Involvement of intermediary metabolites in the pathway of extracellular Ca2+-induced mitogen-activated protein kinase activation in human fibroblasts.
Involvement of intermediary metabolites in the pathway of extracellular Ca2+-induced mitogen-activated protein kinase activation in human fibroblasts.
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中间代谢物参与细胞外 Ca2 诱导的人成纤维细胞丝裂原激活蛋白激酶激活途径。
DOI：
10.1016/s0898-6568(98)00051-5
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发表时间：
1999
影响因子：
4.8
通讯作者：
McCormick,J
中科院分区：
文献类型：
--
作者：
Huang,S;Maher,VM;McCormick,J
Human fibroblasts in culture will grow in serum-free medium containing serum replacement factors, but without protein growth factors, as long as the Ca2+level is 1.0–2.0 mM. When the Ca2+is reduced to 0.1 mM, the cells stop cycling, but they can be reinduced to cycle by raising the Ca2+level to 1.0 mM Ca2+or to higher concentrations that result in activation of mitogen-activated protein kinase (MAPK). We now report that exposure of human fibroblasts to extracellular Ca2+increased the level of inositol (1,4,5)-trisphosphate in the cytoplasm and caused a transient rise in the concentration of intracellular free Ca2+. Ca2+-induced MAPK activation was partly abolished by treatment of the cells with pertussis toxin. It was also decreased by treatment of cells with thapsigargin, which depletes intracellular Ca2+stores; with phorbol 12-myristyl 13-acetate (PMA), which down-regulates protein kinase C (PKC); with the calmodulin antagonists N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide HCl (W-7), and calmidazolium (24571); as well as with lanthanum, a Ca2+channel inhibitor. Ca2+stimulation did not result in phosphorylation of the c-raf-1 protein. Our results suggest that extracellular Ca2+stimulates MAPK activation through a pathway(s) involving a pertussis toxin-sensitive G protein, phospholipase C, intracellular free Ca2+, calmodulin, and PKC.
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影响因子：
4
作者：
Estacion,M;Mordan,LJ
通讯作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
7.5
作者：
Hebert,SC;Brown,EM
通讯作者：
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参与人甲状旁腺和胎盘细胞滋养层细胞钙感应的蛋白质属于 LDL 受体蛋白超家族。
影响因子：
3.7
作者：
Stefan Lundgren;Göran Hjälm;P. Hellman;Bo Ek;C. Juhlin;J. Rastad;L. Klareskog;G. Åkerström;Lars Rask
通讯作者：
Lars Rask
DOI：
10.1073/pnas.90.11.4986
发表时间：
1993-06-01
影响因子：
11.1
作者：
SHORT, AD;BIAN, JH;GILL, DL
通讯作者：
GILL, DL