Monaco M E, Mufson R A
Biochem J. 1986 May 15;236(1):171-5. doi: 10.1042/bj2360171.
WRK-1 rat mammary tumour cells respond to vasopressin with increased accumulation of inositol phosphates as well as increased precursor incorporation into phosphatidylinositol. The phorbol ester, phorbol 13-myristate 12-acetate (PMA) inhibits by 80% both inositol phosphate accumulation and increased precursor incorporation. This inhibition is much less evident at early times (2 min) than at later times (25 min). The vasopressin-induced rise in cytosolic free Ca2+ is inhibited in a similar manner. Oleoylacetylglycerol is inactive with respect to inhibition of vasopressin-induced increases in incorporation of 32P into phosphoinositides. PMA has no effect on vasopressin binding at saturating concentrations of the hormone and does not affect the binding affinity.
WRK - 1大鼠乳腺肿瘤细胞对血管加压素产生反应，表现为肌醇磷酸积累增加以及前体掺入磷脂酰肌醇增加。佛波酯，即佛波醇13 - 肉豆蔻酸酯12 - 乙酸酯（PMA）可抑制80%的肌醇磷酸积累和增加的前体掺入。这种抑制在早期（2分钟）比后期（25分钟）不太明显。血管加压素诱导的胞质游离Ca2 +升高以类似方式受到抑制。油酰乙酰甘油对抑制血管加压素诱导的32P掺入磷酸肌醇没有作用。在激素饱和浓度下，PMA对血管加压素结合没有影响，也不影响结合亲和力。
