ライフサイエンスコーパス: JNK pathway

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

2 engulfing follicle cells, and activates the JNK pathway.

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

4 ary keratinocytes through attenuation of the JNK pathway.

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

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

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

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

9 egulated Cdk5 induces biphasic activation of JNK pathway.

10 t, without activation of the proinflammatory JNK pathway.

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

12 Finally, K13 does not activate the JNK pathway.

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

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

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

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

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

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

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

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

21 its ability to maximally signal through the JNK pathway.

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

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

24 t dramatically inhibited Dvl activity in the JNK pathway.

25 potentiates cell death signaling through the JNK pathway.

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

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

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

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

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

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

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

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

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

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

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

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

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

39 triggers and involvement of both IKKbeta and JNK pathways.

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

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

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

43 Live bacteria also activated the p38 and JNK pathways.

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

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

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

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

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

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

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

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

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

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

54 a component of the c-Jun N-terminal kinase (JNK) pathway.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 Inactivation of Gish resulted in aberrant JNK pathway activation and excessive production of multi

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

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

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

73 lex ensures germ cell survival by preventing JNK pathway activation, and that the mechanism by which

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 this reduces viability and decreases ERK and JNK pathway activation.

78 JNK pathway components facilitating nuclear JNK pathway activation.

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

80 hila adult midgut homeostasis by restricting JNK pathway activity and that Gish is essential for inte

81 It appears that the JNK pathway activity divergently attenuates IL-23p19 exp

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

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

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

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

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

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

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

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

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

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

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

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

94 terized that MBIP mediates activation of the JNK pathway and induces expression of matrix metalloprot

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

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

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

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

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

100 ation is required for full activation of the JNK pathway and the secondary phase of the NF-kappaB pat

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

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

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

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

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

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

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

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

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

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

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

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

113 s suggested that histone methylation and the JNK pathway are involved in LPS-trained immunomodulation

114 Signals via the Gp130/JAK/STAT3 and DLK/JNK pathways are important for axonal injury responses,

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

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

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

118 cal interneurons, and further implicates the JNK pathway as an important regulator of cortical develo

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

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

121 cently identified the Jun N-terminal kinase (JNK) pathway as an important mediator of cortical intern

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

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

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

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

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

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

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

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

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

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

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

133 on the inhibition of a feedback-loop in the JNK-pathway by the immune effector and antimicrobial pep

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

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

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

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

138 RNAi-mediated depletion of JNK pathway components inhibits oviposition in mated fem

139 Knocking down expression of JNK pathway components or the GTPase Rab35 in cyst cells

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

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

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

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

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

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

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

147 The MAPK/ERK and MAPK/JNK pathways, crucial for normal cellular responses to e

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

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

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

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

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

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

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

155 0 and this synergized with inhibition of the JNK pathway for limiting IL-27p28.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 IL-10 production by MCG, implicating miR-21-JNK pathway in MCG-mediated IL-10 production by macropha

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

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

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

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

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

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

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

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

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

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

182 ion of WT MAP3K19 activates both the ERK and JNK pathways in a panel of cancer cell lines.

183 nt understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer

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

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

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

187 e-specific overactivation of the Jun-kinase (JNK) pathway in cyst cells.

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

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

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

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

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

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

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

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

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

197 JNK pathway induction bypassed cell cycle restraints ind

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 When the JNK pathway is ectopically activated to overexpress Mmp1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 The JNK pathway promotes axonal degeneration shortly after a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 Genes regulated by the TGFB and JNK pathway were overexpressed specifically in EAC and d

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