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Titolo:
ACTIVATION OF THE RECEPTOR FOR ADVANCED GLYCATION END-PRODUCTS TRIGGERS A P21(RAS)-DEPENDENT MITOGEN-ACTIVATED PROTEIN-KINASE PATHWAY REGULATED BY OXIDANT STRESS
Autore:
LANDER HM; TAURAS JM; OGISTE JS; HORI O; MOSS RA; SCHMIDT AM;
Indirizzi:
CORNELL UNIV,COLL MED,DEPT BIOCHEM,1300 YORK AVE NEW YORK NY 10021 COLUMBIA UNIV COLL PHYS & SURG,DEPT PHYSIOL NEW YORK NY 10032 COLUMBIA UNIV COLL PHYS & SURG,DEPT MED NEW YORK NY 10032 COLUMBIA UNIV COLL PHYS & SURG,DEPT SURG NEW YORK NY 10032
Titolo Testata:
The Journal of biological chemistry
fascicolo: 28, volume: 272, anno: 1997,
pagine: 17810 - 17814
SICI:
0021-9258(1997)272:28<17810:AOTRFA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; SIGNAL-TRANSDUCTION; BINDING-PROTEINS; CELL-SURFACE; EXPRESSION; INDUCTION; MECHANISM; GLUCOSE; IDENTIFICATION; COMPLICATIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
H.M. Lander et al., "ACTIVATION OF THE RECEPTOR FOR ADVANCED GLYCATION END-PRODUCTS TRIGGERS A P21(RAS)-DEPENDENT MITOGEN-ACTIVATED PROTEIN-KINASE PATHWAY REGULATED BY OXIDANT STRESS", The Journal of biological chemistry, 272(28), 1997, pp. 17810-17814

Abstract

Advanced glycation end products (AGEs) exert their cellular effects on cells by interacting with specific cellular receptors, the best characterized of which is the receptor for AGE (RAGE), The transductional processes by which RAGE ligation transmits signals to the nuclei of cells is unknown and was investigated, AGE-albumin, a prototypic ligand,activated p21(ras) in rat pulmonary artery smooth muscle cells that express RAGE, whereas nonglycated albumin was without effect, MAP kinase activity was enhanced at concentrations of AGE-albumin, which activated p21(ras) and NF-kappa B, Depletion of intracellular glutathione rendered cells more sensitive to AGE-mediated activation of this signaling pathway, in contrast, signaling was blocked by preventing p21(ras) from associating with the plasma membrane or mutating Cys(118) on p21(ras) to Ser. Signaling was receptor-dependent, because it was prevented by blocking access to RAGE with either anti-RAGE IgG or by excess soluble RAGE, These data suggest that RAGE-mediated induction of cellular oxidant stress triggers a cascade of intracellular signals involvingp21(ras) and MAP kinase, culminating in transcription factor activation, The molecular mechanism that triggers this pathway likely involvesoxidant modification and activation of p21(ras).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 15:26:07