I'm a molecular cell biologist, currently (May, 2019 - present) investigating the effect of macromolecular crowding in health and disease. In my doctoral research (2014 - 2019), I developed a tool "Transcription Factor - Fluorescence Recovery After Photobleaching (TF-FRAP)" to quantify transcription factor dynamics and activity. I also worked as a Junior Research Fellow at the Centre for Cellular and Molecular Biology (CCMB), Hyderabad, India. Where, I investigated trailing edge vesicles in osteoblast cells. I hold a master's degree in Molecular Biosciences from Bishop Heber College (Bharathidasan University), Trichy, India.
Osteoarthritis (OA) is a cartilage degenerative disease and millions are suffering worldwide. Cartilage degeneration is the result of imbalance between anabolic and catabolic processes. In addition to that, increased expression of proteolytic enzymes such as matrix metalloproteinases and aggrecanases also play an important role in the onset of the disease. Treating OA is limited to symptomatic treatments as drugs curing OA is not yet developed as our current understanding about molecular mechanisms involved in this disease progression is not yet fully explored.
Understanding the switching mechanism between hypertrophic cartilage and permanent cartilage will give new insights in to therapeutic possibilities in the cartilage disease. SOX9 and RUNX2 are the master transcription factors for the cartilage and bone development respectively and and their dysfunction is often detected in osteoarthritis (OA). My reasearch is focus on the differential regulation of these transcription factors during chondrocyte development, homeostasis and cartilage disease. To study their activity, we apply biophysical techniques, such as Transcription Factor - Fluorescence Recovery After Photobleaching (TF-FRAP), and measure the dynamics of these transcription factors in human primary chondrocytes and mesenchymal stem cells. To further understand the role of SOX9 in OA pathophysiology, we study their activity in response to extracellular stimuli.