Pathog. 2007 Mar;3(3):e44
High-content screening of functional genomic libraries.
Rines DR, Tu B, Miraglia L, Welch GL, Zhang J, Hull MV, Orth AP, Chanda SK
Methods Enzymol. 2006;414:530-65
Identification of the tyrosine phosphatase PTP-MEG2 as an antagonist of hepatic insulin signaling.
Cho CY, Koo SH, Wang Y, Callaway S, Hedrick S, Mak PA, Orth AP, Peters EC, Saez E, Montminy M, Schultz PG, Chanda SK
Cell Metab. 2006 May;3(5):367-78
View All Publications
Positive Regulation of TRAF6-Dependent Innate Immune Responses by Protein Phosphatase PP1-γ.
Opaluch AM, Schneider M, Chiang CY, Nguyen QT, Maestre AM, Mulder LC, Secundino I, De Jesus PD, König R, Simon V, Nizet V, Macleod G, Varmuza S, Fernandez-Sesma A, Chanda SK
PLoS One. 2014;9(2):e89284
Sumit Chanda's Research Focus
Infectious Diseases, HIV/AIDS, Pandemic Influenza, Inflammatory/Autoimmune Disease, Arthritis, Crohn’s Disease (Colitis), Psoriasis, Scleroderma, Systemic Lupus Erythematosus
Viruses are obligate pathogens, and therefore their survival is dependent upon their ability to exploit host cellular machinery. Concurrently, viruses must also successfully evade immune surveillance mechanisms, including first-line (innate) defense systems. The Chanda lab is interested in unraveling the molecular bases for these complex host-pathogen interactions.
Sumit Chanda's Research Report
We are studying cellular proteins required for both influenza A and retrovirus/HIV infection. Also, we are investigating novel molecules that regulate or respond to Pattern Recognition Receptor (PRR) signaling. Taken together, we aim to elucidate the repertoire of host proteins required for viral infection, and understand the molecular strategies adapted by these viruses as countermeasures to innate immune responses.
To understand these events on a global level, our lab uses a series of systems-level approaches, including genome-wide RNAi, proteomics and protein-protein interaction (PPI) analysis, and high content imaging. These, and other, tools are helping us to build a comprehensive cellular 'roadmap' exploited by these viruses to enable their propagation within a cell. These studies are expected to provide unprecedented insight into the molecular circuitry commandeered by these pathogens to establish infection, and will offer new opportunities for the development of 'next generation' host factor and immune-mediated antivirals.
About Sumit Chanda
Sumit Chanda earned his Ph.D. from Stanford University in 2001, and received his post-doctoral training at the Genomics Institute of the Novartis Research Foundation (GNF). He subsequently transitioned to a Group Leader position, and established his research group in the Division of Cellular Genomics at GNF. In 2007, he joined the Infectious and Inflammatory Disease Center at Sanford-Burnham Medical Research Institute as an Associate Professor. Dr. Chanda also holds an Adjunct Professor appointment at the Salk Institute for Biological Studies, as well as a Visiting Scientist position at the Genomics Institute of the Novartis Research Foundation.
Adjunct Professor, Salk Institute for Biological Sciences
Visiting Scientist, The Genomics Institute of the Novartis Research Foundation
Visiting Scientist, The Scripps Research Institute