scispace - formally typeset
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.
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
More filters
Journal ArticleDOI

Cysteine residues in mitochondrial intermembrane space proteins: more than just import

TL;DR: Different functions of human IMS proteins, the involvement of cysteine residues in these functions, the consequences of Cysteine modifications and the consequences in the machinery for disulfide bond formation in terms of human health are discussed.
Journal ArticleDOI

Loss of CHCHD2 and CHCHD10 activates OMA1 peptidase to disrupt mitochondrial cristae phenocopying patient mutations.

TL;DR: It is reported that C10 pathogenesis and the normal function of C2/C10 are intimately linked, and C2 and C10 are partially functionally redundant, and some but not all disease-causing mutations have retained activity.
Journal ArticleDOI

A cold-stress-inducible PERK/OGT axis controls TOM70-assisted mitochondrial protein import and cristae formation.

TL;DR: In this article, cold stress or β-adrenergic stimulation activates PERK that phosphorylates O-linked Nacetylglucosamine transferase (OGT), which enhances MIC19 protein import into mitochondria and promotes cristae formation and respiration.
Journal ArticleDOI

Interplay of mitochondrial fission-fusion with cell cycle regulation: Possible impacts on stem cell and organismal aging.

TL;DR: This review discus literature leading to the understanding on how shifts in the dynamic balance of mitochondrial fission and fusion can modulate progression through, exit from, and re-entry to the cell cycle or undergo senescence and proposes a few hypotheses that may provide direction.
Book ChapterDOI

Mitochondrial dynamics in aging and disease.

TL;DR: In this paper, it was shown that the mobility of proteins and small molecules within the mitochondria is necessary to reach the functional goals of fusion and fission, although cristae and a large fraction of proteins of the respiratory complexes proved to be stable for hours after fusion and perform slow exchange of material.
References
More filters
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.
Related Papers (5)