ライフサイエンスコーパス: c-Jun NH2-terminal kinase

1 olin-induced cAMP accumulation and activated c-Jun NH2-terminal kinase.

2 and inhibited the TNF-induced activation of c-Jun NH2-terminal kinase.

3 hosphorylated but not total p44/42, p38, and c-Jun NH2-terminal kinase.

4 thout affecting the levels of phosphorylated-c-jun-NH2-terminal kinase.

5 factor 2alpha (eIF2alpha) and stress kinase c-Jun NH2-terminal kinase 1 (JNK1) (all P values <0.05).

6 causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and triggers developm

7 CE)/Ced-3 family of proteases (caspases) and c-Jun NH2-terminal kinase 1 (JNK1), which have been show

8 ment of PC-3 cells with TRAIL also activated c-Jun NH2-terminal kinase 1 (JNK1); however, inhibition

9 activate the stress-activated protein kinase/c-Jun NH2-terminal kinase 1 (SAPK/JNK1), and it also pot

10 In this study, we found that c-Jun NH2-terminal kinase 1 activation triggered CtBP ph

11 d with decreased Akt signaling but increased c-Jun NH2-terminal kinase 1/2 (JNK1/2), p38, and extrace

12 sitization was also, in part, dependent upon c-Jun NH2-terminal kinase 1/2 signaling.

13 kinase 1/2, stress-activated protein kinase/c-JUN NH2-terminal kinase 1/2, and p38 mitogen-activated

14 also induced an immediate activation of the c-Jun-NH2-terminal kinase 1 (JNK1) pathway that was foll

15 t was associated with the phosphorylation of c-Jun-NH2-terminal kinase 1/2 and p38 mitogen-activated

16 llular signal-regulated kinase-2 (ERK-2) and c-jun NH2 terminal kinase-1 (JNK-1) phosphorylation of P

17 ivation of stress-activated protein kinase-1/c-Jun NH2-terminal kinase-1, whereas both alpha-PDGFR an

18 Here we show that c-Jun NH2-terminal kinase 2 (JNK2) inhibits IFN-gamma pr

19 bits IH development might include decreasing c-Jun NH2 terminal kinase activation and preventing apop

20 ation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation

21 r p53, but is sensitive to the inhibition of c-Jun NH2-terminal kinase activation and the antioxidant

22 ge, Mkp-1-/- cells exhibit prolonged p38 and c-Jun NH2-terminal kinase activation as well as enhanced

23 ns such as the G12,13 family members mediate c-Jun NH2-terminal kinase activation by neuropeptides an

24 n of cAMP accumulation, but had no effect on c-Jun NH2-terminal kinase activation or inhibition of ER

25 paB signaling was completely inhibited while c-Jun NH2-terminal kinase activation was partially inhib

26 e neutrophil phenotype resulted in a loss in c-Jun NH2-terminal kinase activation with concomitant ac

27 -Dock180 signaling complex, elevated Rac and c-Jun NH2-terminal kinase activation, and increased matr

28 stress precedes 2-methoxyestradiol-mediated c-Jun NH2-terminal kinase activation, leading to elevate

29 s leading to stress-activated protein kinase/c-Jun NH2-terminal kinase activation.

30 ld-type MMP-9 promoter by MEKK-1, a specific c-Jun NH2-terminal kinase activator, was only marginally

31 ar factor-kappaB ligand-induced p38 MAPK and c-Jun NH2-terminal kinase activities were enhanced in os

32 In addition, both ERK and c-Jun NH2-terminal kinase activities were increased afte

33 he RANK-dependent induction of NF-kappaB and c-Jun NH2-terminal kinase activities.

34 Inhibitors caused an increase in c-jun NH2-terminal kinase activity in CLL, but this did

35 The c-jun NH2-terminal kinase activity was increased to the

36 xtracellular signal-regulated kinase but not c-Jun NH2-terminal kinase activity.

37 2 levels, manganese superoxide dismutase, or c-Jun NH2-terminal kinase activity.

38 s well as manganese superoxide dismutase and c-Jun NH2-terminal kinase activity.

