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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Ultrastructure of the mitochondrion and its bearing on function and bioenergetics.
TL;DR: This review delves into the link between mitochondrial structure and energy metabolism, suggesting a tight and mutual control between mitochondrial form and bioenergetics.
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FUNDC1 regulates mitochondrial dynamics at the ER-mitochondrial contact site under hypoxic conditions
Wenxian Wu,Chunxia Lin,Keng Wu,Lei Jiang,Xiaojing Wang,Wen Li,Haixia Zhuang,Xingliang Zhang,Hao Chen,Shupeng Li,Yue Yang,Yue Lu,Jingjing Wang,Runzhi Zhu,Liangqing Zhang,Sen-Fang Sui,Ning Tan,Bin Zhao,Jingjing Zhang,Longxuan Li,Du Feng,Du Feng +21 more
TL;DR: FUNDC1 integrates mitochondrial fission and mitophagy at the interface of the MAM by working in concert with DRP1 and calnexin under hypoxic conditions in mammalian cells.
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Mitochondria in traumatic brain injury and mitochondrial‐targeted multipotential therapeutic strategies
TL;DR: Preclinical and clinical results of mitochondria‐targeted therapy show promise and mitochondrial‐ targeted multipotential therapeutic strategies offer new hope for the successful treatment of TBI and other acute brain injuries.
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MAPL SUMOylation of Drp1 Stabilizes an ER/Mitochondrial Platform Required for Cell Death
TL;DR: It is demonstrated how interorganellar contacts are dynamically regulated through active SUMOylation during apoptosis, creating a stabilized platform that signals cytochrome c release.
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Regulation of mitochondrial fusion and division.
TL;DR: How mitochondrial dynamics are controlled and how these events are coordinated with cell growth, mitosis, apoptosis and human diseases are discussed.
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.