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 Overexpression Ameliorates the Phenotype of Two Mitochondrial Disease Mouse Models
Gabriele Civiletto,Tatiana Varanita,Raffaele Cerutti,Tatiana Gorletta,Serena Barbaro,Silvia Marchet,Costanza Lamperti,Carlo Viscomi,Luca Scorrano,Massimo Zeviani +9 more
TL;DR: Increased levels of the mitochondria-shaping protein Opa1 improve respiratory chain efficiency and protect from tissue damage, suggesting that it could be an attractive target to counteract mitochondrial dysfunction.
Journal ArticleDOI
The E3 Ligase Parkin Maintains Mitochondrial Integrity by Increasing Linear Ubiquitination of NEMO
Anne Kathrin Müller-Rischart,Anna Pilsl,Patrick Beaudette,Maria Patra,Kamyar Hadian,Maria Funke,Regina Peis,Alexandra Deinlein,Carolin Schweimer,Peer-Hendrik Kuhn,Stefan F. Lichtenthaler,Elisa Motori,Elisa Motori,Silvana Hrelia,Wolfgang Wurst,Dietrich Trümbach,Thomas Langer,Daniel Krappmann,Gunnar Dittmar,Jörg Tatzelt,Jörg Tatzelt,Konstanze F. Winklhofer,Konstanze F. Winklhofer +22 more
TL;DR: Parkin, a RING-between-RING-type E3 ubiquitin ligase associated with Parkinson's disease, has a wide neuroprotective activity, preventing cell death in various stress paradigms.
Journal ArticleDOI
OPA1 Processing Reconstituted in Yeast Depends on the Subunit Composition of the m-AAA Protease in Mitochondria
Stéphane Duvezin-Caubet,Mirko Koppen,Johannes Wagener,Michael Zick,Lars Israel,Andrea Bernacchia,Ravi Jagasia,Elena I. Rugarli,Axel Imhof,Walter Neupert,Thomas Langer,Andreas S. Reichert +11 more
TL;DR: These results provide evidence for different substrate specificities of m-AAA proteases composed of different subunits and reveal a striking evolutionary switch of proteases involved in the proteolytic processing of dynamin-like GTPases in mitochondria.
Journal ArticleDOI
LETM1, deleted in Wolf-Hirschhorn syndrome is required for normal mitochondrial morphology and cellular viability
Kai Stefan Dimmer,Francesca Navoni,Alberto Casarin,Eva Trevisson,Sabine Endele,Andreas Winterpacht,Leonardo Salviati,Luca Scorrano +7 more
TL;DR: It is shown that human LETM1 is located in the inner membrane, exposed to the matrix and oligomerized in higher molecular weight complexes of unknown composition, and caused 'necrosis-like' death, without activation of caspases and not inhibited by overexpression of Bcl-2.
Journal ArticleDOI
Mitochondrial Dynamics in Diabetes
TL;DR: This review describes an overview of mechanistic and functional aspects of mitochondrial fission and fusion, and comments on the recent advances connecting mitochondrial dynamics with diabetes and diabetic complications.
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.
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.
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.