Elucidating the repertoire of host proteins required for host-pathogen interaction, as well as cellular control of immune responses.
Dr. Chanda earned his Ph.D. from Stanford University in 2001.
Telomere-independent Rap1 is an IKK adaptor and regulates NF-kappaB-dependent gene expression.
Teo H, Ghosh S, Luesch H, Ghosh A, Wong ET, Malik N, Orth A, de Jesus P, Perry AS, Oliver JD, Tran NL, Speiser LJ, Wong M, Saez E, Schultz P, Chanda SK, Verma IM, Tergaonkar V
Nat Cell Biol. 2010 Aug;12(8):758-67
Human Cep192 is required for mitotic centrosome and spindle assembly.
Gomez-Ferreria MA, Rath U, Buster DW, Chanda SK, Caldwell JS, Rines DR, Sharp DJ
Curr Biol. 2007 Nov 20;17(22):1960-6
B cell terminal differentiation factor XBP-1 induces reactivation of Kaposi's sarcoma-associated herpesvirus.
Yu F, Feng J, Harada JN, Chanda SK, Kenney SC, Sun R
FEBS Lett. 2007 Jul 24;581(18):3485-8
Isolation and characterization of extragenic suppressor mutants of the tolA-876 periplasmic-leaky allele in Escherichia coli K-12.
Amouroux C, Lazzaroni JC, Portalier R
FEMS Microbiol Lett. 1991 Mar 1;62(2-3):305-13
Nucleotide sequence of a hamster cDNA highly homologous to the Xenopus laevis S19 ribosomal protein.
Klein H, Gervais C, Suh M
Nucleic Acids Res. 1990 Jul 11;18(13):3997
A novel replicating agent isolated from the human intestinal tract having characteristics shared with Creutzfeldt-Jakob and related agents.
J Med Microbiol. 1989 Jun;29(2):145-57
Heterotransplantation of malignant human gliomas in neonatal rats.
Tamargo RJ, Epstein JI, Brem H
J Neurosurg. 1988 Dec;69(6):928-33
[Epidemiology and development of chronic renal insufficiency].
Coevoet B, Goubet JM, Brasseur J, Demontis R
Presse Med. 1988 Apr 2;17(12):593
[Butylhydroxytoluene inhibition of the mutagenic activity of carcinogenic nitroso compounds and cyclophosphamide: the role of the glutathione conjugation reaction].
Kalinina EV, Loknitskaia NN, Shuliakovskaia TS, Fonshteĭn LM
Vopr Onkol. 1987;33(9):59-63
Typing of Pseudomonas aeruginosa on the basis of low and high molecular weight aeruginocins.
Pai SR, Joshi LM
J Postgrad Med. 1985 Jan;31(1):52-6
A comparative evaluation of induced hypotension with spinal block and with halothane-d-tubocurarine combination.
J Indian Med Assoc. 1979 Dec 1;73(11):185-7
[In memoriam Leonid Semenovich Persianinov].
Akush Ginekol (Mosk). 1979 Mar;(3):61-2
On the activities in a continuous neural network.
Biol Cybern. 1975;18(1):41-8
Nursing care of babies with cleft lip and palate. 4. The immediate pre- and postoperative nursing care.
Wood BG, Kevill GA
Nurs Times. 1970 Nov 19;66(47):1490-3
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BIRC2/cIAP1 Is a Negative Regulator of HIV-1 Transcription and Can Be Targeted by Smac Mimetics to Promote Reversal of Viral Latency.
Pache L, Dutra MS, Spivak AM, Marlett JM, Murry JP, Hwang Y, Maestre AM, Manganaro L, Vamos M, Teriete P, Martins LJ, König R, Simon V, Bosque A, Fernandez-Sesma A, Cosford ND, Bushman FD, Young JA, Planelles V, Chanda SK
Cell Host Microbe. 2015 Sep 9;18(3):345-53
Sumit Chanda's Research Focus
Infectious Diseases, HIV/AIDS, Pandemic Influenza, Inflammatory/Autoimmune Disease, Arthritis, Crohn’s Disease (Colitis), Psoriasis, Scleroderma, Systemic Lupus Erythematosus, Cancer
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, which will not only provide insight into viral pathogenesis, but key regulators of inflammation and innate immunity in cancer.
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