Garte S J
Biochem Biophys Res Commun. 1985 Dec 17;133(2):702-8. doi: 10.1016/0006-291x(85)90961-1.
The basal and isoproterenol stimulated levels of cyclic AMP in NIH3T3 and H-ras transformed NIH3T3 cells were equivalent. In exponentially growing cells, the phorbol ester 12-O-tetradecanoyl-13-acetate (TPA) inhibited the beta-adrenergic response of NIH3T3 cells, but not of the ras-transformed line. Another line of NIH3T3 cells transformed by a non-ras gene exhibited the normal loss of beta-adrenergic response by the tumor promoter. These results are consistent with a role for p21 in signal transduction related to the effects of TPA.
NIH3T3细胞及H-ras转化的NIH3T3细胞中环磷酸腺苷(cAMP)的基础水平及异丙肾上腺素刺激后的水平相当。在指数生长期的细胞中,佛波酯12-O-十四酰基-13-乙酸酯(TPA)抑制NIH3T3细胞的β-肾上腺素能反应,但不抑制ras转化细胞系的该反应。另一株由非ras基因转化的NIH3T3细胞系表现出肿瘤启动子使其β-肾上腺素能反应正常丧失。这些结果与p21在与TPA作用相关的信号转导中的作用一致。