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Journal ArticleDOI

Oxidative lipidomics of apoptosis: redox catalytic interactions of cytochrome c with cardiolipin and phosphatidylserine.

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TLDR
A new concept is presented that cyt c actuates both of these oxidative roles through a uniform mechanism: its specific interactions with each of these phospholipids result in the conversion and activation of cyt c, transforming it from an innocuous electron transporter into a calamitous peroxidase capable of oxidizing the activating phospholIPids.
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This article is published in Free Radical Biology and Medicine.The article was published on 2004-12-15. It has received 337 citations till now. The article focuses on the topics: Cytochrome c & Cardiolipin.

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Aggregation-Induced Emission: Together We Shine, United We Soar!

TL;DR: This paper presents a meta-analysis of the chiral stationary phase transition of Na6(CO3)(SO4)2, a major component of the response of the immune system to Na2CO3.
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Reactive oxygen species, cellular redox systems and apoptosis

TL;DR: A full understanding of the redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders.
Journal ArticleDOI

Reactive Oxygen Species in Inflammation and Tissue Injury

TL;DR: The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
Journal ArticleDOI

Mechanisms of cytochrome c release from mitochondria

TL;DR: Cyt c has been associated also to vital cell functions (i.e. differentiation), suggesting that its release not always occurs in an all-or-nothing fashion and that mitochondrial outer membrane permeabilization may not invariably lead to cell death.
Journal ArticleDOI

Engulfment of apoptotic cells: signals for a good meal

TL;DR: Several new factors that regulate engulfment have been identified, whereas the roles of some of the older players require revision.
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Journal Article

Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages.

TL;DR: The data suggest that macrophages specifically recognize phosphatidylserine that is exposed on the surface of lymphocytes during the development of apoptosis, and suggest that apoptotic lymphocytes lose membrane phospholipid asymmetry and expose phosphorus on the outer leaflet of the plasma membrane.
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 ArticleDOI

Mitochondrial control of cell death

TL;DR: In many instances, permeabilization of mitochondrial membranes is a rate-limiting step of apoptotic or necrotic cell demise, which has important consequences for the pathophysiology of cell death, as well as for its pharmacological control.
Journal ArticleDOI

Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.

TL;DR: The results suggest that binding and/or phagocytosis of apoptotic cells induces active antiinflammatory or suppressive properties in human macrophages, likely that resolution of inflammation depends not only on the removal of apoptosis but on active suppression of inflammatory mediator production.
Book ChapterDOI

[44] Glutathione peroxidase

TL;DR: This chapter presents a procedure for the preparation of glutathione peroxidase, which is regarded as a major protective system against endogenously and exogenously induced lipid peroxidation.
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