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Hydrogen sulfide-induced GAPDH sulfhydration disrupts the CCAR2-SIRT1 interaction to initiate autophagy

Autophagy. 2021-01; 
Iram Khan Iqbal, Sapna Bajeli, Shivani Sahu, Shabir Ahmad Bhat, Ashwani Kumar
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PCR Cloning and Subcloning Mouse Gapdh (Genbank: NM_008084.3) was cloned in pcDNA3.1 (Invitrogen, V795-20) with N-terminal GFP or C-terminal FLAG using KpnI & XhoI or HindIII & ApaI, respectively by Genscript® custom synthesis service Get A Quote

摘要

The deacetylase SIRT1 (sirtuin 1) has emerged as a major regulator of nucleocytoplasmic distribution of macroautophagy/autophagy marker MAP1LC3/LC3 (microtubule-associated protein 1 light chain 3). Activation of SIRT1 leads to the deacetylation of LC3 and its translocation from the nucleus into the cytoplasm leading to an increase in the autophagy flux. Notably, hydrogen sulfide (HS) is a cytoprotective gasotransmitter known to activate SIRT1 and autophagy; however, the underlying mechanism for both remains unknown. Herein, we demonstrate that HS sulfhydrates the active site cysteine of the glycolytic enzyme GAPDH (glyceraldehyde-3-phosphate dehydrogenase). Sulfhydration of GAPDH leads to its redistribution int... More

关键词

Autophagy, CCAR2, GAPDH, Mycobacterium tuberculosis, PRKAA, SIRT1, hydrogen sulfide, starvation, sulfhydration, tuberculosis