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1 cellular signal-regulated kinase 1/2 and the c-Jun amino-terminal kinase.
2 ression was reduced, including the genes for c-Jun amino-terminal kinase.
3 as well as the activation of the downstream c-Jun amino-terminal kinase.
4 f MKP-1 was associated with an activation of c-Jun amino-terminal kinase.
5 fferentiation and constitutive activation of c-Jun amino-terminal kinase.
6 ty of rac proteins to activate the family of c-jun amino-terminal kinases.
7 ated protein kinase 1 (ERK1)/ERK2 as well as c-Jun amino-terminal kinase 1 (JNK1)/stress-activated pr
8 Expression of the dominant negative form of c-Jun amino-terminal kinase 1 blocked both the activatio
9 ransection resulted in chronic activation of c-Jun amino-terminal kinase-1 (JNK) in L4/L5 DRGs concom
11 comitant reduction in the phosphorylation of c-jun amino-terminal kinase, a serine threonine kinase a
12 ream of the p53 response and upstream of the c-Jun amino-terminal kinase activation in DNA damage-ind
16 verexpression of RAFTK induces activation of c-Jun amino-terminal kinase (also known as stress-activa
17 ility of DUSP1/MKP-1 to dephosphorylate ERK, c-Jun amino-terminal kinase and p38 in the cell nucleus.
18 inal kinase 1 blocked both the activation of c-Jun amino-terminal kinase and the induction of endoder
19 tive oxygen species that cause activation of c-Jun amino-terminal kinase and transcription factor For
20 racellular signal-regulated protein kinases, c-Jun amino-terminal kinases and p38 MAP kinases, which
22 differentiation and sustained activation of c-Jun amino-terminal kinase, but not of ERK1,2 or of p38
23 C-1 and was not accompanied by disruption of c-Jun amino-terminal kinase-dependent signaling events r
24 PAK1 could be dissociated from activation of c-Jun amino-terminal kinase, even though activation of b
25 3 kinase, mammalian target of rapamycin, and c-Jun amino-terminal kinase failed to block NO donor-ind
27 ogen stimulation of cytoskeletal changes and c-jun amino-terminal kinases is mediated by Rac small gu
30 lar signal regulated kinase (ERK1/2) and the c-Jun amino terminal kinase (JNK) signaling pathways.
32 e formation of long filopodia; (2) activated c-Jun amino terminal kinase (JNK); (3) activated serum r
33 ne-expanded huntingtin induces apoptosis via c-Jun amino-terminal kinase (JNK) activation in HN33 cel
34 hypothesis that arachidonic acid stimulates c-jun amino-terminal kinase (JNK) activity in the murine
35 ained increase of intracellular ceramide and c-Jun amino-terminal kinase (JNK) activity, which are th
38 rt that NF-kappaB complexes downregulate the c-Jun amino-terminal kinase (JNK) cascade, thus establis
39 expression of c-Jun protein, as well as the c-Jun amino-terminal kinase (JNK) group of mitogen-activ
40 cate that glutamate toxicity may involve the c-Jun amino-terminal kinase (JNK) group of mitogen-activ
46 kinase kinase (MAP3K) that can regulate the c-Jun amino-terminal kinase (JNK) MAP kinase cascade.
47 ting kinase (NIK) specifically activates the c-Jun amino-terminal kinase (JNK) mitogen-activated prot
48 osure requires the activation of a conserved c-jun amino-terminal kinase (JNK) mitogen-activated prot
49 ogen-activated protein kinase (ERK), but not c-jun amino-terminal kinase (JNK) or p38, in a dose- and
53 ure (DC) requires both integrin function and c-Jun amino-terminal kinase (JNK) signaling for opposed
56 om mice had lost or altered responses of the c-Jun amino-terminal kinase (JNK) to microtubule disrupt
58 ffect of angiotensin II (Ang II) to activate c-Jun amino-terminal kinase (JNK) was studied in a Chine
59 the phosphorylated protein levels of p38 and c-Jun amino-terminal kinase (JNK) were significantly inc
65 vated protein kinase superfamily, designated c-Jun amino-terminal kinase (JNK), has been recently ide
66 togen-activated protein (MAP) kinase family, c-Jun amino-terminal kinase (JNK), p38 MAP kinase (p38),
67 and dose-related activation of p38 MAPK and c-Jun amino-terminal kinase (JNK), whereas extracellular
70 onstitutively activates two protein kinases, c-Jun amino-terminal kinase (JNK)/stress-activated prote
71 related with enhanced phosphorylation of the c-Jun amino-terminal kinases JNK1 and JNK2 and activatio
73 th 48 or 89 polyglutamine repeats stimulated c-Jun amino-terminal kinases (JNKs) activity and induced
77 al at dosages that inhibit activation of the c-Jun amino-terminal kinases (JNKs) in primary embryonic
79 tracellular signal-regulated kinases (ERKs), c-Jun amino-terminal kinases (JNKs), and the p38 mitogen
80 response kinases (ERKs or p42/44(MAPK)), the c-Jun amino-terminal kinases (JNKs), and the p38/Hog 1 p
81 vated protein kinases (SAPKs), also known as c-Jun amino-terminal kinases (JNKs), are activated in re
82 tracellular signal-regulated kinases (ERKs), c-Jun amino-terminal kinases (JNKs), or p38 stress-respo
84 ut not p38 mitogen-activated protein kinase, c-Jun amino-terminal kinase or mitogen activated protein
86 g the extracellular signal-regulated kinase, c-Jun amino-terminal kinase, p38, and nuclear factor kap
87 othelial Akt/NO synthase activation, reduced c-Jun amino terminal kinase phosphorylation, and decreas
89 d kinase and stress-activated protein kinase/c-Jun amino-terminal kinase signaling pathways and calci
90 for EGF-induced MAPK activation, but not for c-Jun amino-terminal kinase stimulation or MAPK activati
91 activated protein kinase (MAPK) superfamily, c-Jun amino-terminal kinase/stress-activated protein kin
92 the MAPK family, namely p42(mapk/erk2), p46 c-Jun amino-terminal kinase/stress-activated protein kin
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