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Uni‐axial cyclic stretch induces c‐src activation and translocation in human endothelial cells via SA channel activation
Author(s) -
Naruse Keiji,
Sai Xaurui,
Yokoyama Nagao,
Sokabe Masahiro
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01528-2
Subject(s) - proto oncogene tyrosine protein kinase src , phosphorylation , chemistry , microbiology and biotechnology , extracellular , tyrosine kinase , biophysics , tyrosine phosphorylation , chromosomal translocation , signal transduction , biochemistry , biology , gene
The kinase activity of c‐src increased and peaked at 15 min after an application of uni‐axial cyclic stretch in HUVECs followed by a translocation of c‐src to Triton‐insoluble fraction. Suppression of c‐src by an antisense S ‐oligodeoxynucleotide inhibited the stretch‐induced tyrosine phosphorylation and morphological changes. The stretch‐induced increase in c‐src activity was inhibited by FK506, a specific inhibitor for calcineurin, by Gd 3+ , a blocker for stretch activated channels, and by the extracellular Ca 2+ depletion suggesting the involvement of SA channels. These results strongly suggest c‐src plays an important role in the downstream of SA channel activation followed by the morphological changes.