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His recent research has focused on the role of the glucose-dependent, post-translational modifications of proteins by O-linked beta-N-acetylglucosamine moiety (O-GlcNAc) in mediating cardiomyocyte stress responses. Work from his laboratory has demonstrated that acute increases of O-GlcNAc levels are cardioprotective; conversely, in the setting of diabetes where O-GlcNAc levels are chronically elevated cardiomyocytes cell survival pathways such as autophagy are impaired in an O-GlcNAc dependent manner. Additional interests include the role of store-operated calcium entry (SOCE) in cardiomyocytes and how this is regulated by O-GlcNAc.
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Research square (2024)
Nature Reviews Cardiologypp.1-20, (2024)
American Journal of Physiology-heart and Circulatory Physiologyno. 4 (2023): H601-H616
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JOURNAL OF NEUROCHEMISTRYno. 5 (2023): 682-700
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Journal of the American Heart Associationno. 19 (2023)
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CIRCULATION RESEARCHno. Suppl_1 (2023)
CIRCULATION RESEARCHno. Suppl_1 (2023)
Cell reports methodsno. 7 (2023): 100537-100537
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