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(Received for publication, June 30, 1995; and in revised form, August 22, 1995) The receptor for advanced glycation end products (RAGE), a
newly-identified member of the immunoglobulin superfamily, mediates
interactions of advanced glycation end product (AGE)-modified proteins
with endothelium and other cell types. Survey of normal tissues
demonstrated RAGE expression in situations in which accumulation of
AGEs would be unexpected, leading to the hypothesis that under
physiologic circumstances, RAGE might mediate interaction with ligands
distinct from AGEs. Sequential chromatography of bovine lung extract
identified polypeptides with M
Volume 270,
Number 43,
Issue of October 27, 1995 pp. 25752-25761
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
MEDIATION OF NEURITE OUTGROWTH AND CO-EXPRESSION OF RAGE AND
AMPHOTERIN IN THE DEVELOPING NERVOUS SYSTEM
values of
12,000 (p12) and 23,000 (p23) which bound RAGE.
NH
-terminal and internal protein sequence data for p23
matched that reported previously for amphoterin. Amphoterin purified
from rat brain or recombinant rat amphoterin bound to purified sRAGE in
a saturable and dose-dependent manner, blocked by anti-RAGE IgG or a
soluble form of RAGE (sRAGE). Cultured embryonic rat neurons, which
express RAGE, displayed dose-dependent binding of I-amphoterin which was prevented by blockade of RAGE
using antibody to the receptor or excess soluble receptor (sRAGE). A
functional correlate of RAGE-amphoterin interaction was inhibition by
anti-RAGE F(ab`)
and sRAGE of neurite formation by cortical
neurons specifically on amphoterin-coated substrates. Consistent with a
potential role for RAGE-amphoterin interaction in development,
amphoterin and RAGE mRNA/antigen were co-localized in developing rat
brain. These data indicate that RAGE has physiologically relevant
ligands distinct from AGEs which are likely, via their interaction with
the receptor, to participate in physiologic processes outside of the
context of diabetes and accumulation of AGEs.
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 R. Ramasamy, S. J. Vannucci, S. S. D. Yan, K. Herold, S. F. Yan, and A. M. Schmidt Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation Glycobiology, July 1, 2005; 15(7): 16R - 28R. [Abstract] [Full Text] [PDF]
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I. E. Dumitriu, P. Baruah, B. Valentinis, R. E. Voll, M. Herrmann, P. P. Nawroth, B. Arnold, M. E. Bianchi, A. A. Manfredi, and P. Rovere-Querini Release of High Mobility Group Box 1 by Dendritic Cells Controls T Cell Activation via the Receptor for Advanced Glycation End Products J. Immunol., June 15, 2005; 174(12): 7506 - 7515. [Abstract] [Full Text] [PDF]
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L. Feng, C. Matsumoto, A. Schwartz, A. M. Schmidt, D. M. Stern, and J. Pile-Spellman Chronic Vascular Inflammation in Patients With Type 2 Diabetes: Endothelial biopsy and RT-PCR analysis Diabetes Care, February 1, 2005; 28(2): 379 - 384. [Abstract] [Full Text] [PDF]
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L. L. RONG, W. TROJABORG, W. QU, K. KOSTOV, S. D. YAN, C. GOOCH, M. SZABOLCS, A. P. HAYS, and A. M. SCHMIDT Antagonism of RAGE suppresses peripheral nerve regeneration FASEB J, December 1, 2004; 18(15): 1812 - 1817. [Abstract] [Full Text] [PDF]
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