Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling.

  title={Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling.},
  author={Anastasia Z. Kalea and Fiona See and Evis Harja and Mar{\'i}a del Mar Arriero and Ann Marie Schmidt and Barry I. Hudson},
  journal={Cancer research},
  volume={70 13},
Receptor for advanced glycation end products (RAGE) and its ligands are overexpressed in multiple cancers. RAGE has been implicated in tumorigenesis and metastasis, but little is known of the mechanisms involved. In this study, we define a specific functional role for an alternate splice variant termed RAGE splice variant 1 (RAGEv1), which encodes a soluble endogenous form of the receptor that inhibits tumorigenesis. RAGEv1 was downregulated in lung, prostate, and brain tumors relative to… CONTINUE READING


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Publications referenced by this paper.
Showing 1-10 of 40 references

Identification, classification, and expression of RAGE gene splice variants.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology • 2008
View 2 Excerpts

Interaction of the RAGE cytoplasmic domain with diaphanous-1 is required for ligand-stimulated cellular migration through activation of Rac1 and Cdc42

BI Hudson, AZ Kalea, MD Arriero
J Biol Chem 2008;283:34457–68 • 2008
View 1 Excerpt

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