- Genetic and Pathophysiological Basis of Cardiac and Skeletal Muscle Laminopathies. Genes (Basel) doi: 10.3390/genes15081095. 2024
- Automated assessment of cardiac dynamics in aging and dilated cardiomyopathy Drosophila models using machine learning. Communications Biology volume 7, Article number: 702 (2024)
- Diurnal expression of Dgat2 induced by time-restricted feeding maintains cardiac health in the Drosophila model of circadian disruption. Aging Cell. doi: 10.1111/acel.14169. 2024
- O-GlcNAc transferase regulates collagen deposition and fibrosis resolution in idiopathic pulmonary fibrosis. Front. Immunol. doi:10.3389/fimmu.2024
- Time-restricted feeding regulates lipid metabolism under metabolic challenges. Bioessays. doi: 10.1002/bies.202300157. 2023
- Time-restricted feeding promotes muscle function through purine cycle and AMPK signaling in Drosophila obesity models. Nat Commun. 14:949. 2023
- Mitochondrial epigenetic modifications and nuclear-mitochondrial communication: A new dimension towards understanding and attenuating the pathogenesis in women with PCOS. Rev Endocr Metab Disord. doi: 10.1007/s11154-023-09789-2. 2023.
- Circadian-mediated regulation of cardiometabolic disorders and aging with time-restricted feeding. Obesity. Suppl 1:40-49. 2023
- A skeletal muscle-centric view on time-restricted feeding and obesity under various metabolic challenges in humans and animals. Int J Mol Sci. 24:422. 2022
- Time-restricted feeding restores muscle function in Drosophila models of obesity and circadian-rhythm disruption. Nat Commun. 10, 2700. 2019
- Time-Restricted Eating to Prevent and Manage Chronic Metabolic Diseases. Annual Review of Nutrition. 39:291-315. 2019
- Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling. Human Molecular Genetics. 28:351-371. 2019
- Increasing autophagy and blocking Nrf2 suppress laminopathy-induced age-dependent cardiac dysfunction and shortened lifespan. Aging Cell. 17:e12747-e12747. 2018
- Prolonged cross-bridge binding triggers muscle dysfunction in a Drosophila model of myosin-based hypertrophic cardiomyopathy. eLife. 7. 2018
- TRiC/CCT chaperonins are essential for maintaining myofibril organization, cardiac physiological rhythm, and lifespan. FEBS Letters. 591:3447-3458. 2017
- Time-restricted feeding for prevention and treatment of cardiometabolic disorders. J Physiol, 595: 3691-3700. 2017
- A Drosophila model of dominant inclusion body myopathy 3 shows diminished myosin kinetics that reduce muscle power and yield myofibrillar defects. Dis Model Mech, 10(6): 761–771. 2017
- A Restrictive Cardiomyopathy Mutation in an Invariant Proline at the Myosin Head/Rod Junction Enhances Head Flexibility and Function, Yielding Muscle Defects in Drosophila. Journal of Molecular Biology. 428:2446-2461. 2016
- Using Drosophila as an integrated model to study mild repetitive traumatic brain injury. Scientific Reports. 6. 2016
- Huntington’s Disease-Induced Cardiac Disorders Affect Multiple Cellular Pathways. Reactive Oxygen Species, 2(5), 325–338. 2016
- The Relay/Converter Interface Influences Hydrolysis of ATP by Skeletal Muscle Myosin II. Journal of Biological Chemistry. 291:1763-1773. 2016
- A Failure to Communicate. Journal of Biological Chemistry. 290:29270-29280. 2015
- Time-restricted feeding attenuates age-related cardiac decline in Drosophila. Science. 347:1265-1269. 2015
- Mapping Interactions between Myosin Relay and Converter Domains That Power Muscle Function. Journal of Biological Chemistry. 289:12779-12790. 2014
- Drosophila as a potential model to ameliorate mutant Huntington-mediated cardiac amyloidosis. Rare Diseases. 2:e968003-e968003. 2014
