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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Plasmalogen loss caused by remodeling deficiency in mitochondria
Tomohiro Kimura,Atsuko K. Kimura,Mindong Ren,Vernon Monteiro,Yang Xu,Bob Berno,Michael Schlame,Richard M. Epand +7 more
TL;DR: Tafazzin function thus critically relates to homeostasis of plasmalogen, which in the ethanolamine class has conceivably analogous and more potent molecular functions in mitochondria than diacyl phosphatidylethanolamine.
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EGCG protects cardiomyocytes against hypoxia-reperfusion injury through inhibition of OMA1 activation
Jinliang Nan,Cunjin Nan,Jian Ye,Lu Qian,Ya Geng,Dawei Xing,Muhammad Saif Ur Rahman,Mingyuan Huang +7 more
TL;DR: EGCG inhibits OMA1 self-cleavage and attenuates OPA1 cleavage, suggesting that EGCG can be used to treat ischemia-reperfusion injury (IRI), and to use Oma1 inhibition induced by EGCg to treat cardiac IRI.
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Opa1 relies on cristae preservation and ATP synthase to curtail reactive oxygen species accumulation in mitochondria.
Ruben Quintana-Cabrera,Israel Manjarrés-Raza,Carlos Vicente-Gutierrez,Mauro Corrado,Juan P. Bolaños,Luca Scorrano +5 more
TL;DR: In this paper, the mitochondrial fusion and cristae shape protein Opa1 requires mitochondrial ATP synthase oligomers to reduce reactive oxygen species (ROS) accumulation in cells fueled with galactose.
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Selenoprotein S silencing triggers mouse hepatoma cells apoptosis and necrosis involving in intracellular calcium imbalance and ROS-mPTP-ATP.
TL;DR: The results indicate that SelenoS silencing triggers mouse hepatoma cells apoptosis and necrosis through affecting intracellular calcium homeostasis and ROS-mPTP-ATP participates in cell death transformation from apoptosis to necrosis to rise damage.
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Oligomeric state study of prokaryotic rhomboid proteases.
Padmapriya Sampathkumar,Michelle W. Mak,Sarah J. Fischer-Witholt,Emmanuel Guigard,Cyril M. Kay,M. Joanne Lemieux +5 more
TL;DR: Results indicate that rhomboids form oligomers which are facilitated by the membrane domain, and it is shown that these oligomers exist in the lipid bilayer for hiGlpG.
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.