Biography & Research:
Human genome is constantly damaged due to intrinsic and extrinsic genotoxic agents that contribute towards oxidative DNA base damages. These oxidative DNA base lesions often mutagenic and toxic, and are repaired via the base excision repair pathway (BER) in which the abasic (AP) endonuclease, APE1, a multifunctional essential protein, plays a central role. APE1 also functions as a transcriptional co-regulator reductively activating several transcription factors (TFs, e.g., AP-l, NF-kB, and named Ref-1). Amyloid beta (Aβ) protein deposition in Alzheimer's disease (AD) brain induces oxidative damage in neuronal genomes causing their death. The neuroprotective role played by APE1, i.e. the mechanism(s) by which it counters the Aβ-induced oxidative damages is/are poorly understood. Elucidating the molecular mechanisms associated with AD is our lab’s current focus.