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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Novel intracellular functions of apolipoproteins: the ApoO protein family as constituents of the Mitofilin/MINOS complex determines cristae morphology in mitochondria.
TL;DR: In this paper, the authors highlight the current view on the mammalian Mitofilin/MINOS complex and focus on APOOL and the role of CL in determining cristae morphology.
Journal ArticleDOI
Targeting cell death.
Derek J. Hausenloy,Luca Scorrano +1 more
TL;DR: Changes in mitochondrial inner membrane permeability and in the morphology of the organelle are regulated, perhaps interconnected processes that are starting to emerge as novel therapeutic targets for reducing cell death induced by ischemia‐reperfusion.
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Carboxy-Terminal Modulator Protein (CTMP) is a mitochondrial protein that sensitizes cells to apoptosis.
Arnaud Parcellier,Lionel A. Tintignac,Elena Zhuravleva,Peter Cron,Susanne Schenk,Lana Bozulic,Brian A. Hemmings +6 more
TL;DR: The Carboxy-Terminal Modulator Protein (CTMP) protein was identified as a PKB inhibitor that binds to its hydrophobic motif as mentioned in this paper, and it exhibits a dual sub-mitochondrial localization as a membrane bound pool and a free pool of mature CTMP in the inter-membrane space.
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UCP2-dependent improvement of mitochondrial dynamics protects against acute kidney injury.
Nan Qin,Ting Cai,Qingqing Ke,Qi Yuan,Jing Luo,Xiaoming Mao,Lei Jiang,Hongdi Cao,Ping Wen,Ke Zen,Yang Zhou,Junwei Yang +11 more
TL;DR: It is suggested that enhancing UCP2 to improve mitochondrial dynamics has potential as a strategy for improving outcomes of renal injury and that U CP2 has a role in preserving mitochondrial integrity by preventing loss of membrane potential and reducing subsequent mitophagy.
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Cryo-EM structures of S-OPA1 reveal its interactions with membrane and changes upon nucleotide binding.
Danyang Zhang,Yan Zhang,Jun Ma,Chunmei Zhu,Tongxin Niu,Wenbo Chen,Xiaoyun Pang,Yujia Zhai,Fei Sun +8 more
TL;DR: Cryo-electron microscopic structures of S-OPA1–coated liposomes in nucleotide-free and GTPγS-bound states reveal that hydrophobic residues in its extended membrane-binding domain are critical for its tubulation activity and indicate that S-opa1 adopts a dynamin-like power stroke membrane remodeling mechanism during mitochondrial inner membrane fusion.
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.