39 Deletion of NQO2 also abolished TNF-induced c-Jun NH2-terminal kinase, Akt, p38, and p44/p42 mitogen

40 trate that CpG DNA induces the activation of c-Jun NH2-terminal kinase and p38 but does not activate

41 Norepinephrine also activated c-Jun NH2-terminal kinase and p38 MAPK in alpha1A-transf

42 In some cell types, c-Jun NH2-terminal kinase and p38 mitogen-activated prot

43 review the novel contribution of p38(SAPK), c-Jun NH2-terminal kinase and PKR-like endoplasmic retic

44 otein tyrosine phosphorylation and activates c-Jun NH2-terminal kinase and suggest that these pathway

45 ation of the stress-activated protein kinase/c-Jun NH2-terminal kinase and the p38 mitogen-activated

46 HER2 with HER3 as well as the activation of c-Jun-NH2-terminal kinase and PI3-K activities.

47 bring together Max and c-Myc along with JNK (c-Jun NH2-terminal kinase) and p38MAPK, as well as their

48 racellular signal-regulated kinase 1/2, p38, c-Jun NH2-terminal kinase, and extracellular signal-regu

49 , extracellular signal-regulated kinase 1/2, c-Jun NH2-terminal kinase, and p38 mitogen-activated pro

50 blunted the activation of protein kinase C, c-Jun NH2-terminal kinase, and p38, as well as phosphory

51 tTG expression is mediated by the p38 MAPK, c-Jun NH2-terminal kinase, and phosphatidylinositol 3-ki

52 the extracellular signal-regulated kinases, c-Jun NH2-terminal kinases, and p38 kinase and induced A

53 the extracellular signal-regulated kinases, c-Jun NH2-terminal kinases, and p38 kinase; degradation

54 n of extracellular signal-regulated kinases, c-Jun NH2-terminal kinases, and p38 MAPK with different

55 hways extracellular signal-regulated kinase, c-Jun-NH2-terminal kinase, and p38.

56 s, the nonspecific activator of p38 MAPK and c-Jun NH2-terminal kinase, anisomycin, protected cardiac

57 Transient activation of the c-Jun-NH2-terminal kinase/AP-1 pathway, together with do

58 Here we describe a protein, JLP (c-Jun NH2-terminal kinase-associated leucine zipper prot

59 Heregulin, but not ID5, activated the c-Jun-NH2-terminal kinase cascade.

60 augments bortezomib-induced cytotoxicity by c-Jun NH2-terminal kinase/caspase activation.

61 ctivation occurs through the inhibition of a c-Jun NH2-terminal kinase-dependent, but not an extracel

62 and of downstream signaling pathways through c-Jun NH2-terminal kinases, extracellular signal-regulat

63 of the extracellular regulated kinase 2 and c-Jun NH2-terminal kinase groups of mitogen-activated pr

64 cell death has not been determined; however, c-Jun NH2-terminal kinase has been implicated as an esse

65 We propose therefore that c-Jun acts as a c-Jun NH2-terminal kinase-independent coactivator of PU.

66 2'-amino-3'-methoxyflavone (PD 98059) or the c-Jun NH2-terminal kinase inhibitor 1, 9-pyrazoloanthron

67 26, the p38 MAPK inhibitor SB203580, and the c-Jun NH2-terminal kinase inhibitor SP600125.

68 c-Jun NH2-terminal kinase inhibitors blocked MGBG-induce

69 n this study, we identify ARF6 together with c-Jun NH2-terminal kinase-interacting protein 3 and 4 (J

70 Recent data suggest that c-Jun NH2-terminal kinase is also activated, possibly th

71 inase (ERK) 1 and ERK2, moderately activated c-Jun NH2 terminal kinase (JNK), and weakly activated p3

72 Furthermore, PK + bortezomib activates c-Jun NH2 terminal kinase (JNK), which translocates to m

73 family showed that chondrocytes also express c-Jun NH2 terminal kinase (JNK)-1, JNK-2, and p38 protei

74 TAM also stimulated c-Jun NH2-terminal kinase (JNK) 1 activity, and interfer

75 3, with the exception of moderately enhanced c-Jun NH2-terminal kinase (JNK) activation and antibody

76 ls and suppresses ionizing radiation-induced c-Jun NH2-terminal kinase (JNK) activation and apoptosis

77 locked both S. typhimurium- and SopE-induced c-Jun NH2-terminal kinase (JNK) activation but did not i

78 e and caspase activation, was abrogated when c-Jun NH2-terminal kinase (JNK) activation was blocked w

