Associate Professor

The major focus of our lab is to understand the molecular mechanisms that lead to cellular transformation, ultimately leading to cancer. We predominantly study the role of various protein kinases and phosphatases that regulate cellular processes like cell cycle/ mitosis and promote tumorigenesis. We have been using the small T antigen of Polyoma virus as a model to study the impact of such 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. Using inducible small T expression system as a tool, we have already screened library of protein kinases to identify the ones that enable mitotically arrested cells to overcome cell death, and hence promote resistance. This system thus provides an excellent model to understand how cancer cells develop resistance against anti-mitotic and anti-cancer agents that are used for the treatment of cancer. Some of the prominent candidates that we are studying are Mastl/Greatwall kinase, FAK/PTK2, PCTAIRE1/CDK16, PLK1, DBC1/CCAR2, UNC5B, lipin1 and protein phosphatase 2A (PP2A). 

Faculty Details

  • Email shaida.andrabi@uok.edu.in
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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. https://doi.org/10.1007/s12079 {ISSN: 1873-961X} Impact Factor= 5.9