Saranga MV

Parkinson's disease (PD) is the second most prevalent neurodegenerative disease. Neurodegeneration

accompanied with neuroinflammation , protein degradation dysfunction and mitochondrial dysfunction

is commonly associated with the pathogenesis of PD. Although the exact pathogenic mechanism is still

not well understood evidence has suggested the role of impaired ubiquitin/proteasome pathway (UPP),

lysosome pathway and autophagy machinery in α-synuclein accumulation and degeneration of

dopaminergic neurons. The Tripartite Motif (TRIM) family proteins typically have E3 ubiquitin ligase

activities and play crucial roles in the degradation of target proteins. TRIM family proteins are known to

play important role in various cellular processes like autophagy, innate immune response and

inflammation. TRIM proteins having RNA/miRNA binding NHL domain (TRIM2, TRIM3, TRIM32, TRIM 71)

are known to regulate neurons. I am currently interested to understand the role of these TRIM-NHL

proteins in TNF driven neuroinflammatory stress condition in the cellular model and its implication in

mitochondrial dysfunction. This study will provide a better insight into the mitochondrial functions

regulated by TRIM proteins which can modulate neuronal health further.