ライフサイエンスコーパス: JNK pathway

1 llular calcium and used PI3K, PICK-1 and the JNK pathway.

2 e damage or activation of the damage-sensing Jnk pathway.

3 Slipper (Slpr), an upstream activator of the JNK pathway.

4 l growth factor (VEGF) all increased via the JNK pathway.

5 nt, in part via the p38 MAPK pathway and the JNK pathway.

6 egulated Cdk5 induces biphasic activation of JNK pathway.

7 t, without activation of the proinflammatory JNK pathway.

8 ein-1) was strongly induced by the TNF-alpha/JNK pathway.

9 Finally, K13 does not activate the JNK pathway.

10 esting that miR-155-inducing signals use the JNK pathway.

11 the NF-kappaB pathway without affecting the JNK pathway.

12 asome activity and an activation of the MLK2-JNK pathway.

13 at central Ang II activates the AT(1)R, SAPK/JNK pathway.

14 iated inhibition of the stress response MKK4-JNK pathway.

15 tive control samples, failed to activate the JNK pathway.

16 PK kinase kinase for TRAF4 regulation of the JNK pathway.

17 urons and other cell types by activating the JNK pathway.

18 activity deprivation activates the LZK-MKK4-JNK pathway.

19 its ability to maximally signal through the JNK pathway.

20 d AP-1 activation specific through impairing JNK pathway.

21 ss-induced cell death via the IRE1alpha-ASK1-JNK pathway.

22 y of Dvl in the beta-catenin pathway and the JNK pathway.

23 t dramatically inhibited Dvl activity in the JNK pathway.

24 potentiates cell death signaling through the JNK pathway.

25 Dvl and negatively regulates the Dvl-induced JNK pathway.

26 kinase) and activate JNK through a TAK1-MKK4-JNK pathway.

27 e MAPK kinase kinase kinases (MAP4Ks) in the JNK pathway.

28 ch was, at least in part, dependent upon the JNK pathway.

29 ications for the design of inhibitors of the JNK pathway.

30 e resistant to DCA-induced activation of the JNK pathway.

31 n evolutionarily conserved VANGL2-p62/SQSTM1-JNK pathway.

32 kinase kinase (MAP3K) of the stress-induced JNK pathway.

33 38 MAPK, and SAPK/ERK kinase-1 (SEK1) of the JNK pathway.

34 tes, which associated with activation of the JNK pathway.

35 f HSCs to TGF-beta through activation of the JNK pathway.

36 p-regulation is mediated by PI3K/Akt and the JNK pathway.

37 engulfing follicle cells, and activates the JNK pathway.

38 not the AKT/mammalian target of rapamycin or JNK pathways.

39 operatively targeting the RB1, PI3K/AKT, and JNK pathways.

40 mediated through the NFkappaB, PKC, Src, and JNK pathways.

41 triggers and involvement of both IKKbeta and JNK pathways.

42 ssion requires activation of both ERK1/2 and JNK pathways.

43 ator of p38, but not of activators of ERK or JNK pathways.

44 ion appears to regulate both the ERK and the JNK pathways.

45 Live bacteria also activated the p38 and JNK pathways.

46 is critically dependent on the NF-kappaB and JNK pathways.

47 gnaling pathways including the p38, Akt, and Jnk pathways.

48 ellular signal-regulated kinase 5 (ERK5) and JNK pathways.

49 ion in a process that involves Src, ERK, and JNK pathways.

50 alancing TGF-beta signaling via the Smad and JNK pathways.

51 ivating genes critical for the NF-kappaB and JNK pathways.

52 protein depends on Wnt5a/CaMKII and/or Wnt5a/JNK pathways.

53 oinduction through Smad2-independent Ras/ERK/JNK pathways.

54 vation of the Jun N-terminal protein kinase (JNK) pathway.

55 that activates the c-Jun N-terminal kinase (JNK) pathway.

56 n of the ASK1/Jun N-terminal protein kinase (JNK) pathway.

