Artigo Revisado por pares

Roles of c‐Src and PKC in production of persistent calcium sparklet activity

2009; Wiley; Volume: 23; Issue: S1 Linguagem: Inglês

10.1096/fasebj.23.1_supplement.1000.19

ISSN

1530-6860

Autores

Jyoti Gulia, Peichun Gui, Jun‐Tzu Chao, Manuel F. Navedo, Luis F. Santana, Michael J. Davis,

Tópico(s)

Neuroscience and Neuropharmacology Research

Resumo

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.

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