alexa Synaptotagmin-1 is required for fibroblast growth factor-1 release.
Cardiology

Cardiology

Angiology: Open Access

Author(s): LaVallee TM

Abstract Share this page

By using p65 synaptotagmin-1 and fibroblast growth factor (FGF)-1:beta-galactosidase (beta-gal) NIH 3T3 cell co-transfectants, we demonstrate that a proteolytic fragment consisting of the extravesicular domain of synaptotagmin-1 is released into the extracellular compartment in response to temperature stress with similar kinetics and pharmacological properties as FGF-1:beta-gal. Using a deletion mutant that lacks 95 amino acids from the extravesicular domain of synaptotagmin-1, neither synaptotagmin-1 nor FGF-1:beta-gal are able to access the stress-induced release pathway. Furthermore, the p40 extravesicular fragment of synaptotagmin-1 is constitutively released in p40 synaptotagmin-1 NIH 3T3 cell transfectants, and this release is potentiated when the cells are subjected to temperature stress. These data demonstrate that the p40 fragment derived from synaptotagmin-1 is able to utilize the FGF-1 non-classical exocytotic pathway and that the release of FGF-1 is dependent on synaptotagmin-1.

This article was published in J Biol Chem and referenced in Angiology: Open Access

Relevant Expert PPTs

Relevant Speaker PPTs

Recommended Conferences

  • International Conference on Vascular Biology & Medicine
    July 24-25, 2017 Chicago, USA
  • International Conference on Angiology
    Oct 16-17, 2017, Budapest, Hungary
  • 21st International Conference on Clinical & Experimental Cardiology
    October 16-18, 2017 Chicago, USA

Relevant Topics

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords