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Activation of endogenous c‐Src or a related tyrosine kinase by intracellular (pY)EEI peptide increases voltage‐operated calcium channel currents in rabbit ear artery cells
Author(s) -
Wijetunge S.,
Hughes A.D.
Publication year - 1996
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(96)01177-5
Subject(s) - proto oncogene tyrosine protein kinase src , tyrosine kinase , vascular smooth muscle , calcium , peptide , intracellular , calcium in biology , endogeny , chemistry , calcium channel , tyrosine , microbiology and biotechnology , kinase , biophysics , medicine , biochemistry , endocrinology , biology , smooth muscle , signal transduction , organic chemistry
The effect of activation of endogenous c‐Src tyrosine kinase by (pY)EEI peptide was examined on voltage‐operated calcium channel (VOC) currents in arterial smooth muscle cells. In single rabbit ear artery cells intracellular application of (pY)EEI peptide increased calcium channel currents. Inactive, non‐phosphorylated YEEI peptide had no effect on currents. Peptide‐A, a 21 amino acid inhibitor of c‐Src inhibited currents and prevented the effect of (pY)EEI peptide on calcium channel currents. These results indicate that activation of intrinsic c‐Src increases VOC and support a role for c‐Src in the regulation of VOC in vascular smooth muscle cells.