Ramakrishnan Shyam Kumar
Birla Institute of Technology and Science, Pilani, SASTRA University, Bharathiar University
About
I am a doctoral researcher in BITS Pilani, working in epigenetics and endothelial biology, where I delve into the molecular underpinnings of vascular health and diseases. Our research focuses on Histone and RNA modifications that shape endothelial cell behavior during homeostasis and pathological conditions. We use various high-throughput molecular biology techniques, In vitro and In vivo models, and basic bioinformatics tools to validate our findings. I believe by combining insights from epigenetics and epitranscriptomics, we can uncover innovative biomarkers and therapeutic targets for endothelial dysfunction. These findings may lead to the development of RNA-based diagnostics and precision medicine strategies addressing prevention and treatment.
Employment
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Birla Institute of Technology and Science, Pilani DST-INSPIRE Fellow2021 - Present
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Birla Institute of Technology and Science, Pilani DBT-JRF2021 - 2022
Education
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SASTRA University M.Sc. Molecular Genetics2017 - 2019
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Bharathiar University B.Sc. Microbiology with Nanotechnology2014 - 2017
Projects & Funding
Projects & funding information is unavailable.
Publications (7)
- YTHDF proteins differentially regulate a subset of m6A-modified transcripts to restrain endothelial inflammation during homeostasis Save
- Histone H4K5 deacetylation by enhanced HDAC1 expression drives endothelial inflammation in diabetes through repression of the KLF2-eNOS axis Save
- Binuclear iridium( <scp>iii</scp> ) chloro-bridged complex as a selective luminescent probe for human serum albumin: sensing studies in rat and human urine Save
- Regulation of shelterin proteins TERF2IP and TRF2 by the MLL2-H3K4me3-p65 axis drives hyperglycemia-dependent endothelial senescence Save
- S-nitrosylation of EZH2 alters PRC2 assembly, methyltransferase activity, and EZH2 stability to maintain endothelial homeostasis Save
- Elevated H3K4me3 Through MLL2-WDR82 upon Hyperglycemia Causes Jagged Ligand Dependent Notch Activation to Interplay with Differentiation State of Endothelial Cells Save
- Intermittent High Glucose Elevates Nuclear Localization of EZH2 to Cause H3K27me3-Dependent Repression of KLF2 Leading to Endothelial Inflammation Save