Liu A Y, Kamalakannan V, Chen K Y
Biochim Biophys Acta. 1987 Apr 22;928(2):235-9. doi: 10.1016/0167-4889(87)90126-1.
We have characterized and quantitated the level of cAMP-dependent protein kinase in the NS-20, N1E-115, N-18 and N1A-103 mouse neuroblastoma clonal cell lines, and we have correlated the occurrence of functional cAMP-dependent protein kinase with the dibutyryl cAMP-induced differentiated functions in these cells. Our results demonstrate the presence of functional cAMP-dependent protein kinase in extracts of all four cell lines examined, including the 'neurite minus' N1A-103 cell line. Dibutyryl cAMP induced neurite outgrowth and acetylcholinesterase activity in the NS-20, N1E-115 and N-18 neuroblastoma cell lines, but not in the N1A-103 cell line. However, dibutyryl cAMP caused a 2-3-fold increase in the R1 regulatory subunit protein and cAMP-phosphodiesterase activity in the 'neurite minus' N1A-103 cells in a manner similar to that of the other three 'neurite positive' cell lines. These results suggest that the biochemical lesion(s) subserving the neurite-minus phenotype of the N1A-103 cells may be distal to the activation of cAMP-dependent protein kinase and is in a biochemical pathway distinct from the induction of R1 regulatory subunit protein and cAMP-phosphodiesterase activity.
我们已经对NS - 20、N1E - 115、N - 18和N1A - 103小鼠神经母细胞瘤克隆细胞系中cAMP依赖性蛋白激酶的水平进行了表征和定量，并且将功能性cAMP依赖性蛋白激酶的出现与这些细胞中双丁酰cAMP诱导的分化功能相关联。我们的结果表明，在所检测的所有四种细胞系的提取物中都存在功能性cAMP依赖性蛋白激酶，包括“无神经突”的N1A - 103细胞系。双丁酰cAMP在NS - 20、N1E - 115和N - 18神经母细胞瘤细胞系中诱导神经突生长和乙酰胆碱酯酶活性，但在N1A - 103细胞系中则不然。然而，双丁酰cAMP使“无神经突”的N1A - 103细胞中的R1调节亚基蛋白和cAMP磷酸二酯酶活性增加了2至3倍，其方式与其他三种“有神经突”的细胞系类似。这些结果表明，导致N1A - 103细胞无神经突表型的生化损伤可能位于cAMP依赖性蛋白激酶激活的下游，并且处于与R1调节亚基蛋白和cAMP磷酸二酯酶活性诱导不同的生化途径中。
