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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Mitochondrial protein Preli-like is required for development of dendritic arbors and prevents their regression in the Drosophila sensory nervous system.
Asako Tsubouchi,Taiichi Tsuyama,Makio Fujioka,Haruyasu Kohda,Keiko Okamoto-Furuta,Toshiro Aigaki,Tadashi Uemura +6 more
TL;DR: It is shown that the Drosophila mitochondrial protein Preli-like (Prel), a member of the conserved PRELI/MSF1 family, contributes to the integrity of mitochondrial structures, the activity of respiratory chain complex IV and the cellular ATP level.
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A proteomic screen with Drosophila Opa1-like identifies Hsc70-5/Mortalin as a regulator of mitochondrial morphology and cellular homeostasis.
TL;DR: A novel interaction between Hsc70-5/Mortalin and Opa1-like that influences cellular homeostasis through mitochondrial fusion is identified.
Journal ArticleDOI
Targeting Mitochondrial Network Architecture in Down Syndrome and Aging.
Nunzia Mollo,Rita Cicatiello,Miriam Aurilia,Roberta Scognamiglio,Rita Genesio,Maria Charalambous,Simona Paladino,Anna Conti,Lucio Nitsch,Lucio Nitsch,Antonella Izzo +10 more
TL;DR: Evidence is summarized suggesting that drugs targeting either PGC-1α/PPARGC1A or mTOR signaling or other factors affecting the mitochondrial network may represent therapeutic approaches to improve and/or prevent the effects of altered mitochondrial function.
Journal ArticleDOI
Mitochondrial Dysfunctions: A Thread Sewing Together Alzheimer's Disease, Diabetes, and Obesity.
TL;DR: Mitochondrial alterations have emerged as a feature common to all metabolic disorders, underlining perhaps an impaired coordination between cellular needs and mitochondrial responses that could contribute to their development and/or progression.
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Mitochondrial fission augments capsaicin-induced axonal degeneration
Hao Chiang,Hao Chiang,Nobuhiko Ohno,Nobuhiko Ohno,Yu Lin Hsieh,Yu Lin Hsieh,Don J. Mahad,Don J. Mahad,Shin Kikuchi,Shin Kikuchi,Hitoshi Komuro,Sung-Tsang Hsieh,Bruce D. Trapp +12 more
TL;DR: It is established that mitochondrial stationary site size significantly affects axonal integrity and suggested that inhibition of Ca2+-dependent mitochondrial fission facilitates mitochondrial function and axonal survival following activation of axonal cationic channels.
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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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.