Description
Title: Cancer’s TRAP1 chaperones the metabolic switch
Abstract: The formation of respiratory complexes and the removal of misfolded proteins both depend on molecular chaperones for proper mitochondrial function. A subset of molecular chaperones called heat shock proteins (Hsps) work in all subcellular compartments both normally and in response to stress. The Hsp90 chaperone TNF-receptor-associated protein-1 (TRAP1) is mainly found in the mitochondria and regulates mitochondrial apoptosis as well as metabolic reprogramming in cells. By encouraging glycolytic metabolism and inhibiting the mitochondrial permeability transition that comes before numerous cell death pathways, TRAP1 upregulation aids in the growth and progression of many cancers. In cellular models of cancer, TRAP1 attenuation causes apoptosis, indicating TRAP1 as a potential therapeutic target. Post-translational modifications (PTM), which also affect cytosolic Hsp90 proteins, control TRAP1’s function and moderate its effects on downstream effectors, or “clients.” Few effectors have, however, been found so far. Here, we’ll talk about how TRAP1 dysregulation affects cancer and how post-translational modifications affect TRAP1’s known functions.
Keywords: TRAP1; Hsp90; chaperone; post-translational modification; cancer; mitochondria; metabolism;
Warburg effect
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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