57 e regulation of the c-Jun N-terminal kinase (JNK) pathway.

58 the stress-responsive Jun-N-terminal kinase (JNK) pathway.

59 activating the c-Jun NH(2)-terminal kinase (JNK) pathway.

60 pathways, such as the jun N-terminal kinase (JNK) pathway.

61 ator of the MEKK1-c-Jun NH2-terminal kinase (JNK) pathway.

62 fold protein of the c-Jun N-terminal kinase (JNK) pathway.

63 was mediated by the c-Jun N-terminal kinase (JNK) pathway.

64 c regulator for the c-Jun N-terminal kinase (JNK) pathway.

65 KT and proapoptotic c-Jun N-terminal kinase (JNK) pathways.

66 Activation of the JNK pathway (2-3-fold) in response to tumor necrosis fac

67 ogen, activates the c-Jun N-terminal kinase (JNK) pathway, a hallmark of the host stress response.

68 regulating kinase 1/c-Jun N-terminal Kinase (JNK) pathway, a module known to stimulate insulin resist

69 mediated by the NF-kappaB pathway and c-JUN/JNK pathway acting in parallel to elicit focal adhesion

70 RC overexpression diminishes amyloid-induced JNK pathway activation and apoptosis in the beta-cell, a

71 This stabilization requires JNK pathway activation and interaction with POSH and is

72 ctivity of the recombinant kinase domain and JNK pathway activation driven by full-length MLK1 expres

73 e data indicate that endogenous MIF inhibits JNK pathway activation during reperfusion and protects t

74 We found ARC knockdown enhances JNK pathway activation, whereas ARC overexpression reduc

75 t is dependent upon increased downstream p38/JNK pathway activation.

76 mechanism of apoptosis by p38 MAP kinase and JNK pathway activation.

77 JNK pathway components facilitating nuclear JNK pathway activation.

78 t amyloid increases c-Jun N-terminal kinase (JNK) pathway activation, we investigated whether ARC aff

79 n neurons, yet the factors that initiate DLK/JNK pathway activity remain poorly defined.

80 e show that skipping of MKK7 exon 2 enhances JNK pathway activity, as indicated by c-Jun phosphorylat

81 e Cno, is not involved in the stimulation of JNK pathway activity, indicating that Cno has both a Rap

82 Surprisingly, they were also regulators of Jnk pathway activity: both Src and the small GTPase Rho1

83 Our genetic analysis suggests that the JNK pathway acts in parallel with the insulin-like signa

84 Specific inhibitors of the Ras, ERK, and JNK pathways all reduced the synthesis of viral proteins

85 evelopmental activation of the Toll, ERK, or JNK pathways alone fail to activate wound repair loci.

86 logic or genetic (siRNA) interruption of the JNK pathway also significantly attenuated the lethality

87 KK1 activation, we propose a RhoA-ROCK-MEKK1-JNK pathway and a MEKK1-p38 pathway as Smad-independent

88 ons that lead to diminished signaling in the JNK pathway and enhanced proliferation in colon cancer.

89 cycle arrest, p53 mutant cells activate the JNK pathway and expression of the pro-apoptotic gene hid

90 ha-induced activation of the Rho kinase/MKK4/JNK pathway and IL-6 production, but not p38 activation

91 hile knockdown of USP48 attenuates TNF-alpha/JNK pathway and increases E-cadherin expression and cell

92 Activation of the JNK pathway and induction of the AP-1 transcription fact

93 the function of MLK4 selectively induced the JNK pathway and its downstream targets, cJUN, ATF3, and

94 otic tumor suppressor acting through the ROS-JNK pathway and support the therapeutic potential for th

95 d FLS appeared to activate c-Jun through the JNK pathway and TAK1 activation of c-Jun was dependent o

96 h signaling is stimulated by DSS through the JNK pathway and that inhibition of Hh signaling in EBs p

97 antagonists reaper and hid can activate the JNK pathway and that this pathway is required for induci

98 lk relationship between the stress-activated JNK pathway and the mitogen-activated ERK pathway.

