Liebermann D, Sachs L
Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.
Exp Cell Res. 1978 May;113(2):383-90. doi: 10.1016/0014-4827(78)90379-8.
Induction of neurite formation in neuroblastoma cells by dibutyryl cyclic 3':5'-AMP (db-cAMP) or prostaglandin EI (PGE1) was enhanced after enucleation. Cells selected for resistance to db-cAMP were induced to form neurites by db-cAMP or PGE1 only after, but not before enucleation. Inhibition of protein synthesis inhibited neurite induction in nucleated, but not in enucleated cells, and enucleated cells were less sensitive to inhibition of neurite formation by concanavalin A (ConA). Colchicine, vinblastine and cytochalasin B (CB), compounds that interfere with the assembly of microtubules and microfilaments, inhibited induction in both types of cells. It is suggested that enucleation removes a nuclear inhibitor of neurite induction by db-cAMP and PGE1, and that neurite induction in nucleated cells requires that cAMP activates the assembly of microtubules and microfilaments and inactivates the nuclear inhibitor.
去核后，二丁酰环3':5'-腺苷（db-cAMP）或前列腺素E1（PGE1）诱导神经母细胞瘤细胞形成神经突的能力增强。仅在去核后而非去核前，对db-cAMP具有抗性的细胞才会被db-cAMP或PGE1诱导形成神经突。蛋白质合成的抑制可抑制有核细胞中的神经突诱导，但对去核细胞无此作用，并且去核细胞对伴刀豆球蛋白A（ConA）抑制神经突形成的敏感性较低。秋水仙碱、长春碱和细胞松弛素B（CB）这些干扰微管和微丝组装的化合物，可抑制这两种类型细胞中的神经突诱导。有人提出，去核去除了db-cAMP和PGE1诱导神经突的核抑制剂，并且有核细胞中的神经突诱导需要cAMP激活微管和微丝的组装并使核抑制剂失活。
