Bozou J C, Couvineau A, Rouyer-Fessard C, Laburthe M, Vincent J P, Kitabgi P
FEBS Lett. 1987 Jan 26;211(2):151-4. doi: 10.1016/0014-5793(87)81426-6.
Treatment of HT29 cells with the tumor promoting phorbol ester PMA resulted in an attenuation of VIP-stimulated cAMP production in intact cells and VIP-stimulated adenylate cyclase activity in cell membranes. PMA did not decrease the ability of cholera toxin and forskolin to elevate cAMP levels in intact cells. Fluoride-stimulated adenylate cyclase activity in HT29 cells homogenates was not affected by PMA. The maximal VIP binding capacity of homogenates prepared from HT29 cells treated with PMA was decreased by 50%. It is concluded that protein kinase C regulates VIP receptor function possibly through phosphorylation of the VIP receptor.
用促肿瘤佛波酯PMA处理HT29细胞，导致完整细胞中VIP刺激的cAMP生成以及细胞膜中VIP刺激的腺苷酸环化酶活性减弱。PMA并未降低霍乱毒素和福斯高林升高完整细胞中cAMP水平的能力。PMA不影响HT29细胞匀浆中氟化物刺激的腺苷酸环化酶活性。用PMA处理的HT29细胞制备的匀浆的最大VIP结合能力降低了50%。得出的结论是，蛋白激酶C可能通过VIP受体的磷酸化来调节VIP受体功能。
