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Open AccessJournal ArticleDOI

OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion

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.
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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.

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Citations
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Journal ArticleDOI

Keeping mitochondria in shape: a matter of life and death.

TL;DR: Mitochondria are dynamic organelles that participate in energy conversion, metabolism, signaling and apoptosis and are in close contact with the endoplasmic reticulum generating an essential interface in cell physiology and death.
Journal ArticleDOI

Regulation of mitochondrial morphological dynamics during apoptosis by Bcl-2 family proteins: a key in Bak?

TL;DR: Emerging evidence has now suggested a regulation of mitochondrial morphological dynamics by Bcl-2 family proteins, and Bak appears to be a key in this regulation.
Book ChapterDOI

Drosophila Models of Parkinson's Disease

TL;DR: The methodologies employed in developing the various Drosophila models, and the recent advances that these models in particular have contributed to the understanding of the mechanisms that underlie PD pathogenesis and possible treatment strategies are reviewed.
Journal ArticleDOI

Structural implications of mitochondrial dynamics.

TL;DR: Electron micrographs of serial sections of human umbilical vein endothelial cells reveal perinuclear mitochondria of extreme length and with branches in those cells that also have short peripheral mitochondria, indicating novel fast inner membrane reorganizations.
References
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Journal ArticleDOI

Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

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.
Journal ArticleDOI

The Pathophysiology of Mitochondrial Cell Death

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

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.
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