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• W2104479178 endingPage "507" @default.
• W2104479178 startingPage "497" @default.
• W2104479178 abstract "<h3>Background</h3> Mitochondria are dynamic organelles that undergo fission and fusion. During cell stress, mitochondrial dynamics shift to fission, leading to mitochondrial fragmentation, membrane leakage, and apoptosis. Mitochondrial fragmentation requires the cleavage of both outer and inner membranes, but the mechanism of inner membrane cleavage is unclear. Bif-1 and prohibitin-2 may regulate mitochondrial dynamics. <h3>Methods</h3> We used azide-induced ATP depletion to incite cell stress in mouse embryonic fibroblasts and renal proximal tubular cells, and renal ischemia-reperfusion to induce stress in mice. We also used knockout cells and mice to determine the role of Bif-1, and used multiple techniques to analyze the molecular interaction between Bif-1 and prohibitin-2. <h3>Results</h3> Upon cell stress, Bif-1 translocated to mitochondria to bind prohibitin-2, resulting in the disruption of prohibitin complex and proteolytic inactivation of the inner membrane fusion protein OPA1. Bif-1-deficiency inhibited prohibitin complex disruption, OPA1 proteolysis, mitochondrial fragmentation, and apoptosis. Domain deletion analysis indicated that Bif-1 interacted with prohibitin-2 via its C-terminus. Notably, mutation of Bif-1 at its C-terminal tryptophan-344 not only prevented Bif-1/prohibitin-2 interaction but also reduced prohibitin complex disruption, OPA1 proteolysis, mitochondrial fragmentation, and apoptosis, supporting a pathogenic role of Bif-1/prohibitin-2 interaction. In mice, Bif-1 bound prohibitin-2 during renal ischemia/reperfusion injury, and Bif-1-deficiency protected against OPA1 proteolysis, mitochondrial fragmentation, apoptosis and kidney injury. <h3>Conclusions</h3> These findings suggest that during cell stress, Bif-1 regulates mitochondrial inner membrane by interacting with prohibitin-2 to disrupt prohibitin complexes and induce OPA1 proteolysis and inactivation." @default.
• W2104479178 created "2016-06-24" @default.
• W2104479178 creator A5072357628 @default.
• W2104479178 date "2001-08-01" @default.
• W2104479178 modified "2023-10-18" @default.
• W2104479178 title "Complex and segmental uniparental disomy (UPD): review and lessons from rare chromosomal complements" @default.
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• W2104479178 doi "https://doi.org/10.1136/jmg.38.8.497" @default.
• W2104479178 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1734925" @default.
• W2104479178 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11483637" @default.
• W2104479178 hasPublicationYear "2001" @default.

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