Burgun C, Esteve L, Humblot N, Aunis D, Zwiller J
INSERM U338, Centre de Neurochimie, 5 rue Blaise Pascal, 67084, Strasbourg, France.
FEBS Lett. 2000 Nov 10;484(3):189-93. doi: 10.1016/s0014-5793(00)02153-0.
Stimulation of pheochromocytoma PC12 cells by cAMP-elevating agents caused the induction of the immediate early gene 3CH134, which encodes MAP kinase phosphatase-1 (MKP-1). Forskolin was as potent as serum in stimulating MKP-1 gene expression, whereas dibutyryl-cAMP and neuropeptide PACAP were less effective. Induction of the MKP-1 gene was accompanied by neo-synthesis of MKP-1 protein. MAP kinase activation was not involved in the cAMP-induced MKP-1 gene expression. The MAP kinase inactivation, that would result from MKP-1 induction in response to increased intracellular cAMP level, contributes to explain how hormones or neurotransmitters signaling through cAMP influence cell growth and differentiation.
能提高环磷酸腺苷（cAMP）水平的试剂刺激嗜铬细胞瘤PC12细胞，会诱导即早基因3CH134的表达，该基因编码丝裂原活化蛋白激酶磷酸酶-1（MKP-1）。福斯高林在刺激MKP-1基因表达方面与血清的效力相当，而二丁酰环磷腺苷和神经肽垂体腺苷酸环化酶激活肽（PACAP）的效果则较差。MKP-1基因的诱导伴随着MKP-1蛋白的重新合成。丝裂原活化蛋白激酶的激活不参与cAMP诱导的MKP-1基因表达。因细胞内cAMP水平升高而诱导产生MKP-1所导致的丝裂原活化蛋白激酶失活，有助于解释激素或神经递质通过cAMP发出的信号如何影响细胞生长和分化。
