Fibronectin type I repeat is a nonactivating ligand for EphA1 and inhibits ATF3-dependent angiogenesis

Junko Masuda, Ryosuke Usui, Yoshiro Maru

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

ATF3 stimulated promoter activity of EphA1 by 3.4-fold in ATF3-dependent angiogenesis in vitro. Although tyrosine kinase activation of EphA1 was dispensable, binding of EphA1 to fibronectin through its type I repeat played an essential role in the angiogenesis. Recombinant proteins containing fibronectin 10th to 12th type I repeat (I 10-12) but not I 12 could inhibit the angiogenesis in vitro by competitively targeting EphA1 with the full-length fibronectin. However, I 12 acquired a higher affinity toward EphA2 with K d 18 nM and inhibited vascular endothelial growth factor-dependent angiogenic invasion in a Matrigel plug assay.

Original languageEnglish
Pages (from-to)13148-13155
Number of pages8
JournalJournal of Biological Chemistry
Volume283
Issue number19
DOIs
Publication statusPublished - May 9 2008
Externally publishedYes

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Fibronectins
Ligands
Recombinant Proteins
Protein-Tyrosine Kinases
Vascular Endothelial Growth Factor A
Assays
Chemical activation
In Vitro Techniques

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

Fibronectin type I repeat is a nonactivating ligand for EphA1 and inhibits ATF3-dependent angiogenesis. / Masuda, Junko; Usui, Ryosuke; Maru, Yoshiro.

In: Journal of Biological Chemistry, Vol. 283, No. 19, 09.05.2008, p. 13148-13155.

Research output: Contribution to journalArticle

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