79 betaAR stimulation caused c-Jun NH2-terminal kinase (JNK) activation, which was ab

80 PTEN protein and mRNA expression and induced c-Jun NH2-terminal kinase (JNK) activation.

81 Levels of c-Jun and c-Jun NH2-terminal kinase (JNK) activity are also high i

82 lly, serum starvation-induced suppression of c-jun NH2-terminal kinase (JNK) activity in C4-2B cells

83 xel caused a rapid and transient increase in c-Jun NH2-terminal kinase (JNK) activity, a proposed med

84 s in the active, GTP-bound state, stimulated c-Jun NH2-terminal kinase (JNK) activity, and enhanced t

85 KT/protein kinase B, only Deltap85 inhibited c-Jun NH2-terminal kinase (JNK) activity.

86 tantly, SCIO-469 enhanced phosphorylation of c-Jun NH2-terminal kinase (JNK) and augmented cleavage o

87 ) and late (16 h) activation of proapoptotic c-Jun NH2-terminal kinase (JNK) and decreased the antiap

88 markedly by NH2-terminal phosphorylation by c-Jun NH2-terminal kinase (JNK) and mediates stress resp

89 ase (IRAK) to the receptor and activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor (NF)-

90 ctivated protein kinase signalling molecules c-Jun NH2-terminal kinase (JNK) and p38 kinase in skelet

91 ted mitogen-activated protein (MAP) kinases, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase, as w

92 rongly the stress-activated protein kinases, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase.

93 l-regulating kinase 1 (ASK1) which activates c-Jun NH2-terminal kinase (JNK) and p38 pathways in resp

94 The c-Jun NH2-terminal kinase (JNK) branch of the mitogen-ac

95 but decreased that of p53; and 4) activated c-Jun NH2-terminal kinase (JNK) but not p38 kinase.

96 IF enhanced TRAF6-mediated activation of the c-Jun NH2-terminal kinase (JNK) by 3-fold, while only mo

97 The c-Jun NH2-terminal kinase (Jnk) family is implicated in

98 ignal-regulated kinase (Erk) family, and the c-Jun NH2-terminal kinase (JNK) family.

99 CDK4 up-regulation required intact TNFR1 and c-Jun NH2-terminal kinase (JNK) function.

100 The c-Jun NH2-terminal kinase (JNK) group of mitogen-activat

101 The c-Jun NH2-terminal kinase (JNK) group of mitogen-activat

102 The c-Jun NH2-terminal kinase (JNK) has been implicated in t

103 c-Jun NH2-terminal kinase (JNK) has been shown recently

104 racellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) have been implicated in

105 racellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) in bovine aortic endothe

106 rR stimulation and Ras can also activate the c-Jun NH2-terminal kinase (JNK) in cardiomyocytes.

107 hepatocyte cell death as well as the role of c-Jun NH2-terminal kinase (JNK) in the ConA and ConA/D-g

108 er the same conditions, THANK also activated c-jun NH2-terminal kinase (JNK) in U937 cells.

109 inases that functions as an activator of the c-Jun NH2-terminal kinase (JNK) in vitro.

110 kinase inhibitor SB203580 (5 microM) and the c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 (25 m

111 g kinase 1 (ASK1) inhibitor thioredoxin, and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 (anth

112 c-Jun NH2-terminal kinase (JNK) is activated by a number

113 The c-Jun NH2-terminal kinase (JNK) is activated during obes

114 The c-Jun NH2-terminal kinase (JNK) is activated when cells

115 the proapoptotic Bcl-2 family protein BAD by c-Jun NH2-terminal kinase (JNK) is controversial.

116 The c-Jun NH2-terminal kinase (JNK) is involved in the regul

117 We have previously identified c-Jun NH2-terminal kinase (JNK) kinase 1/mitogen-activat

118 racellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) mitogen-activated protei

119 assays indicated that NGF neither activated c-Jun NH2-terminal kinase (JNK) nor p38 mitogen-activate

120 fects on ERK, PTEN expression did not affect c-Jun NH2-terminal kinase (JNK) or PDGF-stimulated Akt.

