ライフサイエンスコーパス: JNK

1 JNK activation was confirmed in livers of patients homoz

2 JNK activation was not triggered by reactive immune cell

3 JNK activity was critical for ICAM-1-induced F-actin rea

4 JNK activity was not affected by TLR2 activation.

5 JNK and p38 MAPK drive the recruitment of transcription

6 JNK further promotes and amplifies caspase activity, the

7 JNK inhibition with SP600125 shows off-target effects.

8 JNK is known to mediate many cellular events via activat

9 JNK proteins are activated via phosphorylation in respon

10 JNK was suppressed by SP600125 or Jnk siRNA.

11 JNKs and ERK1/2 also phosphorylated p21 at S130 and T57,

12 evity of nematodes by activating the TIR-1 - JNK-1 - DAF-16 signaling pathway, and the cell wall comp

13 urthermore, activation of endothelial ICAM-1/JNK led to phosphorylation of paxillin, its association

14 s remarkably independent of DLK-1/DLK, KGB-1/JNK, and other MAPK signaling factors known to mediate r

15 hemoattractant-induced activation of ERK1/2, JNK and PI3K pathways, but only the MEK inhibitor UO126

16 oylation of receptor-associated Galphai in a JNK-dependent manner.

17 d pluripotent stem cell-hepatic cells with a JNK inhibitor reduced accumulation of ATZ.

18 gosertib and paclitaxel/Taxol, that activate JNK through mitotic and oxidative stress as well as by p

19 from DILI patients contained more activated JNK, predominantly in nuclei of hepatocytes and in immun

20 also exhibited elevated levels of activated JNK as well as enhanced p70S6K1 autoinhibitory domain ph

21 tes reactive oxygen species (ROS), activates JNK and p38 pathways, and prompts apoptosis.

22 lly, AGGF1 initiates autophagy by activating JNK, which leads to activation of Vps34 lipid kinase and

23 In addition, JNK inhibition limits viral reactivation, exhibiting par

24 ivation, we investigated whether ARC affects JNK signaling in amyloid-forming islets.

25 ti-inflammatory brake in hepatocytes against JNK and NF-kappaB and limits their activation and downst

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

27 orescence microscopy revealed that TIR-1 and JNK-1 are involved in the phosphorylation and activation

28 Inhibitors of ERK1/2 and JNK kinases abolished and significantly decreased H. pyl

29 ession by specifically activating Erk1/2 and JNK signaling pathways.

30 the combined action of JAK, SRC, c-ABL, and JNK kinases.

31 rylation, MKK4 (but not MKK7) activation and JNK/AP-1 induction, leading to a Bak- and Bax-dependent

32 ention to protect against ALF; autophagy and JNK may also provide therapeutic targets for ALF treatme

33 ant transformation of different cancers, and JNK is highly activated in basal-like triple-negative br

34 -kappaB and three major MAPKs (P38, ERK, and JNK), the essential components of signaling pathways dow

35 required for the induction of NF-kappaB and JNK and for the recruitment of macrophages.

36 stream signaling intermediates NF-kappaB and JNK.

37 uced nitroxidative stress, IKK/NF-kappaB and JNK/AP-1 activation, inflammatory cytokine, chemokine, a

38 vated protein kinases (SAPKs), p38 MAPK, and JNK.

39 ncy also promotes the activation of MKK4 and JNK and cytokine production independently of RIPK1 kinas

40 rying some loser mutations activate Nrf2 and JNK signalling, which contribute to the loser status.

41 dox activation of the stress kinases p38 and JNK is instrumental in neuronal death by oxidative stres

42 s (ASK1-3) are apical kinases of the p38 and JNK MAP kinase pathways.

43 Furthermore, ERK1/2, p38 and JNK MAPKs, but not PI3K, were individually necessary for

44 n we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessa

45 Stress-associated p38 and JNK mitogen-activated protein (MAP) kinase signaling cas

46 asic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT

47 ly infected cells, and activation of p38 and JNK signaling by anisomycin resulted in increased cell d

48 CsA and FK506 inhibited PAN-induced p38 and JNK signaling, thereby protecting podocytes from PAN-ind

49 ifically, the stress kinase pathways p38 and JNK were modified in latently infected cells, and activa

50 Prolonged LPS-induced activation of p38 and JNK, phosphorylation of downstream transcription factors

51 osphorylation of IkappaBalpha, ERK, p38, and JNK in HIV-infected cells across two in vitro latency mo

52 we show that endothelial MAPKs ERK, p38, and JNK mediate diapedesis-related and diapedesis-unrelated

53 by which heparanase activates Erk, p38, and JNK signaling in macrophages, leading to increased c-Fos

54 Signaling through p38MAPK and JNK in reprogrammed macrophages was enhanced by CCL5-bou

55 ation of stress related kinases (p38MAPK and JNK).