99 gramming is mediated by up regulation of the JNK pathway and transient debilitation of the epigenetic

100 l apoptosis was independent of the classical JNK pathway and was mediated by a novel c-Jun kinase.

101 ion and in which SIAH1 in turn activates the JNK pathway and, ultimately, contributes to cell death.

102 Activation of the NF-kappaB and JNK pathways and Gadd45beta expression were analyzed in

103 ed in part by loss of control of the MEK and JNK pathways and involved downstream activation of the E

104 paired activation of the NF-kappaB, p38, and JNK pathways and reduced production of IL-8 and TNF-alph

105 ignals via both the Wnt/beta-catenin and Wnt/JNK pathways and that different thresholds of Wnt-Fzd7 a

106 that the activation of ERK, p38 kinase, and JNK pathways and the hypertonicity response element in t

107 X protein (pX) activates p38 MAP kinase and JNK pathways and, in response to weak apoptotic signals,

108 MKK7 activates the c-Jun N-terminal kinase (JNK) pathway and is the only MKK containing three motifs

109 th the activation of the c-Jun-NH(2)-kinase (JNK) pathway and requires localization of a small unique

110 SH3s), a scaffold component of the apoptotic JNK pathway, and that Siah contributes to death of neuro

111 with other signaling mutants, such as in the JNK pathway, and we demonstrate that JNK signaling is no

112 of the ERK and c-Jun NH(2)-terminal kinase (JNK) pathways, and downstream transcription factors, in

113 Members of the JNK pathway are organized together by virtue of interact

114 protein kinase/c-Jun N-terminal kinase (MAPK/JNK) pathways are both implicated in Alzheimer's disease

115 appaB pathway, and MAP kinase (ERK, p38, and JNK) pathways are important for VEGF-A-induced TR3-TV2 a

116 ed B-cell expansion in vivo and identify the JNK pathway as a therapeutic target for ABC-DLBCL.

117 Thus, we identified JNK pathway as another signaling mode for the antiapopto

118 pathway activities, thereby pointing to FAK/JNK pathway as the downstream effector of MUCL1 signalin

119 JNK pathway-associated phosphatase (JKAP, also known as

120 sion revealed that Tollo signals through the JNK pathway at the NMJ.

121 Inhibition of the JNK pathway attenuated BIM(EL) expression, prevented BIM

122 se studies show that inhibition of the MLK 3/JNK pathway attenuates MPP(+)-mediated SH-SY5Y cell deat

123 Inhibition of the JNK pathway blocked viral replication in a manner distin

124 omoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinas

125 ed kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways but not the p38 pathway.

126 and Sprouty-4 expression and stimulated the JNK pathway, but not beta-catenin/T cell factor activity

127 valuate the expression and regulation of the JNK pathway by MAP3K in arthritis.

128 Interruption of the JNK pathway by pharmacologic or genetic (e.g. siRNA) mea

129 rogates signaling through the MAPK, PI3K and JNK pathways by downregulation of both KRAS and RREB1 in

130 Furthermore, blockade of the ERK or JNK pathways by U0126 and SP600125, respectively, abolis

131 ion of the MKK4-c-Jun NH(2)-terminal kinase (JNK) pathway, c-Jun phosphorylation, and apoptosis.

132 th canonical and noncanonical members of the JNK pathway caused open wounds, as did several genes inv

133 Disruption of the MLK-JNK pathway causes decreased Dll4/Notch signaling, exces

134 the mutants provide a scaffold for multiple JNK pathway components facilitating nuclear JNK pathway

135 Our analysis of JNK pathway components reveals redundancy among the upst

136 optotic stimuli promote the stabilization of JNK pathway components, thereby contributing to cell dea

137 -suppressing functions have been ascribed to JNK pathway components.

