0000-0003-1443-219X About
Organisms have been my special interest since schooling, and I found it as a best opportunity to learn biological root which causes various issues in human life. I determined to establish my career path in biology by studying of chemistry and bioscience. From the beginning of my graduation level, I become skilled with molecular biology, protein chemistry and structural biology to elucidate the structures of transcription factors in bacteriophage. My PhD thesis was primarily based on determination the structure of bacteriophage P22 C1 protein which is a transcriptional activator of its own gene and it regulates lysis vs lysogeny switch when it infects its host cell E. coli. I was able to co-crystallize the protein along with its cognate DNA and was also become able to determine the structure of this protein partially along with its promoter DNA. Personally, I am highly motivated and hardworking student which in turn made me develop to think and work independently. Although my academic training preliminary based on prokaryotic system, I become interested to understand the pathogenic mechanisms underlying various neurological diseases in human. After the completion of my Ph.D. degree, I joined the Section on Developmental Genetics (SDG) at Eunice Kennedy Shriver National Institute of Child Health and Disease (NICHD), NIH, Bethesda as a Visiting Fellow. My post-doctoral work involves studies to understand the molecular mechanism(s) of a group of childhood neurodegenerative lysosomal storage disorders (LSDs) called neuronal ceroid lipofuscinoses (NCLs), commonly known as Batten disease. Even though mutations in >13 different genes cause various NCLs, at the cellular level, all the NCLs characteristically exhibit similar pathology. Infantile NCL (or INCL) is caused inactivating mutations in the CLN1 gene encoding palmitoyl protein thioesterase1 (PPT1). INCL is a devastating neurodegenerative LSD that has no effective treatment. Understanding the mechanism(s) underlying pathogenesis of these rare diseases may provide a window to unravel the pathogenic mechanism(s) of more common neurodegenerative diseases like Alzheimer’s and Parkinson’s. Since neurodegenerative diseases share some common pathological mechanisms like mitochondrial dysfunctions, oxidative stress, calcium dysregulation, lysosomal storage disorders and by some genetic determinants, I think understanding the relationship of these shared molecular mechanism(s) of pathogenesis of neurodegenerative diseases can develop novel therapeutic strategies and will lead us to a bench-to-bedside clinical trial.
Employment
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International Institute of Innovation and Technology Research Scientist2021 - Present
Education
Education history is unavailable.
Projects & Funding
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