56 the accumulation of autophagosomes, p62, and JNK signaling.

57 connection between loss-of-cell polarity and JNK activation, much less is known about the molecular m

58 ced pro-inflammatory cytokine production and JNK activity under hypoxia were prevented by inhibiting

59 In this study, we found that ROS and JNK inhibitors block HCV up-regulation of ER stress and

60 ys including Ras, PI3K/Akt, Raf/ERK, Src and JNK.

61 vation of key inflammatory mediators such as JNK and IkappaB kinase (IKK) occurs rapidly upon consump

62 nally, TAT.ARC treatment inhibited DAXX-ASK1-JNK signaling in the ischemic brain.

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

64 on of the proapoptotic proteins BIM and BAX, JNK signaling, and endoplasmic reticulum stress, explain

65 RC binds JNK, suggesting interaction between JNK and ARC decreases amyloid-induced JNK phosphorylatio

66 RC from mouse islet lysates showed ARC binds JNK, suggesting interaction between JNK and ARC decrease

67 Blocking JNK activation failed to further reduce cytokine-induced

68 paB, and TGF-beta1 signaling were blocked by JNK specific siRNA.

69 ls: an invasive population, characterized by JNK-dependent elevation of Mmp1 expression, and a hyperp

70 thogenic stimuli, a process also mediated by JNK activation.

71 and TIMP-3 in CD146(+) TSCs are regulated by JNK/signal transducer and activator of transcription 3 s

72 c subunit of telomerase that was reversed by JNK inhibition.

73 ikely involve the downregulation of SOCS3 by JNK inhibition.

74 id not impair the phosphorylation of CDK4 by JNKs.

75 rosis factor (Tnf) from Kupffer cells caused JNK-mediated cholangiocellular proliferation and oncogen

76 In cells, JNK activation enhanced p70S6K1 phosphorylation and mTOR

77 pression near ICC lesions, cholangiocellular JNK-phosphorylation, and ROS accumulation in surrounding

78 city and increased autophagy while decreased JNK activation.

79 cies (ROS) or intervening with ROS-dependent JNK activation that leads to its activation-induced cell

80 In two selected tumor cells, two different JNK inhibitors inhibited the phosphorylation and activat

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

82 IK or MAP4K7), as upstream regulators of DLK/JNK signaling in neurons.

83 kinase 1 (MINK1 or MAP4K6) in regulating DLK/JNK signaling in neurons.

84 on MAP4Ks as important regulators of the DLK/JNK signaling pathway.SIGNIFICANCE STATEMENT Neuronal de

85 ly to regulate DLK activation and downstream JNK-dependent phosphorylation of c-Jun in response to st

86 perproliferative population lacking elevated JNK signalling.

87 Endothelial JNK and to a much lesser degree p38 were the principal M

88 Silencing IGFBP-3 in Huh7 cells enhanced JNK and NF-kappaB activity and increased palmitate-induc

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

90 proliferation and apoptosis while enhancing JNK signaling.

91 ion was observed in MAPK pathways (p38, ERK, JNK) and the NF-kappaB pathway (IKKalpha/beta, NF-kappaB

92 small GTPases, which ultimately lead to ERK, JNK, and p38 phosphorylation.

93 LP-induced phosphorylation of PAK1/2 and ERK/JNK MAPK (P < 0.05).

94 associated with modulation of PAK1/2 and ERK/JNK MAPK signaling and F-actin dynamics.

95 tivated multiple intracellular pathways (ERK/JNK, MYC/MAX, WNT, retinoblastoma), altered oncogenes an

96 These findings establish JNK-dependent PRDX6 recruitment and oxidation-induced Ga

97 cancer cells, probably mediated via the FAK/JNK signaling pathway.

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

99 expression of pro-apoptotic and pro-fibrotic JNK and TGFbeta1 proteins in Ppif-/- females.

100 ed in the overexpression of IFN-beta: first, JNK-mediated activation of c-jun, which binds to the IFN

101 poorly characterized scaffolding protein for JNK signaling.

102 Moreover, they establish a causal role for JNK in the hippocampal neurogenic niche and anxiety beha

103 Previously unobserved negative feedback from JNK also contributes to Wnd repression at both time poin

104 Motivated by these problems, we identified JNK-interacting protein 3 (JIP3) as an important regulat

105 est of IkB-alpha activation and reduction in JNK(MAPK) phosphorylation.

