Assistant Professor

The major focus of our lab is to understand the molecular mechanisms that lead to cellular transformation, ultimately leading to cancer. We study the role of various oncogenes and tumor suppressors that regulate cell cycle progression, particularly during mitosis. We are looking at the impact of various proteins that affect the regulation of spindle assembly checkpoint (SAC) during mitosis. We have been predominantly using the small T antigen of Polyoma virus as a model to study the impact of these proteins on mitotic regulation. Expression of small T antigen is known to cause major mitotic abnormalities in mammalian cells like abnormal spindles, lack of chromosomal congression, aneuploidy etc, which lead to mitotic arrest, followed by apoptosis in mammalian cells. We use various genetic, biochemical, molecular and cell biology approaches to identify the cellular proteins that allow the “abnormal cells” to repair such anomalies and overcome apoptosis. These approaches will possibly help us understand the role of such proteins in enabling cancer cells to overcome cell death induced by internal cellular signaling as well as by anticancer drugs and develop resistance against them. Some of the prominent candidates that we are studying are Mastl, DBC1, UNC5B, and lipin1. In addition, our lab also studies the role of kinases and phosphatases in the regulation of cell division (particularly mitosis), apoptosis/ cell survival and resistance against cell death during tumorigenesis.

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Research Papers Published

  • "Polyomavirus small T antigen interacts with yes-associated protein to regulate cell survival and differentiation." Journal of Virology, 88(20): 12055 -12064 {ISSN: 0022-538X} Impact Factor= 4.65
  • "Polyoma small T antigen triggers cell death via mitotic catastrophe" Oncogene, 10(192): 1038 -1048 {ISSN: ISSN: 0950} Impact Factor= 8.65
  • "Polyoma Small T Antigen Induces Apoptosis In Mammalian Cells Through UNC5B Pathway In A PP2A Dependent Manner" Journal of virology, 194(14): DOI No. 10.1128/JVI.02187-19 {ISSN: 0022-538X} Impact Factor= 4.3
  • "AKT Regulates Mitotic Progression of Mammalian Cells by Phosphorylating MASTL, Leading to Protein Phosphatase 2A Inactivation" Molecular and Cellular Biology, 40(10): DOI No. 10.1128/MCB.00366-18 {ISSN: 0270-7306} Impact Factor= 3.5
  • "PCTAIRE1 promotes mitotic progression and resistance against antimitotic and apoptotic signals" Journal of Cell Science, 135(3): 258831 - {ISSN: 0021-9533} Impact Factor= 5.28
  • "Interaction of DBC1 with polyoma small T antigen promotes its degradation and negatively regulates tumorigenesis" Journal of Biological Chemistry, 298(2): 101496 - {ISSN: 0021-9258} Impact Factor= 5.15
  • "PCTAIRE promotes mitotic progression and survival of cancer cells against apoptotic signals" Journal of Cell Science, 135(3): DOI No. jcs258831 {ISSN: 1477-9137} Impact Factor= 5.2
  • "Polyoma Small T antigen promotes DBC1 protein degradation to antagonize AKT signaling via activation of LKB1." Journal of Biological Chemistry, 298(2): DOI No. 101496 {ISSN: 1083-351X} Impact Factor= 5.48
  • "Lipin-1 stability and its adipogenesis functions are regulated in contrasting ways by AKT1 and LKB1" Journal of Cell Communications and Signaling, 16(3): DOI No. {ISSN: 1873-961X} Impact Factor= 5.9


DepartmentSubjectCourse TaughtSemester
Bio-ChemistryMScCell Biology1
Bio-ChemistryMScMolecular Biology2
Bio-ChemistryMScMolecular Biology2
Bio-ChemistryMScSignal Transduction4