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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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Regulation of Mitochondrial Electron Transport Chain Assembly.

TL;DR: The initial idea that the respiratory chain protein complexes (RCCs) were independent structures in the inner mitochondrial membrane evolved after the identification of higher quaternary structures called supercomplexes (SCs), whose formation is dynamically regulated in order to accommodate cellular metabolic demands.
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Genome-wide linkage scan and association study of PARL to the expression of LHON families in Thailand

TL;DR: A genome-wide linkage scan with 400 microsatellite markers in 9 large Thai LHON G11778A pedigrees showed the most evidence of association between two SNPs, rs3749446 and rs1402000, located in PARL presenilins-associated rhomboid-like and LHON expression, which has long been believed to intrigue the neurodegeneration of LHON.
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Mitochondrial quality control mechanisms as potential therapeutic targets in sepsis-induced multiple organ failure.

TL;DR: This review will focus on advances concerning potential mechanisms in regulating mitochondria quality control and impacts of mitochondrial quality control on the progression of sepsis.
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OMA1 reprograms metabolism under hypoxia to promote colorectal cancer development

TL;DR: It is demonstrated that OMA1, a stress‐activated mitochondrial protease, promotes colorectal cancer development by driving metabolic reprogramming and suppresses OXPHOS in coloreCTal cancer models.
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Cell death: Insights into the ultrastructure of mitochondria

TL;DR: The current knowledge of mitochondrial inner membrane remodelling during cell death is summarized and the role of mitochondrial proteins in governing structural alterations is discussed, including the adaptor protein p66Shc as a regulator of mitochondrial metabolism during apoptosis.
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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