121 protein kinase (MAPK) family, which includes c-jun NH2-terminal kinase (JNK) or stress-activated prot

122 MEK kinase 1 (MEKK1) activates the c-Jun NH2-terminal kinase (JNK) pathway in response to e

123 of dominant-negative protein mutants of the c-Jun NH2-terminal kinase (JNK) pathway revealed that th

124 fects of contractile activity in vivo on the c-Jun NH2-terminal kinase (JNK) pathway, a signaling cas

125 role of two specific signaling pathways, the c-Jun NH2-terminal kinase (JNK) pathway, and the extrace

126 lular processes, including activation of the c-Jun NH2-terminal kinase (JNK) pathway.

127 a dynamic junctional regulator of the MEKK1-c-Jun NH2-terminal kinase (JNK) pathway.

128 mmatory pathways, which was achieved through c-Jun NH2-terminal kinase (JNK) phosphorylation and fact

129 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) regulate liver metabolis

130 hikers on axonal vesicles, we focused on the c-Jun NH2-terminal kinase (JNK) scaffolding protein Sund

131 racellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) signal transduction path

132 Although c-Jun NH2-terminal kinase (JNK) signaling is involved in

133 een identified as a scaffold protein for the c-Jun NH2-terminal kinase (JNK) signaling pathway and as

134 The c-Jun NH2-terminal kinase (JNK) signaling pathway has be

135 may be via their reported activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway in KS

136 We report that the c-Jun NH2-terminal kinase (JNK) signaling pathway mediat

137 ular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) subgroups of MAP kinases

138 hen (APAP) model is known to be regulated by c-Jun NH2-terminal kinase (JNK) through interaction with

139 The FAK-p130Cas complex activates c-Jun NH2-terminal kinase (JNK) via a Ras/Rac1/Pak1/MAPK

140 le caspases and of the stress kinase p38 and c-Jun NH2-terminal kinase (JNK) was completely blocked i

141 Rac1 and c-Jun NH2-terminal kinase (JNK) were activated when cell

142 Tpi, breaks ligand binding interactions with c-Jun NH2-terminal kinase (JNK), and causes GSTpi multim

143 acellular signal-regulated kinase (ERK), the c-Jun NH2-terminal kinase (JNK), and p38 MAP kinase path

144 extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 mitogen-activat

145 extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 were activated

146 tivated protein kinases (MAPKs): p38MAPK and c-Jun NH2-terminal kinase (JNK), as well as signal trans

147 acellular signal-regulated kinase (ERK), and c-jun NH2-terminal kinase (JNK), but not p38 mitogen-act

148 Furthermore, the c-Jun NH2-terminal kinase (JNK), involved in growth acti

149 cyte apoptosis is mediated via activation of c-Jun NH2-terminal kinase (JNK), leading to activation o

150 e expressed and treatment with TNF activated c-Jun NH2-terminal kinase (JNK), needed for AP-1 activat

151 We found that c-Jun NH2-terminal kinase (JNK), not cyclin-dependent ki

152 t affect the stimulation of either p38 MAPK, c-jun NH2-terminal kinase (JNK), or protein kinase B (PK

153 s of p53 with murine double minute 2 (Mdm2), c-Jun NH2-terminal kinase (JNK), p300/CBP, and p14ARF du

154 p44 mitogen-activated protein kinase (MAPK), c-Jun NH2-terminal kinase (JNK), p38, p65, NF-kappaB) we

155 by inhibitors of MAPK/ERK kinase (MEK), p38, c-Jun NH2-terminal kinase (JNK), protein tyrosine kinase

156 racellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK), the inactivation of p38

157 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK), which, in turn, regulat

158 alcineurin-NFAT signaling indirectly through c-Jun NH2-terminal kinase (JNK)- and p38-mediated phosph

159 ellular signal-regulated kinase (ERK)-1/2/3, c-Jun NH2-terminal kinase (JNK)-1/2, p38 kinase, mitogen

160 gen-activated protein kinase (MAPK) kinase 4/c-Jun NH2-terminal kinase (JNK)-activating kinase (MKK4/

161 The c-Jun NH2-terminal kinase (JNK)-interacting protein (JIP

162 Here, we report that c-Jun NH2-terminal kinase (JNK)-interacting protein-3 (J

163 ress associated with sustained activation of c-Jun NH2-terminal kinase (JNK)-signaling cascades, pro-

164 idylinositol 3-kinase, sphingomyelinase, and c-Jun NH2-terminal kinase (JNK).

