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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Drp1 mediates caspase-independent type III cell death in normal and leukemic cells.
Marlène Bras,Victor J. Yuste,Gaël Roué,Sandrine Barbier,Patricia Sancho,Clémence Virely,Manuel Rubio,Sylvie Baudet,Josep E. Esquerda,Hélène Merle-Béral,Marika Sarfati,Santos A. Susin +11 more
TL;DR: This previously unknown mechanism controlling caspase-independent type III PCD may provide the basis for novel therapeutic approaches to overcome apoptotic avoidance in malignant cells.
Journal ArticleDOI
Opening the doors to cytochrome c: changes in mitochondrial shape and apoptosis
TL;DR: The molecular mechanisms that control mitochondrial shape, their changes during apoptosis and the role that these changes might play in the amplification of the apoptotic cascade are reviewed.
Journal ArticleDOI
SENP1-Sirt3 Signaling Controls Mitochondrial Protein Acetylation and Metabolism.
Tianshi Wang,Ying Cao,Quan Zheng,Jun Tu,Wei Zhou,Jianli He,Jie Zhong,Yalan Chen,Jiqiu Wang,Rong Cai,Yong Zuo,Bo Wei,Qiuju Fan,Jie Yang,Yicheng Wu,Jing Yi,Dali Li,Mingyao Liu,Chuangui Wang,Aiwu Zhou,Aiwu Zhou,Yu Li,Xuefeng Wu,Wen Yang,Y. Eugene Chin,Guo-Qiang Chen,Jinke Cheng +26 more
TL;DR: Sirt3 SUMOylation mutation reduces fat mass and antagonizes high-fat diet (HFD)-induced obesity via increasing oxidative phosphorylation and energy expenditure and the results reveal that SENP1-Sirt 3 signaling modulates Sirt3 activation and mitochondrial metabolism during metabolic stress.
Journal ArticleDOI
OPA1 mutations cause cytochrome c oxidase deficiency due to loss of wild-type mtDNA molecules
Patrick Yu-Wai-Man,Patrick Yu-Wai-Man,Kamil S. Sitarz,David C. Samuels,Philip G. Griffiths,Philip G. Griffiths,Amy K. Reeve,Laurence A. Bindoff,Laurence A. Bindoff,Rita Horvath,Patrick F. Chinnery +10 more
TL;DR: The mtDNA changes induced by OPA1 mutations in skeletal muscle biopsies from 15 patients with both pure DOA and DOA+ phenotypes are investigated, and they are consistent with the ‘maintenance of wild-type’ hypothesis, the secondary mtDNA deletions induced by EMTs triggering a compensatory mitochondrial proliferative response in order to maintain an optimal level ofWild-type mtDNA genomes.
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OMA1 mediates OPA1 proteolysis and mitochondrial fragmentation in experimental models of ischemic kidney injury
TL;DR: Oma1-mediated OPA1 proteolysis plays an important role in the disruption of mitochondrial dynamics in ischemic AKI as indicated by better renal function, less tubular damage, and lower apoptosis in OMA1-deficient mice.
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.
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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.
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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.
Journal ArticleDOI
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.