OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
Christian Frezza,Sara Cipolat,Olga Martins de Brito,Massimo Micaroni,Galina V. Beznoussenko,Tomasz Rudka,Davide Bartoli,Roman S. Polishuck,Nika N. Danial,Bart De Strooper,Luca Scorrano +10 more
TLDR
Evidence is provided that Optic Atrophy 1 (OPA1), a profusion dynamin-related protein of the inner mitochondrial membrane mutated in dominant optic atrophy, protects from apoptosis by preventing cytochrome c release independently from mitochondrial fusion.About:
This article is published in Cell.The article was published on 2006-07-14 and is currently open access. It has received 1444 citations till now. The article focuses on the topics: Optic Atrophy 1 & Inner mitochondrial membrane.read more
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Opa1 is required for proper mitochondrial metabolism in early development.
TL;DR: Opa1 was successfully depleted in zebrafish embryos using antisense morpholinos, which resulted in disrupted mitochondrial morphology and a new Opa1-associated phenotype in a vertebrate model system, which further elucidates the absolute requirement of OPA1 for successful vertebrate development.
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Intersection of mitochondrial fission and fusion machinery with apoptotic pathways: Role of Mcl-1
TL;DR: Findings on how the mitochondrial fission and fusion machinery may intersect apoptotic pathways focusing on recent advances on the key role played by Mcl‐1 will be covered.
Journal ArticleDOI
Endophilin B1/Bif-1 stimulates BAX activation independently from its capacity to produce large scale membrane morphological rearrangements.
Aitor Etxebarria,Oihana Terrones,Hirohito Yamaguchi,Ane Landajuela,Olatz Landeta,Bruno Antonsson,Hong Gang Wang,Gorka Basañez +7 more
TL;DR: These findings provide direct evidence for a functional interplay between Bif-1, BAX, and cardiolipin during MOMP but also add significantly to the growing body of evidence indicating that components of the mitochondrial morphogenesis machinery possess proapoptotic functions that are independent from their recognized roles in normal mitochondrial dynamics.
Journal ArticleDOI
Membrane Nanoparticles Derived from ACE2-Rich Cells Block SARS-CoV-2 Infection.
Cheng Wang,Shaobo Wang,Yin Chen,Jianqi Zhao,Songling Han,Gaomei Zhao,Jing Kang,Yong Liu,Liting Wang,Xiaoyang Wang,Yang Xu,Song Wang,Yi Huang,Junping Wang,Jinghong Zhao +14 more
TL;DR: In this paper, membrane nanoparticles (NPs) prepared from ACE2-rich human renal tubular epithelial cells were discovered to have potent capacity to block SARS-CoV-2 infection.
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A Small Molecule That Protects the Integrity of the Electron Transfer Chain Blocks the Mitochondrial Apoptotic Pathway
Xian Jiang,Li Li,Zhengxin Ying,Chenjie Pan,Shaoqiang Huang,Lin Li,Miaomiao Dai,Bo Yan,Ming Li,Hui Jiang,She Chen,Zhiyuan Zhang,Xiaodong Wang +12 more
TL;DR: The discovery of a small molecule that efficiently blocks Bim-induced apoptosis after Bax is activated on the mitochondria and protects the integrity of the ETC and allows treated cells to continue to proliferate after apoptosis induction is reported.
References
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Michael C. Wei,Michael C. Wei,Wei-Xing Zong,Emily H. Cheng,Tullia Lindsten,Vily Panoutsakopoulou,Andrea J. Ross,Kevin A. Roth,Grant R. MacGregor,Craig B. Thompson,Stanley J. Korsmeyer +10 more
TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
Journal ArticleDOI
The Pathophysiology of Mitochondrial Cell Death
Douglas R. Green,Guido Kroemer +1 more
TL;DR: The therapeutic induction of MOMP may restore apoptosis in cancer cells in which it is disabled, and the general rules governing the pathophysiology and controversial issues regarding its regulation are discussed.
Journal ArticleDOI
Two CD95 (APO-1/Fas) signaling pathways
Carsten Scaffidi,Simone Fulda,Anu Srinivasan,Claudia Friesen,Feng Li,Kevin J. Tomaselli,Klaus-Michael Debatin,Peter H. Krammer,Marcus E. Peter +8 more
TL;DR: In the presence of caspase‐3 the amount of active casp enzyme‐8 generated at the DISC determines whether a mitochondria‐independent apoptosis pathway is used (type I cells) or not (type II cells).
Journal Article
The expanding role of mitochondria in apoptosis
TL;DR: The complexity of the apoptotic program began to increase with the discovery of Bcl-2, a gene whose product causes resistance to apoptosis in lymphocytes, and the complex role of mitochondria in apoptosis came into focus when biochemical studies identified several mitochondrial proteins that are able to activate cellular apoptotic programs directly.
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Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development
TL;DR: It is concluded that Mfn1 and Mfn2 have both redundant and distinct functions and act in three separate molecular complexes to promote mitochondrial fusion, and by enabling cooperation between mitochondria, has protective effects on the mitochondrial population.