165 quitination by its association with inactive c-Jun NH2-terminal kinase (JNK).

166 ted in an increase in RAFTK activity and the c-Jun NH2-terminal kinase (JNK).

167 a and membrane ruffling, and to activate the c-Jun NH2-terminal kinase (JNK).

168 regulated kinase (ERK) kinase (MEK)-ERK, and c-jun NH2-terminal kinase (JNK).

169 aggregates correlated with activation of the c-jun NH2-terminal kinase (JNK).

170 ressful stimuli results in activation of the c-Jun NH2-terminal kinase (JNK)/stress-activated protein

171 nase (MAPK) family members p42MAPK, p38, and c-Jun NH2-terminal kinase (JNK)/stress-activated protein

172 xtracellular signal-regulated kinase (ERK)2, c-jun NH2-terminal kinase (JNK)1, and p38 MAPK.

173 The other pathway involves c-Jun NH2-terminal kinase (JNK)2, which is activated by

174 he c-Abl nonreceptor tyrosine kinase and the c-Jun NH2-terminal kinase (JNK/stress-activated protein

175 mitogen-activated protein kinases (MAPK) and c-Jun NH2-terminal kinases (JNK) and that the activation

176 We show that viral activation of the c-Jun NH2-terminal kinases (JNK) family of MAP kinases a

177 lular signal-regulated kinases (ERK) and the c-Jun NH2-terminal kinases (JNK), are transiently activa

178 ), and the stress-activated protein kinases, c-Jun NH2-terminal kinases (JNK), but not p38, are criti

179 d protein kinases, including the p38 and the c-Jun NH2-terminal kinases (JNK), have been associated w

180 Basal c-Jun-NH2-terminal kinase (JNK) activity was increased 3

181 lastine, but not paclitaxel, increasing both c-Jun-NH2-terminal kinase (JNK) and p38 activity.

182 We tested the role of c-jun-NH2-terminal kinase (JNK) on PS1 gene expression u

183 y shown that inhibition of basal activity of c-jun-NH2-terminal kinase (JNK) with JNK-specific inhibi

184 tivation of IkappaB kinase complex (IKK) and c-Jun-NH2-terminal kinase (JNK), and subsequently activa

185 to induce lipoapoptosis in liver cells in a c-Jun-NH2-terminal kinase (JNK)-dependent, but death rec

186 In contrast, c-jun-NH2-terminal kinase (JNK)/stress-activated protein

187 cellular signal regulated kinases (ERKs) and c-jun-NH2-terminal kinases (JNK).

188 lated protein kinase [ERK] 1 and 2, p38, and c-Jun NH2-terminal kinase [JNK]) and nuclear factor kapp

189 of mitogen-activated protein (MAP) kinases (c-Jun NH2-terminal kinase [JNK], p38, extracellular sign

190 ation of p21ras and preferentially activated c-Jun NH2 terminal kinases (JNK1 and JNK2) over extracel

191 t shock element binding activity, as well as c-Jun NH2-terminal kinase (JNK1) activation.

192 so abolished the hypoxia-induced increase in c-Jun NH2-terminal kinase (JNK1) catalytic activity and

193 xtracellular signal-regulated kinase (ERK2), c-Jun NH2-terminal kinase (JNK1), and p38 in response to

194 to the activation of AP-1, specifically the c-Jun NH2-terminal kinase (JNK1), p38, and the extracell

195 C-Jun NH2 terminal kinases (JNKs) are important cell sig

196 l and functional homology to p38 include the c-Jun NH2-terminal kinases (JNKs or SAPKs) and the extra

197 pathways that regulate MAP kinases including c-Jun NH2-terminal kinases (JNKs) and extracellular regu

198 We identified c-Jun NH2-terminal kinases (JNKs) as essential upstream

199 we found that arsenic induces activation of c-Jun NH2-terminal kinases (JNKs) at a similar dose rang

200 a panel of SCLC lines and the activation of c-Jun NH2-terminal kinases (JNKs) by UV in the individua

201 signal-regulated protein kinases (Erks) and c-Jun NH2-terminal kinases (JNKs) was strongly inhibited

202 lar-signal-regulated protein kinases (ERKs), c-Jun NH2-terminal kinases (JNKs), and p38 kinase and in

