Down-regulation of protein kinase C activity preferentially attenuates high K(+)-stimulated tyrosine hydroxylase activity in adrenal chromaffin cells cultured with insulin-like growth factor-I.
Down-regulation of protein kinase C activity preferentially attenuates high K(+)-stimulated tyrosine hydroxylase activity in adrenal chromaffin cells cultured with insulin-like growth factor-I.
复制标题
在用胰岛素样生长因子-I 培养的肾上腺嗜铬细胞中，蛋白激酶 C 活性的下调优先减弱高 K( ) 刺激的酪氨酸羟化酶活性。
DOI：
10.1016/0304-3940(95)12144-7
复制
发表时间：
1995
影响因子：
2.5
通讯作者：
Dahmer,MK
中科院分区：
文献类型：
--
作者：
Dahmer,MK
本研究的目的是确定肾上腺嗜铬细胞蛋白激酶C（PKC）的丢失是否影响高K+和毛喉素刺激的酪氨酸羟化酶（酪氨酸3-单加氧酶，EC 1.14.16.2）活性的增强，在用胰岛素样生长因子-I（IGF-I）处理的细胞中观察到。毛喉素刺激的酪氨酸羟化酶的激活不受PKC下调的影响。高K+刺激的酪氨酸羟化酶活性大幅下降后，处理的细胞与活性，但不是无活性的，佛波酯（300 nM）。在PKC下调后，与无IGF-I培养的细胞中的36 ± 8%（n = 14）相比，在有IGF-I培养的细胞中的高K+刺激的酪氨酸羟化酶活性降低了61 ± 5%（n = 14）。这些数据表明，PKC是所需的高K+刺激的酪氨酸羟化酶活性的增强与IGF-I治疗观察。
The purpose of this study was to determine whether the loss of protein kinase C (PKC) from adrenal chromaffin cells affected the enhancement of high K+- and forskolin-stimulated tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2) activity observed in cells treated with insulin-like growth factor-I (IGF-I). Forskolin-stimulated tyrosine hydroxylase activation was not affected by down-regulation of PKC. High K+-stimulated tyrosine hydroxylase activity decreased substantially after treating the cells for ∼18 h with active, but not inactive, phorbol ester (300 nM). After down-regulation of PKC, high K+-stimulated tyrosine hydroxylase activity in cells cultured with IGF-I decreased by 61 ± 5% (n = 14) compared to 36 ± 8% (n = 14) in cells cultured without IGF-I. These data suggest that PKC is required for the enhancement of high K+-stimulated tyrosine hydroxylase activity observed with IGF-I treatment.