Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Redox control of caspases
Autore:
Sen, CK; Roy, S;
Indirizzi:
Ohio State Univ, Med Ctr, Heart & Lung Res Inst 512, Dept Surg,Lab Mol Med, Columbus, OH 43210 USA Ohio State Univ Columbus OH USA 43210 Lab Mol Med, Columbus, OH 43210 USA
Titolo Testata:
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
fascicolo: 4, volume: 10, anno: 2001,
pagine: 215 - 220
SICI:
1382-6689(200109)10:4<215:RCOC>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA-LIPOIC ACID; NITRIC-OXIDE; INDUCED APOPTOSIS; OXIDATIVE STRESS; CELLULAR THIOLS; (CD95)-MEDIATED APOPTOSIS; HYDROGEN-PEROXIDE; MALIGNANT GLIOMA; HUMAN LEUKEMIA; S-NITROSATION;
Keywords:
antioxidant; thiol cell death; nutrition lipoic acid; signal transduction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Sen, CK Ohio State Univ, Med Ctr, Heart & Lung Res Inst 512, Dept Surg,LabMol Med, 473 W 12th Ave, Columbus, OH 43210 USA Ohio State Univ 473 W 12thAve Columbus OH USA 43210 OH 43210 USA
Citazione:
C.K. Sen e S. Roy, "Redox control of caspases", ENV TOX PH, 10(4), 2001, pp. 215-220

Abstract

Caspases are critical mediators of apoptotic cell death. All members of the caspase family contain the sequence QACXG which contains the active site cysteine. The putative active site of caspase 3 contains a cysteine residuethat is subject to redox control. Both thioredoxin and glutathione have been shown to be required for caspase-3 activity to induce apoptosis. The regulation of inducible caspase 3 activity by oxidation-reduction (redox) dependent mechanisms is reviewed. Up until a few years ago, reactive oxygen species (ROS) research mostly focused on oxidative damage and ROS were thoughtto be a key trigger for cell death. This view has been refined, leading tothe understanding that the biological function of ROS is determined by numerous variables such as concentration, chemical type and cellular localization. For example, ROS and reactive nitrogen species may intercept induciblecell death under certain circumstances via the redox regulation of inducible caspase activity and/or by depleting cellular energy stores. Likewise, death of unwanted diseased or degenerative cells may be facilitated by pharmacologically enhancing the thiol status of such cells using redox-active alpha -lipoic acid. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 02:39:33