203 e, attenuated the shear stress activation of c-Jun NH2-terminal kinases (JNKs), suggesting that Cdc42

204 The novel protein kinases, c-Jun NH2-terminal kinases (JNKs)/stress-activated prote

205 lular signal-regulated protein kinase (ERK), c-Jun NH2-terminal kinase kinase (JNKK), and c-Jun/AP-1

206 indicate that CpG DNA activates the p38 and c-Jun NH2-terminal kinase MAPK and leads to the activati

207 ellular ATP and consequent inhibition of the c-JUN NH2-terminal kinase-mediated stress signaling path

208 ited the activation of PKC, ERK1/2, p38, and c-Jun NH2-terminal kinase mitogen-activated protein kina

209 racellular signal-regulated kinase, p38, and c-Jun NH2-terminal kinase mitogen-activated protein kina

210 ta) as a result of activation of the p38 and c-Jun NH2-terminal kinase mitogen-activated protein kina

211 XIAP), Mcl-1, and p21CIP1/WAF1 and activated c-Jun NH2-terminal kinase; moreover, these effects were

212 of interleukin-1 receptor-associated kinase, c-Jun NH2 terminal kinase, nuclear factor-kappaB, and ac

213 Phosphorylation of c-Jun by c-Jun NH2-terminal kinase on Ser-63 and -73 does not alt

214 the stress-activated protein kinases (SAPKs; c-jun NH2-terminal kinases or JNKs).

215 hosphorylation, and phosphorylation of MAPK, c-Jun NH2-terminal kinase, p38 MAPK, and activating tran

216 messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal

217 ogenic acid decreased the phosphorylation of c-Jun NH2-terminal kinases, p38 kinase, and MAPK kinase

218 c-Jun NH2-terminal kinase-p46 is phosphorylated and acti

219 Furthermore, SMAD6 knockdown activated the c-Jun NH2-terminal kinase pathway and reduced phosphoryl

220 urthermore, we found that ATF4 regulated the c-Jun NH2-terminal kinase pathway resulting in VEGF upre

221 induction of c-jun through activation of the c-jun NH2-terminal kinase pathway.

222 p38 MAPK, or stress-activated protein kinase/c-Jun NH2-terminal kinase pathways.

223 l characterization showed that knocking down c-Jun NH2-terminal kinase prevented N-cadherin up-regula

224 (ERKs), stress-activated protein kinases or c-Jun NH2-terminal kinases (SAPKs/JNKs), and p38 kinase.

225 ion factor hypoxia-inducible factor 1 alpha, c-Jun NH2-terminal kinase signaling, and the generation

226 The ability of signaling via the JNK (c-Jun NH2-terminal kinase)/stress-activated protein kina

227 eas PAK (p21-activated kinase) and JNK/SAPK (c-Jun NH2-terminal kinase/ stress-activated protein kina

228 entrations of merbarone caused activation of c-Jun NH2-terminal kinase/stress-activated protein kinas

229 These results further suggest that c-Jun and c-Jun NH2-terminal kinase/stress-activated protein kinas

230 valuate the role of: 1) p42mapk/erk2, 2) p46 c-Jun NH2-terminal kinase/stress-activated protein kinas

231 pendent signaling pathway that activates the c-Jun NH2-terminal kinase/stress-activated protein kinas

232 A possible mechanism implicating the C-Jun NH2-terminal kinase/stress-activated protein kinas

233 extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase/stress-activated protein kinas

234 nd mechanism of activation of members of the c-Jun-NH2-terminal kinase/stress-activated protein kinas

235 s seen on CD40-mediated activation of ERK or c-Jun NH2-terminal kinase, suggesting that the BCR and C

236 Activation of the c-Jun NH2-terminal kinase type 1 (JNK1) signaling pathwa

237 trast, muscarinic agonist stimulation of the c-Jun NH2-terminal kinases was not inhibited in SCLC cel

238 sphorylation of Syk, phospholipase C-g2, and c-Jun NH2-terminal kinase were markedly decreased in WIP

239 ound RhoA and Rac1, phospho-p38, and phospho-c-Jun NH2-terminal kinases were unchanged.

240 ellular signal regulated kinases 1 and 2 and c-Jun NH2-terminal kinase, whereas cyclic-PA did not.

241 Asphalt fumes transiently activated c-Jun NH2-terminal kinases without affecting extracellul