The Ca2+-dependent exocytosis of enlargeosomes is greatly reinforced by genistein via a non-tyrosine kinase-dependent mechanism

Ilaria Prada, Emanuele Cocucci, Gabriella Racchetti, Jacopo Meldolesi

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Studies carried out by immunofluorescence, patch-clamping and FM dye fluorescence consistently showed that the Ca2+-induced exocytosis of enlargeosomes, specific vesicles expressed by many cell types, is strongly reinforced by pre-treatment of the cells with genistein, a wide spectrum blocker of tyrosine kinases, which also induces many additional effects. Various other blockers of tyrosine kinases, however, were ineffective, and the same occurred with drugs mimicking most of the rapid, non-tyrosine kinase-dependent effects of genistein. The reinforcement of enlargeosome-regulated exocytosis, therefore, is a new effect of genistein and a peculiar property of the enlargeosome exocytosis, not shared by analogous processes.

Original languageEnglish
Pages (from-to)4932-4936
Number of pages5
JournalFEBS Letters
Volume581
Issue number25
DOIs
Publication statusPublished - Oct 16 2007

Fingerprint

Genistein
Exocytosis
Phosphotransferases
Protein-Tyrosine Kinases
Constriction
Fluorescent Antibody Technique
Reinforcement
Coloring Agents
Fluorescence
Cells
Pharmaceutical Preparations
Therapeutics

Keywords

  • Desmoyokin/Ahnak
  • FM dye
  • Immunocytochemistry
  • Patch-clamping

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

The Ca2+-dependent exocytosis of enlargeosomes is greatly reinforced by genistein via a non-tyrosine kinase-dependent mechanism. / Prada, Ilaria; Cocucci, Emanuele; Racchetti, Gabriella; Meldolesi, Jacopo.

In: FEBS Letters, Vol. 581, No. 25, 16.10.2007, p. 4932-4936.

Research output: Contribution to journalArticle

Prada, Ilaria ; Cocucci, Emanuele ; Racchetti, Gabriella ; Meldolesi, Jacopo. / The Ca2+-dependent exocytosis of enlargeosomes is greatly reinforced by genistein via a non-tyrosine kinase-dependent mechanism. In: FEBS Letters. 2007 ; Vol. 581, No. 25. pp. 4932-4936.
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