Alternative splicing of RAGE

Roles in biology and disease

Anastasia Z. Kalea, Ann Marie Schmidt, Barry Hudson

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

The Receptor for Advanced Glycation End-products (RAGE) is a complex, multi-ligand signaling system implicated in the pathogenesis of diabetes, cardiovascular disease and various cancers. RAGE undergoes extensive alternative splicing to produce a variety of transcripts with diverse functions, including soluble antagonists and variants with altered ligand binding domains. Studies focused on the major soluble variant (RAGEv1/esRAGE) have revealed this to function by binding RAGE-ligands and preventing activation of RAGE signaling in vascular and tumor cells. Furthermore, measurement of this variant in human serum has revealed that RAGEv1/esRAGE levels may represent a novel biomarker for RAGE-ligand related pathogenic states. Understanding the full plethora of RAGE alternative splicing and its regulation is central to elucidating the role of RAGE in biology and disease.

Original languageEnglish
Pages (from-to)2756-2770
Number of pages15
JournalFrontiers in Bioscience
Volume16
Issue number7
DOIs
StatePublished - Jun 1 2011

Fingerprint

Alternative Splicing
Ligands
Biomarkers
Medical problems
Advanced Glycosylation End Product-Specific Receptor
Blood Vessels
Tumors
Neoplasms
Cardiovascular Diseases
Chemical activation
Cells
Serum

Keywords

  • Advanced Glycation End-products
  • Alternative splicing
  • mRNA
  • Receptors
  • Review

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

Cite this

Alternative splicing of RAGE : Roles in biology and disease. / Kalea, Anastasia Z.; Schmidt, Ann Marie; Hudson, Barry.

In: Frontiers in Bioscience, Vol. 16, No. 7, 01.06.2011, p. 2756-2770.

Research output: Contribution to journalArticle

Kalea, Anastasia Z. ; Schmidt, Ann Marie ; Hudson, Barry. / Alternative splicing of RAGE : Roles in biology and disease. In: Frontiers in Bioscience. 2011 ; Vol. 16, No. 7. pp. 2756-2770.
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