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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SLP-2 negatively modulates mitochondrial sodium-calcium exchange.
Sandrine Da Cruz,Umberto De Marchi,Maud Frieden,Philippe A. Parone,Jean-Claude Martinou,Nicolas Demaurex +5 more
TL;DR: Data show that SLP-2 modulates mitochondrial calcium extrusion, thereby altering the ability of mitochondria to buffer Ca(2+) and to shape cytosolic Ca( 2+) signals.
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Respiratory supercomplexes: plasticity and implications.
TL;DR: This review will investigate the current body of work on supercomplexes including their assembly, regulation, and plasticity, and particularly their role in the generation of reactive oxygen species and aging.
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The vitamin D receptor regulates mitochondrial function in C2C12 myoblasts.
Stephen P. Ashcroft,Joseph J. Bass,Abid A. Kazi,Philip J. Atherton,Andrew Philp,Andrew Philp,Andrew Philp +6 more
TL;DR: A direct role for the VDR is highlighted in regulating skeletal muscle mitochondrial respiration in vitro, providing a potential mechanism as to how vitamin D deficiency might impact upon skeletal muscle oxidative capacity.
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Insights into Substrate Gating in H. influenzae Rhomboid
Cory L. Brooks,Christelle Lazareno-SaezC. Lazareno-Saez,Jason S. Lamoureux,Michelle W. Mak,M. Joanne Lemieux +4 more
TL;DR: A new structure of the Haemophilus influenzae rhomboid hiGlpG is presented, which reveals disorder in loop 5, helix 5, and loop 4, indicating that, together, they represent mobile elements of the substrate gate.
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Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction
Corina T. Madreiter-Sokolowski,Armin Sokolowski,Markus Waldeck-Weiermair,Roland Malli,Wolfgang F. Graier +4 more
TL;DR: Mitochondria’s role in and impact on cellular aging and their potential to serve as a target for therapeutic interventions against age-related cellular dysfunction 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.
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.
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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.