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1 e p70(S6K) and their ability to activate the JNK mitogen-activated protein kinase.
2 ctin polymerization, cell proliferation, and JNK/mitogen-activated protein kinase activation, conceiv
3 the p38, extracellular regulated kinase 1/2, JNK, mitogen-activated protein kinase, and NF-kappaB sig
4 At the same time, HSV activated the p38 and JNK mitogen-activated protein kinases as well as the dow
5 requires the activation of both the ERK and JNK mitogen-activated protein kinase cascade and is inde
6 Activation of the Jun amino-terminal kinase (JNK) mitogen-activated protein kinase cascade after T ce
8 ability to elicit phosphorylation of p38 and JNK mitogen-activated protein kinases, IkappaB-alpha deg
9 aling via the Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase in middle ear muco
11 ponents of the JNK signaling pathway, namely JNK, mitogen-activated protein kinase kinase 7, and mixe
12 of the JNK pathway, including phosphorylated JNKs, mitogen-activated protein kinase kinase 4, mitogen
13 lthough an important contribution of ERK and JNK mitogen-activated protein kinase (MAPK) activation i
14 activity by suppressing the ERK1/2, p38, and JNK mitogen-activated protein kinase (MAPK) pathways.R-P
15 y activation of the c-Jun-N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) cascade.
16 of a conserved c-jun amino-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) module, as
17 tion of the p38/c-Jun NH(2)-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) signaling p
18 ulated kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)] were asse
20 n we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessa
22 RK), p38, and Jun N-terminal protein kinase (JNK) mitogen-activated protein kinases (MAPKs) has been
23 d protein kinase/Jun N-terminal kinase (SAPK/JNK) mitogen-activated protein kinases (MAPKs) in DCs.
25 activation of p38/Jun NH(2)-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs), enhanced
26 ons upstream of the c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase module in Drosophi
28 human aortic endothelial cells, the PKCbeta-JNK mitogen-activated protein kinase pathway importantly
29 , a block has been identified in the ERK and JNK mitogen-activated protein kinase pathways; the block
30 / p44 ERK, p38, and to a lesser extent, SAPK/JNK mitogen-activated protein kinase phosphorylation.
31 antibody-induced hyperactivation of ERK and JNK mitogen activated protein kinase signaling pathways
32 while expression and phosphorylation of the JNK mitogen-activated protein kinase was not observed fo
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