138 NF-kappaB signaling, only BCMA activates the JNK pathway conferring on BCMA the specific ability to a

139 e showed that loss or hyperactivation of the JNK pathway contributes to the development of inflammati

140 ignals from Kit Tyr(567) to activate the Rac/JNK pathway controlling mast cell proliferation, which l

141 and to activate the c-Jun N-terminal kinase (JNK) pathway correlated well with its ototoxic potential

142 ased GFAP accumulation, whereas blocking the JNK pathway decreased GFAP accumulation.

143 inhibit the ERK5 pathway but not the p38 or JNK pathways, demonstrating the specific and unique requ

144 e distinct aspects of Jun N-terminal kinase (JNK) pathway dependent axonal morphogenesis in Drosophil

145 We propose that the JNK pathway described here is required to relieve the in

146 ith or without SB202190, an inhibitor of the JNK pathway; dexamethasone; or doxycycline for different

147 and U0126 inhibitors and inhibition of SAPK/JNK pathway did not suppress C pneumoniae-induced ICAM-1

148 viously been implicated in activation of the JNK pathway during embryonic dorsal epidermal closure.

149 egative cross-talk between the NF-kappaB and JNK pathways during TGF-beta1 signaling has not been det

150 dramatically increased signaling through the JNK pathway, elevated MMP3 and MMP13 gene expression in

151 erize potent pharmacologic inhibitors of the JNK pathway for clinical translation.

152 0 and this synergized with inhibition of the JNK pathway for limiting IL-27p28.

153 se results demonstrate the importance of the JNK pathway for VZV replication and advance the idea tha

154 s, we find that the c-Jun N-terminal kinase (JNK) pathway generates higher noise than the NF-kappaB p

155 Mice deficient in the JNK pathway had decreased serum levels of IL-6 and IL-1b

156 In contrast, inhibiting p38 or JNK pathways had no effect on MMP-1 production.

157 rmation; however, suppression of the ERK and JNK pathways had no effect on these processes.

158 Activation of the JNK pathway has been implicated in the formation of seve

159 While the JNK pathway has been well characterized, the mechanism o

160 onistic cross-talk between NF-kappaB and ROS/JNK pathways have recently been identified.

161 s activation of the c-Jun N-terminal kinase (JNK) pathway; however, the signaling molecules that link

162 Indeed, TG-ODNs were shown to activate the JNK pathway in an ATM-dependent manner as evidenced by e

163 ce and adenovirus-mediated activation of the JNK pathway in cardiomyocytes inhibited peroxisome proli

164 To test the requirement for the JNK pathway in ES cell neurogenesis, ES cell lines beari

165 cate that MEKK2 is a potent activator of the JNK pathway in FLS and that signal complexes including M

166 Overexpression of Draper or the JNK pathway in follicle cells is sufficient to induce de

167 eta-cell apoptosis through activation of the JNK pathway in human islets and in insulinoma (INS 832/1

168 ells and established a critical role for the JNK pathway in infection of these cells.

169 In addition, deficiency of either the ERK or JNK pathway in mouse livers reduced the basal, but not t

170 ckdown of Sh3rf2 activates the pro-apoptotic JNK pathway in neuronal cells.

171 Targeting the JNK pathway in spinal astroglia may present a new and ef

172 MAPK, p38 MAPK, or stress-activated protein/JNK pathway in THC-treated DCs.

173 nterplay between the proteasome and the SAPK/JNK pathway in the context of GFAP accumulation.

174 ol to investigate the functional role of the JNK pathway in the development of heart failure.

175 hat SFRP1 acts through the non-canonical WNT/JNK pathway in the prostate.

176 phila eye to investigate the function of the JNK pathway in three different tumor models of increasin

177 ut that Mmp1 is expressed independent of the JNK pathway in unwounded epidermis.

178 Genetic inhibition of JNK pathway in vivo by Jnk3 knockout results in ameliora

179 The identification of the role of the JNK pathway in VZV infection of neurons reveals potentia

180 the PI3K/Akt while enhancing the ERK/p38MAPK/JNK pathways in LMCs.

