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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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The processing of human rhomboid intramembrane serine protease RHBDL2 is required for its proteolytic activity.

TL;DR: This study has demonstrated that RHBDL2 activity is regulated by proenzyme activation, revealed a role for the conserved WR residues in loop 1 in RHBDl2 activity, and provided critical insights into the regulation and function of this human rhomboid protease.
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Amorphous solid dispersion of Berberine mitigates apoptosis via iPLA2β/Cardiolipin/Opa1 pathway in db/db mice and in Palmitate-treated MIN6 β-cells.

TL;DR: The results indicated that the regulation of iPLA2β/CL/Opa1 by HGSD may prevent beta-cell apoptosis and may improve islet beta- cell function in Type 2 diabetic mice and in palmitate-treated MIN6 cells.
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Lipid droplet meets a mitochondrial protein to regulate adipocyte lipolysis.

TL;DR: A study identifies optic atrophy 1 (OPA1), a protein that regulates mitochondrial dynamics, as perilipin 1 interaction partner and the A‐kinase anchoring protein (AKAP) on LDs that is involved in the induction of stimulated lipolysis.
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Translation of Pharmacogenetics into Clinically Relevant Testing Modalities

TL;DR: Pharmacogenetics relies on the genetic makeup of an individual to predict drug response and efficacy, as well as potential adverse drug events, and the clinical utility and application of PGx are especially apparent in some subspecialty areas of chemotherapeutic, psychotropic drug, and anticoagulant therapies.
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Reconstitutions of mitochondrial inner membrane remodeling.

TL;DR: The current knowledge of inner mitochondrial membrane architecture is reviewed and recent findings and advances in understanding the factors that shape this membrane are discussed.
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.
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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.
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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.
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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.
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