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2 cyte proliferation and dedifferentiation via mitogen-activated protein kinase 1,2 (MAPK1,2) activatio
3 activation of extracellular signal-regulated mitogen-activated protein kinase 1/2 (ERK 1/2(MAPK)) use
4 t3 and extracellular signal-regulated kinase/mitogen-activated protein kinase 1/2 (pErk1/2(MAPK)).
6 at activation of VEGFR1 by VEGFB to increase mitogen-activated protein kinase 1/2 phosphorylation and
7 reased in melanoma cells, when (V600E)B-RAF, mitogen-activated protein kinase 1/2, or extracellular s
9 naling response as assessed by extracellular mitogen-activated protein kinase 1 and 2 (ERK1/2) phosph
10 th atRA and forskolin suppressed HIV-induced mitogen-activated protein kinase 1 and 2 and Stat3 phosp
12 -1 and activation of extracellular-regulated/mitogen-activated protein kinases 1 and 2 in untransfect
13 -1 and activation of extracellular-regulated/mitogen-activated protein kinases 1 and 2 in untransfect
14 rax lethal toxin fails to cleave its target, mitogen-activated protein kinase 1, and anthrax edema to
17 identified MEK5, the MAPK kinase in the big mitogen-activated protein kinase 1 (BMK1)/ERK5 pathway,
18 d phosphorylation of RSK, whereas inhibiting mitogen-activated protein kinase 1 does not affect phosp
19 g, as well as short interfering RNA-mediated mitogen-activated protein kinase-1 down-regulation, show
20 patocyte proliferation, through signaling by mitogen-activated protein kinase 1 (ERK) and the transcr
23 sufficient roles have been described for the mitogen activated protein kinase(1) (MAPK) signaling pat
24 s, hyperglycemia stimulated proliferation by mitogen-activated protein kinase 1 (MAPK1)- and MAPK3-de
27 bition of either receptor with inhibitors of mitogen-activated protein kinase 1 or phosphatidylinosit
28 cellular signal-regulated kinase 1/2 and big mitogen-activated protein kinase 1 signaling pathways le
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