181 nt activation of both the p38 MAP kinase and JNK pathways in pX-mediated apoptosis and suggest that t

182 CL2/MCP-1 was mediated by the PI3K, ERK, and JNK pathways in RA ST fibroblasts and by the PI3K and ER

183 he stress-activated c-Jun N-terminal kinase (JNK) pathway in mice and SH-SY5Y neuroblastoma cells.

184 role of p38 and c-Jun NH(2)-terminal kinase (JNK) pathways in 3,3'-diindolylmethane-induced p21 mRNA

185 e MAP-ERK kinase (MEK) and c-jun-NH2-kinase (JNK) pathways in modifying CSC-like behavior.

186 ess kinase (p38 and c-Jun N-terminal kinase [JNK]) pathways in response to many stimuli.

187 rated milder and transient activation of the JNKs pathway in the CA1 subfield of the hippocampus duri

188 The JNK pathway includes a MAPKKK (Wallenda/DLK), a MAPKK (H

189 paB (NF-kappaB) and c-Jun N-terminal kinase (JNK) pathways, including Ikbkb, Nfkb1, Nfkb2, Rela, Jnk1

190 Inhibition of TRAF2/JNK pathway increases E (epithelial)-cadherin expression

191 ions as a costimulatory molecule through the JNK pathway independent of KARAP/DAP12 and DAP10.

192 nd Fzd-9 signaling through activation of the JNK pathway induces cadherin proteins and the receptor t

193 JNK pathway induction bypassed cell cycle restraints ind

194 th sustained activation of the pro-apoptotic JNK pathway, induction of CHOP, and an absence of the in

195 ts a control mechanism in which an activated JNK pathway influences axonal transport by functioning a

196 endent of Raf activation, and is reversed by JNK pathway inhibition either at the level of SEK-1, JNK

197 Moreover, TAK1 knockdown or JNK pathway inhibition induced the expression of farneso

198 Blocking c-Jun activation by JNK pathway inhibition prevented neuronal death after st

199 Further studies showed that JNK pathway inhibition sensitized BRAF mutant cells to G

200 Furthermore, JNK pathway inhibitor CEP-11004 effectively blocks paraq

201 r findings support the evaluation of MEK and JNK pathway inhibitors as therapeutic agents in BLBC to

202 ctivity was unaffected by a p38 inhibitor or JNK pathway interference.

203 We show that the JNK pathway is activated and required in engulfing folli

204 We identify and validate that the JNK pathway is activated during and strongly modulates b

205 For example, the JNK pathway is activated in psoriatic skin, which makes

206 The JNK pathway is activated in sepsis and has also been imp

207 Furthermore, we show that this Dkk1/wnt-PCP-JNK pathway is active in an Abeta-based mouse model of A

208 lenda (Wnd)/dual leucine zipper kinase (DLK)-Jnk pathway is an evolutionarily conserved MAPK signalin

209 The JNK pathway is critical for H. pylori-dependent cell mot

210 The RelA/NF-kappaB-PKCdelta-JNK pathway is critical for UV-induced apoptosis, as it

211 When the JNK pathway is ectopically activated to overexpress Mmp1

212 ed expression of IL-1beta, whereas the Wnt5a/JNK pathway is for TNF-alpha expression.

213 Finally, the MAPK-JNK pathway is not required for baseline NMJ stabilizati

214 This FFA-stimulated JNK pathway is relevant to hallmarks of metabolic syndro

215 Here, we provide evidence indicating the JNK pathway is required for Netrin signaling in the deve

216 We show that the MLK-JNK pathway is required for the formation of native coll

217 Significantly, the JNK pathway is responsible for the majority of the pheno

218 The proinvasive function of the JNK pathway is revealed in a tumor context when active R

219 We find that the JNK pathway is specifically activated following infectio

220 vation of apoptosis-stimulated kinase (ASK1)-JNK pathways is often detected.

