NDLI: Activation of the Receptor for Advanced Glycation End Products Triggers a p21 ras -dependent Mitogen-activated Protein Kinase Pathway Regulated by Oxidant Stress

Content Provider	Journal of Biological Chemistry (JBC)
Author	Lander, Harry M. Tauras, James M. Ogiste, Jason S. Hori, Osamu Moss, Rebecca A. Schmidt, Ann Marie
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 p21ras 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 p21ras and NF-κB. Depletion of intracellular glutathione rendered cells more sensitive to AGE-mediated activation of this signaling pathway. In contrast, signaling was blocked by preventing p21ras from associating with the plasma membrane or mutating Cys118 on p21ras 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 involving p21ras and MAP kinase, culminating in transcription factor activation. The molecular mechanism that triggers this pathway likely involves oxidant modification and activation of p21ras.
Related Links	http://www.jbc.org/content/272/28/17810.abstract
Ending Page	17814
Starting Page	17810
Page Count	5
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	28
Volume Number	272
DOI	10.1074/jbc.272.28.17810
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	1997-07-11
Access Restriction	Open
Subject Keyword	CELL BIOLOGY AND METABOLISM
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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