Transforming growth factor β regulates the levels of different fibronectin isoforms in normal human cultured fibroblasts

Enrica Balza, Laura Borsi, Giorgio Allemanni, Luciano Zardi

Research output: Contribution to journalArticle

Abstract

Fibronectin (FN) polymorphism is caused by alternative splicing patterns in at least three regions of the primary transcript of a single gene. Using a monoclonal antibody (Mab) specific for an FN segment (ED-A), that can be included or omitted from the molecule depending on the pattern of splicing, we have examined whether transforming growth factor β (TGF-β) and dexamethasone, which are both known to increase the level of total FN, regulate the levels of different FN isoforms. We found that, while dexamethasone does not significantly change the ratio between the total FN and the ED-A containing FN, TGF-β preferentially increases the expression of the FN isoform containing the ED-A sequence.

Original languageEnglish
Pages (from-to)42-44
Number of pages3
JournalFEBS Letters
Volume228
Issue number1
DOIs
Publication statusPublished - Feb 8 1988

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Keywords

  • Fibronectin isoform
  • RNA splicing
  • Transforming growth factor β

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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