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1 inase cascade which include RAF-1, MEK-1 and p42 MAP kinase.
2 like Rsk1, forms a heteromeric complex with p42 MAP kinase.
3 llin, and extracellular-related kinase 2 (or p42 MAP kinase) accounted for the major changes occurrin
9 pproximately 95% with specific inhibitors of p42 MAP kinase and p38 SAP kinase function, respectively
10 the Rsk2 isozyme in the M phase functions of p42 MAP kinase and provide tools for further examining R
11 to be essential for Ag-induced activation of p42 MAP kinase and release of arachidonic acid were unaf
12 ndicate that the sustained activation of p44/p42 MAP kinase and subsequent arachidonate release by cy
13 AP kinase negatively regulated activation of p42 MAP kinase and the responses mediated by this kinase
15 with PD 098059 and SB 203580 indicated that p42 MAP kinase, but not p38 MAP kinase, contributed to t
18 ransduction molecules, including Akt and p44/p42 MAP kinases, by both EGF and IGF, whereas each indiv
25 the rapid but transient activation of ERK2 (p42 MAP kinase) in CD34(+) cells, and we used the MAP ki
27 Mos-induced Cdc2 activation requires active p42 MAP kinase, is inhibited by a MAP kinase phosphatase
28 opus oocyte extract system demonstrated that p42 MAP kinase (MAPK) exhibits a sharp, sigmoidal stimul
30 he inhibition or the depletion of endogenous p42 MAP kinase resulted in defective spindle structures
31 ucleotide phosphate (NADPH)-oxidase, via p44/p42 MAP kinase signaling, and upregulated pro-fibrotic g
33 In PHX cells, the ability of PHE to activate p42 MAP kinase was dramatically reduced, whereas ISO bec
34 phosphorylation of Stat1 and Stat3, whereas p42 MAP kinase was phosphorylated regardless of the pres
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