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Ram P. Chakrabarty on Muck Rack

Ram P. Chakrabarty

As seen in: Nature, Science Magazine
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Articles

Hypoxia-responsive interaction between P-TEFb, BHLHE40, and Tim8-Tim13 regulates hypoxic gene transcription

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By Leticia Pérez-Sisqués, Cindy Reinger, Tianyuan Zheng, Simone De Fabritiis, Marta Iwanaszko, Lawrence Lin, Madhurima Das, Sarah Gold, Grant Andersen, Ram P. Chakrabarty, Navdeep S. Chandel, Ali Shilatifard
| Science Magazine Verified
Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract The P-TEFb transcriptional kinase complex regulates the pause release checkpoint step in transcription by RNA polymerase II (RNAPII). We sought to identify hypoxia-specific interactions that could direct P-TEFb activity to hypoxia-responsive genes.
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Mitochondrial l -2-hydroxyglutarate is a physiological signalling metabolite

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By Ram P. Chakrabarty, Yuki Aoi, Taylor A Poor, Gregory S. McElroy, Karthik Vasan, Shimaa Soliman, Marta Iwanaszko, Rogan A. Grant, Benjamin Howard, Colleen R. Reczek, Anjali Chandel, Michael D. Kahl, Zhaofa Xu, Kathryn A. Helmin, Qiushi Jin, Dongmei Wang, Peng Gao, Jenna Blum, Zachary Sebo, Feng Yue, Shawn M. Davidson, Steven Gygi, Samuel E. Weinberg, Benjamin D. Singer, Seung Hye Han, Ali Shilatifard, Navdeep S. Chandel, Jonathan G. Van Vranken, Yongchao C. Ma
| Nature Verified
Abstract l-2-Hydroxyglutarate (l-2-HG) is a low-abundance metabolite in mammals because the mitochondrial enzyme l-2-HG dehydrogenase (L2HGDH) oxidizes l-2-HG to 2-oxoglutarate (2-OG) to prevent its accumulation1. In humans, a lack of L2HGDH activity leads to l-2-HG accumulation and causes l-2-hydroxyglutaric aciduria2. Thus, l-2-HG is often classified as a toxic metabolite2,3,4,5. However, whether l-2-HG has any physiological function is unclear.
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Metformin inhibits mitochondrial complex I in intestinal epithelium to promote glycaemic control

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By Zachary Sebo, Ram P. Chakrabarty, Rogan A. Grant, Karis B. D’Alessandro, Alec Koss, Jenna Blum, Shawn M. Davidson, Colleen R. Reczek, Navdeep S. Chandel
| Nature Verified
Abstract Metformin is a versatile biguanide drug primarily prescribed for type II diabetes. Despite its extensive use, the mechanisms underlying its clinical effects, including attenuated postprandial glucose excursions and elevated intestinal glucose uptake, remain unclear. Here we map these and other effects of metformin to intestine-specific mitochondrial complex I inhibition.
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