221 pX-mediated activation of p38 MAP kinase and JNK pathways is sustained, inducing the transcription of

222 es, and show that the Jun-N-terminal kinase (JNK) pathway is a key mediator of Anopheles gambiae anti

223 We find that the c-Jun N-terminal kinase (JNK) pathway is activated by VZV infection and that bloc

224 rosophila midgut, the Jun N-Terminal Kinase (JNK) pathway is activated in damaged enterocyte cells (E

225 r, we show that the c-Jun N-terminal kinase (JNK) pathway is involved in the regulation of autophagy

226 The c-Jun-N-terminal kinase (JNK) pathway is strongly activated after partial hepatec

227 y function of Mmp1, under the control of the JNK pathway, is to promote basement membrane repair, whi

228 h activation of the c-Jun N-terminal kinase (JNK) pathway, is able to propagate the initial apoptotic

229 variants with somatic mutations in MAP2K4, a JNK pathway kinase (shown in Figures 4C-E) resulted in a

230 re also known to be scaffolding proteins for JNK pathway kinases [5, 6].

231 Alternatively, sustained activation of JNK pathway led to an increase of the cytotoxicity of th

232 ies to modulate persistent activation of the JNK pathway may be beneficial in preventing disease prog

233 Together, these data demonstrate that the JNK pathway may contribute to the regulation of autocrin

234 Moreover, the activation of the JNK pathway may contribute to this event.

235 e in wildtype mice only, indicating that the JNK pathway may not be critically involved in the absenc

236 ng cells with MKP-1, indicating that p38 and JNK pathways may play important roles in H(2)O(2)-mediat

237 dependent noncanonical pathway(s), i.e., Wnt/JNK pathway, may play a role in the apoptotic inhibition

238 ate that cross-talk between the p38alpha and JNK pathways mediated by induction of DUSP1/MKP-1 regula

239 additional studies indicate that the MEKK-1/JNK pathway mediates critical aspects of neuronal surviv

240 echanism that can suppress the activation of JNK pathways normally induced by oxidative stress.

241 gly, USP48 only targets the TRAF2 related to JNK pathway, not the TRAF2 related to NF-kappaB and p38

242 ated kinase (ERK) and Jun N-terminal kinase (JNK) pathways; OipA activated the p38 pathway.

243 derived xenograft cells by inhibition of the JNK pathway or by disruption of the VANGL2-p62/SQSTM1 in

244 n-activated protein kinases but not the SAPK/JNK pathway; pharmacological inhibition of ERK1/2, but n

245 In summary, the JNK pathway plays an important role in lytic infection a

246 ontrol of tissue renewal through the IKK and JNK pathways plays a key role in liver carcinogenesis.

247 ugh new mechanisms involving Src/p38 and Rho/JNK pathways, possibly contributing to a pro-thrombotic

248 However, deficiency of both ERK and JNK pathways prevented Fgf15-mediated suppression of Cyp

249 o a wild-type phenotype, indicating that the JNK pathway prevents tumor formation.

250 The JNK pathway promotes axonal degeneration shortly after a

251 thus reveal a "loop" mechanism in which the JNK pathway promotes SIAH1 stabilization and in which SI

252 he ERK1/2 and p38 MAPK pathways, but not the JNK pathway, reduced TGF-beta 1-stimulated collagenase-3

253 ecrosis factor-induced signaling through the JNK pathway, reduced the activation of activator protein

254 We provide experimental evidence that JNK pathway regulates activation of caspases in Plasmodi

255 These findings indicate that the MEKK-1/JNK pathway regulates critical aspects of initial outgro

256 itive to the dosage of positive and negative JNK pathway regulators, which attenuate or potentiate SL

257 cules that link the TGFbeta receptors to the JNK pathway remain unknown.

258 zipper kinase (DLK)/c-Jun-N-terminal kinase (JNK) pathway represents a conserved regulator of neurona

259 kinase kinase 1 (MEKK1)/c-Jun-NH(2)-kinase (JNK) pathway represses hTR expression by a mechanism tha

260 y, which converge on the activation of a Rac/JNK pathway required for mast cell proliferation.

