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 mitochondrial cristae remodeling, mitochondrial dysfunction, and neuronal apoptosis in prion diseases.
Wei Wu,Deming Zhao,Syed Zahid Ali Shah,Xixi Zhang,Mengyu Lai,Dongming Yang,Xiaoqian Wu,Zhiling Guan,Jie Li,Huafen Zhao,Wen Li,Hongli Gao,Xiangmei Zhou,Jian Qiao,Lifeng Yang +14 more
TL;DR: Overexpression of OPA1 alleviated prion-induced mitochondrial network fragmentation and mtDNA loss, decrease in intracellular ATP, increase in ADP/ATP ratio, and decrease in mitochondrial membrane potential but also protected neurons from apoptosis by suppressing the release of cytochrome c from mitochondria to cytosol and activation of the apoptotic factor, caspase 3.
Journal ArticleDOI
Intersection between mitochondrial permeability pores and mitochondrial fusion/fission.
TL;DR: Recent developments in the field of mitochondrial membrane processes provide new insights into the relation between mitochondrial fission/fusion events and the mitochondrial permeability transition (MPT), and focuses on cristae remodeling, which may be the intersection between oMPT and iMPT events.
Journal ArticleDOI
Mitochondria and the Brain: Bioenergetics and Beyond.
TL;DR: This review summarizes novel data and technologies that are developed and applied to the identification and clarification of the mitochondrial role in neural plasticity using both cultured cells and in vivo approaches.
Journal ArticleDOI
Dynamic Cardiolipin Synthesis Is Required for CD8+ T Cell Immunity
Mauro Corrado,Joy Edwards-Hicks,Matteo Villa,Lea J. Flachsmann,David E. Sanin,Maaike Jacobs,Francesc Baixauli,Michal A. Stanczak,Eve Anderson,Mai Azuma,Andrea Quintana,Jonathan D. Curtis,Thomas Clapes,Katarzyna M. Grzes,Agnieszka M. Kabat,Ryan Kyle,Annette E. Patterson,Ramon I. Klein Geltink,Borko Amulic,Colin G. Steward,Douglas Strathdee,Eirini Trompouki,David O’Sullivan,Edward J. Pearce,Edward J. Pearce,Erika L. Pearce +25 more
TL;DR: It is shown here that de novo synthesis of the mitochondrial membrane-specific lipid cardiolipin maintains CD8+ T cell function, and the dynamic regulation of a single mitochondrial lipid is crucial for CD8- T cell immunity.
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Mitochondrial fission/fusion and cardiomyopathy.
TL;DR: Accumulating experimental evidence that impairing mitochondrial fission or fusion causes cardiomyopathy in otherwise normal mice is reviewed, and how these data could motivate screening of perinatal carduomyopathy subjects for damaging mutations of mitochondrial fissions and fusion factors is considered.
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.