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New insights on disintegrin-receptor interactions: eristostatin and melanoma cells.

Abstract
Viper venom disintegrins have been used frequently to study the cellular receptors which characterize various types of cells, including platelets, endothelial cells and cancer cells. While the majority of such analyses have pointed to involvement of integrin receptors alphavbeta3, alpha5beta1 or alphaIIbbeta3, this may not always be so. Eristostatin, from Eristocophis macmahoni, is a potent inhibitor of ADP-induced platelet aggregation as well as of human and murine melanoma metastases in mouse model systems. This disintegrin requires an RGDW motif, as well as an intact C-terminus, in order to interact with both platelets and four different types of melanoma cells. Eristostatin causes nonmetastatic SBc12 melanoma cells to show higher susceptibility to specific killing by NK-like TALL-104 cells. While it is known that eristostatin binds to alphaIIbbeta3 on platelets, the receptor with which eristostatin binds to the melanoma cells has not yet been identified.
AuthorsM A McLane, M A Kuchar, C Brando, D Santoli, C A Paquette-Straub, M E Miele
JournalHaemostasis (Haemostasis) 2001 May-Dec Vol. 31 Issue 3-6 Pg. 177-82 ISSN: 0301-0147 [Print] Switzerland
PMID11910183 (Publication Type: Journal Article)
CopyrightCopyright 2002 S. Karger AG, Basel
Chemical References
  • Disintegrins
  • Integrins
  • Oligopeptides
  • Peptides
  • Platelet Aggregation Inhibitors
  • Viper Venoms
  • eristostatin
  • arginyl-glycyl-aspartyl-tryptophan
Topics
  • Binding Sites
  • Cytotoxicity, Immunologic (drug effects)
  • Disintegrins (metabolism)
  • Humans
  • Integrins (metabolism)
  • Killer Cells, Natural (immunology)
  • Melanoma (pathology)
  • Neoplasm Metastasis (prevention & control)
  • Oligopeptides
  • Peptides (genetics, metabolism, pharmacology)
  • Platelet Aggregation Inhibitors (metabolism)
  • Protein Binding
  • Tumor Cells, Cultured (drug effects)
  • Viper Venoms (genetics, metabolism, pharmacology)

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