261 The activation of this cdc42/JNK pathway requires both an intact N terminus and funct

262 we report that propagation of the apoptotic JNK pathway requires the cooperative interaction of two

263 eactivation, we found that inhibition of the JNK pathway resulted in a marked reduction in reactivati

264 xcessive ROS leads to activation of the MKK4-JNK pathway, resulting in apoptosis.

265 These results show that activation of JNK pathway results in CDDO-Me-induced DR up-regulation,

266 t gene, and puc, a negative regulator of the JNK pathway, sensitize p53 mutant cells to ionizing radi

267 m, suggesting that strategies to inhibit the JNK pathway should be considered for the prevention and

268 d protein kinase/Jun N-terminal kinase (SAPK/JNK) pathway showed that phosphorylated c-Jun proteins,

269 ed marked suppression of c-jun-NH(2)-kinase (JNK) pathway signaling, and JNK inhibition suppressed si

270 ctive MEK/ERK or genetic interruption of the JNK pathway significantly diminished adaphostin/MG-132-m

271 d as an endogenous negative regulator of the JNK pathway, since it could block the upstream kinase MK

272 ve caspase 9) or a chemical inhibitor of the JNK pathway (SP600125).

273 armacological inhibitors of both the ERK and JNK pathways stopped the proliferation of primary erythr

274 Mutants in the Wnd-Jnk pathway suppress the overgrowth of SkpA mutants demo

275 kpA is a novel negative regulator of the Wnd-Jnk pathway that functions with Hiw to regulate both syn

276 aB kinase (IKK) and c-Jun N-terminal kinase (JNK) pathways that are coordinately regulated and import

277 A sequential pathway (the JNK pathway) that includes activation of Rac1/Cdc42, mix

278 tely inhibiting the TNF receptor complex and JNK pathway through a negative feedback mechanism.

279 appaB, which can act as the activator of the JNK pathway through the induction of GADD45alpha for tri

280 anscription level through activation of MAPK-JNK pathway, thus TAK1 represents an intrinsic host rest

281 es demonstrate that KSHV ORF36 activates the JNK pathway; thus this cell signaling pathway may functi

282 D3 thus couples tight junctions to the MEKK1-JNK pathway to regulate cell behavior and survival.

283 as a molecular switch to direct Dvl from the JNK pathway to the beta-catenin pathway, possibly by alt

284 ulation and cross talk with parallel ERK and JNK pathways to repress c-Jun activity.

285 hospholipase C signaling and the ERK-1/2 and JNK pathways together with receptor phosphorylation in t

286 n, we report that the jun N-terminal kinase (JNK) pathway upregulates Mmp1 expression after wounding,

287 r, lentiviral-mediated reconstitution of the JNK pathway using a constitutively active construct did

288 his study, the potential role of MLK and the JNK pathway was examined in MPP(+)-induced cell death of

289 nhibitors and siRNAs, we found that the MAPK-JNK pathway was involved in TAK1-mediated HBV suppressio

290 To inhibit the JNK pathway, we used either dominant-negative constructs

291 y which deoxycholic acid (DCA) activates the JNK pathway were examined.

292 In addition, AKT, p38, and JNK pathways were involved in morphine-induced down regu

293 In addition, ERK and/or JNK pathways were shown to be involved in regulating iTr

294 y Abeta induces a clusterin/p53/Dkk1/wnt-PCP-JNK pathway, which drives the upregulation of several ge

295 uR5-to-nucleus communication through the EGF/JNK pathway, which functions to regulate AP-1-mediated t

296 neurons, Abeta signals through a beta2AR-PKA-JNK pathway, which is responsible for most of the phosph

297 Thus, Rap2-JNK pathway, which opposes the action of the NR2A-contai

298 of the c-Jun NH(2)-terminal protein kinase (JNK) pathway, which is associated with cell apoptosis.

299 is signal and for the Jun N-terminal kinase (JNK) pathway, which promotes ISC proliferation in respon

300 Inhibition of the p38 or JNK pathways with pharmacological inhibitors or dominant