Kaberi Datta

Employment

• SAROJINI NAIDU COLLEGE FOR WOMEN ASSISTANT PROFESSOR
  2019 - Present

Education

• University of Calcutta Ph.D.
  2010 - 2017

Projects & Funding

Projects & funding information is unavailable.

Publications (9)

• Corrigendum to “Hsp90/Cdc37 assembly modulates TGFβ receptor-II to act as a profibrotic regulator of TGFβ signaling during cardiac hypertrophy” [Cell. Signal. 27 (12) (2015) 2410–2424](S0898656815002673)(10.1016/j.cellsig.2015.09.005)
  Cellular Signalling 2020 DOI: 10.1016/j.cellsig.2019.109437
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• Key Cellular Effectors in Ros-Mediated Cardiac Diseases
  Modulation of Oxidative Stress in Heart Disease 2019 DOI: 10.1007/978-981-13-8946-7_7
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• Myocyte-derived Hsp90 modulates collagen upregulation via biphasic activation of STAT-3 in fibroblasts during cardiac hypertrophy
  Molecular and Cellular Biology 2017 DOI: 10.1128/MCB.00611-16
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• Quantitative proteomic changes during post myocardial infarction remodeling reveals altered cardiac metabolism and Desmin aggregation in the infarct region
  Journal of Proteomics 2017 DOI: 10.1016/j.jprot.2016.11.017
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• A spatio-temporal cardiomyocyte targeted vector system for efficient delivery of therapeutic payloads to regress cardiac hypertrophy abating bystander effect
  Journal of Controlled Release 2015 DOI: 10.1016/j.jconrel.2015.01.008
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• Comparative proteome profiling during cardiac hypertrophy and myocardial infarction reveals altered glucose oxidation by differential activation of pyruvate dehydrogenase E1 component subunit β
  Journal of Molecular Biology 2015 DOI: 10.1016/j.jmb.2014.10.026
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• Hsp90/Cdc37 assembly modulates TGFβ receptor-II to act as a profibrotic regulator of TGFβ signaling during cardiac hypertrophy
  Cellular Signalling 2015 DOI: 10.1016/j.cellsig.2015.09.005
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• Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy
  PLoS ONE 2014 DOI: 10.1371/journal.pone.0104711
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• Role of α-crystallin B as a regulatory switch in modulating cardiomyocyte apoptosis by mitochondria or endoplasmic reticulum during cardiac hypertrophy and myocardial infarction
  Cell Death and Disease 2013 DOI: 10.1038/cddis.2013.114
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