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1 p44 MAPK/extracellular signal-regulated kinase 1 (ERK1)
3 mitogen-activated protein kinase (MAPK) and p44 MAPK, and membrane translocation of the protein kina
4 82% (immunoblot) after 48 hours, and p42 and p44 MAPK activities were reduced by 44% and 60%, respect
5 with dominant-interfering mutants of p42 and p44 MAPK failed to block phenylephrine-induced ANF expre
6 Immunoblotting confirmed labeling of p42 and p44 MAPK in untreated striatal synaptosomes and HEK 293
7 itiation of translation sites of the p42 and p44 MAPK isoform mRNAs was introduced into cultured card
12 ated kinases 1 and 2 (ERK1/2), also known as p44(MAPK) and p42(MAPK), respectively, are two of the ki
13 orylation of mitogen-activated kinases ERK1 (p44 MAPK) and ERK2 (p42 MAPK) within 5 min, which was bl
14 M-1 microM) elicits significant increases in p44(MAPK) (Erk1) and p42(MAPK) (Erk2) activities in cult
16 , MAP2K2 (MEK2), MAPK1 (p42 MAPK) and MAPK3 (p44 MAPK) phosphorylation in a dose-dependent manner.
18 we have demonstrated that p42 MAPK, but not p44 MAPK, is activated in area CA1 in response to LTP-in
19 tion of mitogen-activated protein kinase p42/p44 (MAPK(p42/p44)), cyclic adenosine monophosphate resp
23 itol 3-kinase, Akt/protein kinase B, and p42/p44 MAPK activation were unchanged in LAMD-SM and ELT3 c
24 uring mitosis, a select pool of MEK1 and p42/p44 MAPK becomes activated at the kinetochores and spind
25 es the Rap-1 G protein and the MEK-1 and p42/p44 MAPK enzymes but is independent of other NGF-activat
28 did not activate p42/p44 MAPK, and basal p42/p44 MAPK activity was not sufficient to account for phos
31 inds to Bim when it is phosphorylated by p42/p44 MAPK but does not interact with a nonphosphorylatabl
32 PK activation in FS-4 cells, we compared p42/p44 MAPK activation by TNF and epidermal growth factor (
34 ts of thrombin could be dissociated from p42/p44 MAPK activation, as selective inhibition of thrombin
37 eby sodium salicylate blocks TNF-induced p42/p44 MAPK activation may help to clarify TNF-activated si
38 KC activation is required for MP-induced p42/p44 MAPK, activation of the stress kinases p38 and JNK1
44 r study indicates that, independently of p42/p44 MAPK activation, PD184161 blocks mtROS generation by
48 to involve raft-dependent activation of p42/p44 MAPK and ligand-induced receptor recruitment to lipi
50 decanoylphorbol-13-acetate activation of p42/p44 MAPK drives Bim ubiquitination in mouse embryonic fi
52 46 blocked the S1P-induced activation of p42/p44 MAPK in airway smooth muscle cells, a response that
53 vation by TNF, blocked the activation of p42/p44 MAPK in response to TNF but not in response to EGF.
54 teins by EGF is blocked by inhibition of p42/p44 MAPK only in the presence of R5020, supporting a shi
58 cer and activator of transcription 3) or p42/p44 MAPK (mitogen-activated protein kinase) phosphorylat
59 lls results in direct activation of PKC, p42/p44 MAPK, p38 kinase, and c-Jun N-terminal kinase (JNK)
60 endent prostaglandin production by a PKC/p42/p44 MAPK/p38 kinase-sensitive pathway in which PI 3-kina
63 he data suggest that a kinase other than p42/p44 MAPK is involved in the estradiol-induced Ser118 pho
64 12 cells are exposed to hypoxia and that p42/p44 MAPK is a critical mediator of EPAS1 activation.
65 APK) after ischemia, and addition of the p42/p44 MAPK kinase (MEK) inhibitor PD98059 during reperfusi
66 lation site mutants were enhanced by the p42/p44 MAPK pathway but were defective in regulation by pro
69 and migration involves activation of the p42/p44 MAPK, possibly through regulation of the cytoskeleta
70 upport a role for TRIM2 in mediating the p42/p44 MAPK-dependent ubiquitination of Bim in rapid ischem
71 protein kinase C nor Gialpha link TNF to p42/p44 MAPK activation, because pretreatment of FS-4 cells
73 pid kinetics; 3) sustained activation of p42/p44 MAPKs lasting for at least 9 h; and 4) prolonged gen
75 PI3K protein, phosphoserine Akt, and p42/p44-MAPK were reduced, however, in both DCR and PF+Exe g
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