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
Citations
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Disruption of cytochrome c heme coordination is responsible for mitochondrial injury during ischemia.
TL;DR: SS-20, which is shown to selectively target CL and protect the Met(80)-Fe ligation, minimizes ischemic injury and promotes ATP recovery, represents a novel target for minimizing ischemia injury.
Journal ArticleDOI
OPA1 mutations associated with dominant optic atrophy influence optic nerve head size.
Piero Barboni,Michele Carbonelli,Giacomo Savini,B. Foscarini,Vincenzo Parisi,Maria Lucia Valentino,Arturo Carta,Annamaria De Negri,Federico Sadun,Massimo Zeviani,Alfredo A. Sadun,Simone Schimpf,Bernd Wissinger,Valerio Carelli +13 more
TL;DR: The DOA patients carrying OPA1 gene mutations present, as a group, a significantly smaller ONH compared with the range of size observed in a control population; this feature may be mutation specific.
Journal ArticleDOI
C11orf83, a Mitochondrial Cardiolipin-Binding Protein Involved in bc1 Complex Assembly and Supercomplex Stabilization
Marjorie Desmurs,Michelangelo Foti,Etienne Raemy,Frédéric M. Vaz,Jean-Claude Martinou,Amos Marc Bairoch,Amos Marc Bairoch,Lydie Lane,Lydie Lane +8 more
TL;DR: It is suggested that C11orf83, now called UQCC3, is the functional human equivalent of Cbp4p, which was lacking experimental characterization, and is involved in the stabilization of bc1 complex-containing supercomplexes, especially the III2/IV supercomplex.
Journal ArticleDOI
TNFR2 Stimulation Promotes Mitochondrial Fusion via Stat3- and NF-kB-Dependent Activation of OPA1 Expression.
Jinliang Nan,Hengxun Hu,Yong Sun,Lianlian Zhu,Yingchao Wang,Zhiwei Zhong,Jing Zhao,Na Zhang,Ya Wang,Yaping Wang,Jian Ye,Ling Zhang,Xinyang Hu,Wei Zhu,Jian-an Wang +14 more
TL;DR: In this article, the authors show that in addition to having proinflammatory properties, mitochondria also play essential roles in maintaining cell structure and function, and that these organs are important cellular organelles.
Journal ArticleDOI
NF-κB pathway controls mitochondrial dynamics.
Mireille Laforge,Vasco Rodrigues,Vasco Rodrigues,Ricardo Silvestre,Clement A. Gautier,Clement A. Gautier,Clement A. Gautier,R. Weil,O. Corti,O. Corti,O. Corti,Jérôme Estaquier,Jérôme Estaquier +12 more
TL;DR: It is demonstrated that the absence of IκB kinase-α, which is a key element of the nonclassical NF-κB pathway, has an impact on the mitochondrial network morphology and OPA1 expression, and PARK2 overexpression did not modify the expression of OPA 1.
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.
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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.