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1                                              p44 MAPK/extracellular signal-regulated kinase 1 (ERK1)
2 ration, GD3 recruits superoxides to activate p44 MAPK and stimulates cell proliferation.
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
8                 The levels of actin, p42 and p44 MAPK, JNK1, JNK2, p38, and PCNA were not substantial
9                   Phosphorylation of p42 and p44 MAPKs, which can be prevented by a mitogen-activated
10       MEKK1 is a strong activator of p42 and p44 MAPKs.
11 so blocked by specific inhibition of p42 and p44 MAPKs.
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
15       For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor
16 , MAP2K2 (MEK2), MAPK1 (p42 MAPK) and MAPK3 (p44 MAPK) phosphorylation in a dose-dependent manner.
17         We have found that p42 MAPK, but not p44 MAPK, is activated in area CA1 following direct stim
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
20               Estradiol did not activate p42/p44 MAPK, and basal p42/p44 MAPK activity was not suffic
21 antibody against phosphorylated (active) p42/p44 MAPK.
22 bited by MAPKK inhibitor U0126, although p42/p44 MAPK was phosphorylated.
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
26 on involves activation of mitoK(ATP) and p42/p44 MAPK.
27 -1alpha-independent and requires PKC and p42/p44 MAPK.
28 did not activate p42/p44 MAPK, and basal p42/p44 MAPK activity was not sufficient to account for phos
29                                 Blocking p42/p44 MAPK activation following preconditioning ischemia w
30 otein expression, which is controlled by p42/p44 MAPK activity and H(2)O(2).
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 (
33 ctivation of the bulk of the cytoplasmic p42/p44 MAPK.
34 ts of thrombin could be dissociated from p42/p44 MAPK activation, as selective inhibition of thrombin
35 ctivated protein kinase kinase (MAPKK)-->p42/p44 MAPK.
36 cription by Cch involved the independent p42/p44 MAPK and PKC pathways.
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
39 nin and LY294002 also blocked MP-induced p42/p44 MAPK, p38, and JNK1 phosphorylation.
40  toxin to block Gialpha does not inhibit p42/p44 MAPK activation by TNF.
41 n of CaMKII were prevented by inhibiting p42/p44 MAPK.
42 at the p55 TNFR is sufficient to mediate p42/p44 MAPK activation.
43 phorylation correlated with the onset of p42/p44 MAPK activation by these agents.
44 r study indicates that, independently of p42/p44 MAPK activation, PD184161 blocks mtROS generation by
45  receptor complex and the stimulation of p42/p44 MAPK and cell migration in response to PDGF.
46                   Finally, activation of p42/p44 MAPK and induction of p21(waf1/cip1) were cGMP-indep
47 C with NO or DFMO leads to activation of p42/p44 MAPK and induction of p21(waf1/cip1).
48  to involve raft-dependent activation of p42/p44 MAPK and ligand-induced receptor recruitment to lipi
49           While MP-induced activation of p42/p44 MAPK and p38 kinase is transient, a sustained activa
50 decanoylphorbol-13-acetate activation of p42/p44 MAPK drives Bim ubiquitination in mouse embryonic fi
51 ls exposed to I/R, whereas inhibition of p42/p44 MAPK had no effect.
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
55 tol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C.
56        While tyrosine phosphorylation of p42/p44 MAPK was detected almost immediately (30 s) after st
57                            Activation of p42/p44 MAPK was determined by Western blot analysis with an
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
61                    FPTIII also prevented p42/p44 MAPK activation and DNA synthesis in response to pla
62 d ODQ inhibited phenylephrine-stimulated p42/p44 MAPK activation.
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
67           This finding suggests that the p42/p44 MAPK pathway is involved in the inhibition of RASMC
68 n involved the PKC/Ca2+ pathway, not the p42/p44 MAPK pathway.
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
72 a receptor kinase to transmit signals to p42/p44 MAPK in response to PDGF.
73 pid kinetics; 3) sustained activation of p42/p44 MAPKs lasting for at least 9 h; and 4) prolonged gen
74 s largely dependent on the activation of p42/p44 MAPKs.
75     PI3K protein, phosphoserine Akt, and p42/p44-MAPK were reduced, however, in both DCR and PF+Exe g
76 transcription factor c-fos downstream to the p44 MAPK signaling cascade.

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