- The UNC-45 Myosin Chaperone. International Review of Cell and Molecular Biology. 103-144. 2014
- Huntington’s Disease Induced Cardiac Amyloidosis Is Reversed by Modulating Protein Folding and Oxidative Stress Pathways in the Drosophila Heart. PLoS Genetics. 9:e1004024-e1004024. 2013
- Expression of the inclusion body myopathy 3 mutation in Drosophila depresses myosin function and stability and recapitulates muscle inclusions and weakness. Molecular Biology of the Cell. 23:11, 2057-2065. 2012
- Interaction of oxidized chaperonin GroEL with an unfolded protein at low temperatures. Biosci Rep 1. 32 (3): 299–303. 2012
- Alternative Relay and Converter Domains Tune Native Muscle Myosin Isoform Function in Drosophila. Journal of Molecular Biology. 416:543-557. 2012
- Transgenic expression and purification of myosin isoforms using the Drosophila melanogaster indirect flight muscle system. Methods. 56:25-32. 2012
- Two Drosophila Myosin Transducer Mutants with Distinct Cardiomyopathies Have Divergent ADP and Actin Affinities. Journal of Biological Chemistry. 286:28435-28443. 2011
- Drosophila UNC-45 accumulates in embryonic blastoderm and in muscles, and is essential for muscle myosin stability. Journal of Cell Science. 124:699-705. 2011
- The UNC-45 Chaperone Is Critical for Establishing Myosin-Based Myofibrillar Organization and Cardiac Contractility in the Drosophila Heart Model. PLoS ONE. 6:e22579-e22579. 2011
- Drosophila UNC-45 prevents heat-induced aggregation of skeletal muscle myosin and facilitates refolding of citrate synthase. Biochemical and Biophysical Research Communications. 396:317-322. 2010
- Mutating the Converter–Relay Interface of Drosophila Myosin Perturbs ATPase Activity, Actin Motility, Myofibril Stability and Flight Ability. Journal of Molecular Biology. 398:625-632. 2010
- Alternative Exon 9-Encoded Relay Domains Affect More than One Communication Pathway in the Drosophila Myosin Head. Journal of Molecular Biology. 389:707-721. 2009
- Divalent cations stabilize GroEL under conditions of oxidative stress. Biochemical and Biophysical Research Communications. 368:625-630. 2008
- Protection of GroEL by its methionine residues against oxidation by hydrogen peroxide. Biochemical and Biophysical Research Communications. 347:534-539. 2006
- αB-Crystallin Maintains Skeletal Muscle Myosin Enzymatic Activity and Prevents its Aggregation under Heat-shock Stress. Journal of Molecular Biology. 358:635-645. 2006
- On the chaperonin activity of GroEL at heat-shock temperature. Int. J. Biochem. Cell Biol., 37(7), 1375–1385. 2005
- Hydrogen peroxide induces the dissociation of GroEL into monomers that can facilitate the reactivation of oxidatively inactivated rhodanese. Int. J. Biochem. Cell Biol., 36(3), 505–518. 2003
- Oxidized GroEL can function as a chaperonin. Frontiers in Bioscience. 9:724-724. 2004
- GroEL interacts transiently with oxidatively inactivated rhodanese facilitating its reactivation. Biochemical and Biophysical Research Communications. 294:893-899. 2002
- Synthesis, conformation and vibrational dynamics of the peptide -Ser-Cys-Lys-Leu-Asp-Phe-, a fragment of apolipoprotein B. Indian J Biochem Biophys. 39(6):410-8. 2002
- Recurrent strokes–an interesting pedigree. Journal of the Association of Physicians of India. 49:765-766. 2001
- Lipoprotein(a) and coronary heart disease in Indian population. Journal of the Association of Physicians of India. 47:1157-1160. 1999
- Oxidative stress and metabolic control in non-insulin dependent diabetes mellitus. Indian J Biochem Biophys. 34(6):512-7. 1997
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