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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Journal ArticleDOI
High-throughput screening identifies suppressors of mitochondrial fragmentation in OPA1 fibroblasts.
Emma Cretin,Emma Cretin,Priscilla Lopes,Elodie Vimont,Takashi Tatsuta,Thomas Langer,Thomas Langer,Anastasia D. Gazi,Martin Sachse,Patrick Yu-Wai-Man,Pascal Reynier,Timothy Wai,Timothy Wai +12 more
TL;DR: In this paper, the entire known mitochondrial proteome (1,531 genes) was used to identify genes that control mitochondrial morphology using a first-in-kind imaging pipeline, including 145 known and novel candidate genes whose depletion promoted elongation or fragmentation of the mitochondrial network in control fibroblasts.
Journal ArticleDOI
Selective killing of human T-ALL cells: an integrated approach targeting redox homeostasis and the OMA1/OPA1 axis.
Micol Silic-Benussi,Gloria Scattolin,Ilaria Cavallari,Sonia Minuzzo,Paola Del Bianco,Samuela Francescato,Giuseppe Basso,Stefano Indraccolo,Donna M. D'Agostino,Vincenzo Ciminale +9 more
TL;DR: The findings provide proof-of-principle for an integrated ROS-based pharmacological approach to target refractory T-ALL and significantly reduced the growth of a glucocorticoid-resistant patient-derived T-all xenograft.
Journal ArticleDOI
Mitochondria in Neuronal Health: From Energy Metabolism to Parkinson's Disease.
Hariharan Murali Mahadevan,Arsalan Hashemiaghdam,Ghazaleh Ashrafi,Angelika B. Harbauer,Angelika B. Harbauer +4 more
TL;DR: In this article, the role of mitochondria in energy metabolism under resting conditions and during synaptic transmission is discussed, and evidence for the contribution of neuronal mitochondrial dysfunction to Parkinson's disease is presented.
Journal ArticleDOI
Prohibitin(g) Cancer: Aurilide and Killing by Opa1-Dependent Cristae Remodeling
TL;DR: Proapoptotic drugs targeting the mitochondrial Bcl-2 rheostat of apoptosis are tools to selectively kill cancer cells by identifying the target of the cytotoxic natural product aurilide in the prohibitin Opa1-dependent apoptotic cristae remodeling.
Book ChapterDOI
MET receptor in oncology: From biomarker to therapeutic target.
TL;DR: This chapter will discuss the history of MET, the genetics of this RTK, and give some background on the receptor biology, and discuss directed therapeutics, mechanisms of resistance, and the future of MET as a therapeutic target.
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.