Bartholin Institute, Rigshospitalet, Copenhagen, Denmark.
FEBS Lett. 2010 Jan 4;584(1):81-5. doi: 10.1016/j.febslet.2009.10.086.
A-kinase anchoring proteins (AKAPs) are known to compartmentalise protein kinase(s) to discrete cellular locations. Here we show that silencing of AKAP 18 alpha or gamma expression results in decreased or increased glucose-stimulated insulin secretion in INS-1E cells. Glucose stimulates AKAP 18 alpha and inhibits AKAP 18 gamma mRNA expressions while palmitate markedly reduces AKAP 18 alpha expression. Human growth hormone (GH) stimulates AKAP 18 alpha expression and attenuates palmitate-induced suppression of AKAP 18 alpha mRNA level. The roles of AKAP 18 alpha and gamma in mediating insulin release are consistent with their respective regulations by glucose.
蛋白激酶锚定蛋白(AKAPs)可将蛋白激酶分隔到特定的细胞位置。本文研究发现沉默 AKAP18α 或γ表达可导致 INS-1E 细胞葡萄糖刺激的胰岛素分泌减少或增加。葡萄糖刺激 AKAP18α,抑制 AKAP18γ mRNA 表达,而棕榈酸则显著降低 AKAP18α 的表达。人生长激素(GH)刺激 AKAP18α 表达,并减弱棕榈酸对 AKAP18α mRNA 水平的抑制作用。AKAP18α 和 γ 在介导胰岛素释放中的作用与其各自受葡萄糖调节的作用一致。