神经生长因子通过环磷酸腺苷依赖性蛋白激酶起作用，以增加PC12细胞中钠通道的数量。
Nerve growth factor acts through cAMP-dependent protein kinase to increase the number of sodium channels in PC12 cells.
作者信息
Kalman D, Wong B, Horvai A E, Cline M J, O'Lague P H
机构信息
Department of Biology, University of California, Los Angeles 90024.
出版信息
Neuron. 1990 Mar;4(3):355-66. doi: 10.1016/0896-6273(90)90048-k.
cAMP-dependent protein kinase (PKA) and phospholipid-dependent protein kinase (PKC) play a role in nerve growth factor (NGF)-mediated differentiation. In PC12 cells, NGF causes neurite outgrowth and increases the number of voltage-gated Na+ channels. Neurite outgrowth involves in part activation of PKC. How NGF regulates Na+ channel number is unknown. Using patch-clamp techniques, we find that agents activating PKC, including phorbol esters and a ras oncogene product (p21) that induces neurites, caused little increase in channel number. In contrast, agents increasing intracellular cAMP were as effective as NGF. A specific protein inhibitor of the PKA catalytic subunit blocked increases by NGF or cAMP. Thus, NGF increases Na+ channel number in PC12 cells in part by activating PKA but apparently not PKC.
环磷酸腺苷依赖性蛋白激酶（PKA）和磷脂依赖性蛋白激酶（PKC）在神经生长因子（NGF）介导的分化过程中发挥作用。在PC12细胞中，NGF可导致神经突生长并增加电压门控性Na⁺通道的数量。神经突生长部分涉及PKC的激活。NGF如何调节Na⁺通道数量尚不清楚。使用膜片钳技术，我们发现激活PKC的试剂，包括佛波酯和一种诱导神经突的ras癌基因产物（p21），对通道数量的增加作用很小。相比之下，增加细胞内cAMP的试剂与NGF的效果相同。PKA催化亚基的一种特异性蛋白抑制剂可阻断NGF或cAMP引起的增加。因此，NGF部分通过激活PKA而非PKC来增加PC12细胞中的Na⁺通道数量。
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