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Research:

DNA Polymerase Theta – Structure function studies and designing novel inhibitors

Cancer cells undergo increased rate of DNA damage due to endogenous stress and exogenous therapeutic agents compared to normal cells. Cancer cells also evolve multiple mechanisms for repairing damaged DNA such as overexpression of several DNA damage repair pathway proteins or utilizing alternate salvage pathways for their survival. Therefore, inhibiting DNA damage repair pathway proteins specifically could be a potential way to eliminate cancer cells. Polymerase Theta (POLQ), is one of the DNA damage repair proteins which participates in Base Excision Repair, VDJ recombination and mainly in MMEJ. Polymerase theta belongs to the family of polymerases, encoded by POLQ gene. Pol theta plays a role in the repair of DSBs via alternative end joining. Also, Pol theta controls the frequency of chromosomal translocations thereby maintaining the genome integrity. It is also known to play a backup role in base excision repair. Pol theta up regulation is strongly correlated with poor clinical outcomes in breast, ovarian, colon and lung cancers. We have initiated structural and functional studies on Pol theta with the aim of characterizing this enzyme and designing novel inhibitors against it.

 

Structural Studies on Actin from Leishmania donovani

Leishmania belongs to the trypanosomatidae family and causes several human diseases including life threatening visceral leishmaniasis. Actin from Leishmania (LdACT) is unique compared to other eukaryotic actinsin terms of its filament forming, toxin and DNase-1-binding properties, in DNA binding and DNA nicking and topoisomerase II regulation properties. We have initiated structural studies on LdACT to understand the structural basis for the unconventional properties of this protein. Detailed structural understanding of LdACT will also help in designing novel anti-leishmanial drugs.