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Roles of c‐Src and PKC in production of persistent calcium sparklet activity
Author(s) -
Gulia Jyoti,
Gui Peichun,
Chao JunTzu,
Navedo Manuel F,
Santana Luis F,
Davis Michael J
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1000.19
Subject(s) - phosphorylation , protein kinase c , proto oncogene tyrosine protein kinase src , chemistry , calcium , kinase , cav1.2 , microbiology and biotechnology , calcium channel , biophysics , biochemistry , biology , organic chemistry
The L‐type calcium channel (Cav1.2) is regulated by multiple kinases, including PKA and c‐Src, which phosphorylate the Cav1.2 C‐terminus at residues S 1901 and Y 2122 (Cav1.2c), respectively, to enhance Ca 2+ entry. PKC also enhances Cav1.2 current under some conditions and promotes persistent Cav1.2 Ca 2+ sparklet activity (quantal Ca 2+ entry events); however, the PKC phosphorylation site is unclear. We addressed two questions using TIRF microscopy to measure Ca 2+ sparklets in patch clamped HEK cells expressing Cav1.2c. 1) Does PKC produce persistent calcium sparklet activity through phosphorylation of S 1901 ? 2) Is c‐Src involved in the production of persistent sparklet activity? Persistent sparklets (indicating a prolonged channel opening state) were defined as nPs > 0.2, where n= # of quantal levels and Ps= probability that a given sparklet site was active. Our results suggest that both PKC and c‐Src promote persistent calcium sparklet activity, possibly by phosphorylating residue Y 2122 rather than S 1901 on Cav1.2c.