Malabika Dutta
Scientist-G |
Decision Unit 5: Functional Biology
Professor |
Academy of Scientific and Innovative Research
Her research focuses on understanding the mechanistic biology underlying obesity, insulin resistance, diabetes, and associated complications. This includes studying non-coding RNA signatures, inter-organellar crosstalk during cell death, and delayed wound healing in diabetes.
Specific Interests
- Role of non-coding RNAs in cellular dysfunction during diabetes
- Impact of reduced Dicer levels on delayed wound healing
- Epigenetic regulation of miRNA machinery
Altered levels of non-coding RNAs such as miR-22, miR-107, and lncRNA H19 regulate key cellular processes in the liver during diabetes. Modulating these RNAs in vivo has been shown to reverse diabetic phenotypes, while their dysregulation in normal models can induce diabetic-like conditions.
Selected Publications
All Citations →- LncRNA H19 inhibition impairs endoplasmic reticulum-mitochondria contact in hepatic cells and augments gluconeogenesis by increasing VDAC1 levels. Nandwani A, Rathore S, Datta M. Redox Biol. 2023 Dec 9;69:102989.
- mir-98-5p regulates gluconeogenesis and lipogenesis by targeting PPP1R15B in hepatocytes. Khan R, Verma AK, Datta M. J Cell Commun Signal. 2023 Sep;17(3):881-895.
- H19 inhibition increases HDAC6 and regulates IRS1 levels and insulin signaling in the skeletal muscle during diabetes. Kumar A, Datta M. Mol Med. 2022 Jul 16;28(1):81.
- GRP75 mediates endoplasmic reticulum-mitochondria coupling during palmitate-induced pancreatic β-cell apoptosis. Tiwary S, Nandwani A, Khan R, Datta M. J Biol Chem. 2021 Dec;297(6):101368.
- RNA sequencing reveals potential interacting networks between the altered transcriptome and ncRNome in the skeletal muscle of diabetic mice. Kesharwani D, Kumar A, Poojary M, Scaria V, Datta M. Biosci Rep. 2021 Jul 30;41(7):BSR20210495.