β-Arrestin1 mediates nicotinic acid–induced flushing, but not its antilipolytic effect, in mice
J. Clin. Invest. 119:5 doi:10.1172/JCI36806 [Go to this article.]

Figure 6
Role of β-arrestin1 in binding and activation of cPLA₂.

(A) GPR109A-expressing HEK-293 cells were transfected with FLAG–β-arrestin1 or FLAG–β-arrestin2. Nicotinic acid stimulation increased binding of cPLA₂ to FLAG–β-arrestin1, but not FLAG–β-arrestin2. (B) Equivalent amounts of cPLA₂ and FLAG–β-arrestins were present in each whole cell lysate. Equal amounts of FLAG–β-arrestin were immunoprecipitated in control and nicotinic acid–treated samples. GPR109A-expressing HEK-293 cells were stimulated with 200 μM nicotinic acid, and cell lysates were analyzed for phosphorylated cPLA₂ at varying times. Agonist-stimulated activation of cPLA₂ in the presence of control siRNA, β-arrestin1 siRNA, or control siRNA plus either pertussis toxin or PD98059 (PD). (C) Binding of FLAG–β-arrestin to cPLA₂. *P = 0.0004 versus respective control. (D) Activation or phosphorylation of cPLA₂ in siRNA-treated cells. **P = 0.0085 versus respective 10-minute value; ***P = 0.0047 versus respective 0-minute value. Data are mean ± SEM of 3 independent experiments.