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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Granzyme B-induced mitochondrial ROS are required for apoptosis
Guillaume Jacquemin,D. Margiotta,Atsuko Kasahara,Esen Yonca Bassoy,Michael Walch,Jerome Thiery,Judy Lieberman,Denis Martinvalet +7 more
TL;DR: GB-induced mitocentric ROS are necessary for optimal apoptogenic factor release, rapid DNA fragmentation and lysosomal rupture, and scavenging the ROS delays and reduces many of the features of GB-induced death.
Lipids in the Assembly of Membrane Proteins and Organization of Protein Supercomplexes
TL;DR: In this paper, the role of phosphatidylethanolamine and cardiolipin in normal assembly and organization of the membrane proteins, multimeric protein complexes, and higher order supercomplexes is discussed.
Journal ArticleDOI
Mitoguardin Regulates Mitochondrial Fusion through MitoPLD and Is Required for Neuronal Homeostasis
Yongping Zhang,Xiao-Man Liu,Jian Bai,Xuejun Tian,Xiaocui Zhao,Wei Liu,Xiuying Duan,Weina Shang,Heng-Yu Fan,Chao Tong +9 more
TL;DR: It is proposed that MIGA proteins promote mitochondrial fusion by regulating mitochondrial phospholipid metabolism via MitoPLD, which function downstream of mitofusin and interact with MinoPLD to stabilize Mito PLD and facilitate MitoplD dimer formation.
Journal ArticleDOI
Loss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity
Yulia Kushnareva,Akos A. Gerencser,Akos A. Gerencser,Blaise Bossy,Blaise Bossy,Won-Kyu Ju,Won-Kyu Ju,A. White,Jenna Waggoner,Mark H. Ellisman,Guy Perkins,Ella Bossy-Wetzel,Ella Bossy-Wetzel +12 more
TL;DR: The data show that whereas OPA1 is required for mitochondrial fusion, maintenance of crista morphology and oxidative phosphorylation, loss of OPA 1 also results in defective Ca2+ homeostasis.
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Mitochondrial fusion and function in Charcot–Marie–Tooth type 2A patient fibroblasts with mitofusin 2 mutations
Elizabeth A. Amiott,Paul Lott,Jamie Soto,Peter B. Kang,J. Michael McCaffery,Salvatore DiMauro,E. Dale Abel,Kevin M. Flanigan,Victoria H. Lawson,Janet M. Shaw +9 more
TL;DR: The results indicate that, in fibroblasts, mitofusin expression, mitochondrial morphology, ultrastructure, mtDNA content, and respiratory capacity are not affected by the presence of mutant Mfn2 protein, and it is shown that mitochondrial fusion occurs efficiently in CMT2A patient-derived fibro Blasts.
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.