106 uce mitotic and oxidative stress, results in JNK-mediated inhibition of RAS-MAPK pathway components S

107 aling cascades downstream of LRP6, including JNK and WNT/beta-catenin, inhibited the biologic activit

108 ted cellular oxidative stress, and increased JNK activity.

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

110 etween JNK and ARC decreases amyloid-induced JNK phosphorylation and downstream signaling.

111 Priming is triggered via calcium-induced JNK signaling, which leads to upregulation of the damage

112 in IBMIR and suppression of cytokine-induced JNK and NF-kappaB activation.

113 MLN9708 also enhanced Dox-induced JNK and p38 phosphorylation and inhibited Dox-induced Ik

114 kinase (DLK) is required for stress-induced JNK signaling in neurons, yet the factors that initiate

115 ting Mule E3 ligase activity and TNF-induced JNK activation and cell death.

116 f ECs resulted in decreased TNFalpha-induced JNK and p38 activity and downstream target phosphorylati

117 nism by which aberrant cell polarity induces JNK-mediated cell migration and tumor invasion.

118 and the therapeutic intervention inhibiting JNK activities represents a promising approach to amelio

119 s H2O2-induced Bim activation via inhibiting JNK phosphorylation, subsequently preventing the apoptos

120 ing GRP78, PERK, eIF2alpha, ATF4, IRE1alpha, JNK, p38, and CHOP.

121 cytokine-induced activation of the IRE1alpha/JNK pro-apoptotic pathway in cytokine-exposed beta cells

122 P2 activates IkappaB kinase (IKK)/NF-kappaB, JNK/AP-1, and c/EBPbeta and stimulates the expression of

123 resulted in the activation of IKK/NF-kappaB, JNK/AP-1, c/EBPbeta, and p38 MAPK and induction of proin

124 increase in activation of the stress kinase JNK and production of the matrix metalloproteinase MMP1.

125 nases p38 and Jun N-terminal protein kinase (JNK).

126 uroinflammation and c-Jun-N-terminal kinase (JNK) activation, which is associated with memory deficit

127 h cell polarity and c-Jun N-terminal kinase (JNK) activity are essential to the maintenance of tissue

128 duces activation of c-Jun N-terminal kinase (JNK) and c-Jun and that genetic ablation of JNK1 or JNK2

129 esion kinase (FAK), Jun NH2-terminal kinase (JNK) and c-Jun signals, but not extracellular signal-reg

130 Moreover, c-Jun N-terminal kinase (JNK) has been implicated in regulation of spontaneous re

131 The role for c-Jun N-terminal Kinase (JNK) in the control of feeding and energy balance is not

132 ted kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected

133 c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase

134 ing through p38 and c-Jun N-terminal kinase (JNK) MAPK pathways alters gene expression and leads to m

135 ulated kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)] were asse

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

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

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

139 s (MAPKs); notably, c-Jun N-terminal kinase (JNK) phosphorylation depends on TLR4 initiation.

140 receptor complex by c-Jun N-terminal kinase (JNK) phosphorylation.

141 d by suppression of c-Jun N-terminal kinase (JNK) phosphorylation.

142 rther show that c-Jun amino-terminal kinase (JNK) plays a pivotal role in mediating vesicle-induced C

143 c-Jun N-terminal kinase (JNK) plays a vital role in malignant transformation of d

144 ression upregulates c-Jun N-terminal kinase (JNK) protein levels, which is required for miR-203 expre

145 tion result in both c-Jun N-terminal Kinase (JNK) signaling and the PERK- and ISR-dependent upregulat

146 tion of ERK 1/2 and c-Jun N terminal kinase (JNK) signaling attenuated TNFalpha-induced DUSP5 express

147 emonstrate that c-Jun amino-terminal kinase (JNK) signaling is crucial for germline cyst breakdown an

148 The c-Jun-N-terminal kinase (JNK) signaling pathway regulates nervous system developm

149 ulin secretion, and c-Jun N-terminal kinase (JNK) signaling.

150 ion of proapoptotic c-Jun N-terminal kinase (JNK) signaling.

151 Draper to activate c-Jun N-terminal kinase (JNK) signalling in glia, resulting in changes in transcr

152 aB kinase (IKK) and c-Jun N-terminal kinase (JNK), and an important mediator of autoimmune and inflam

153 ation of NF-kappaB, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and A

154 one such MAPK, the c-Jun N-terminal kinase (JNK), in VZV lytic infection and reactivation.

155 tivation in turn of c-Jun N-terminal kinase (JNK), the Axl receptor tyrosine kinase and extracellular

156 induced ALF through c-jun-N-terminal kinase (JNK)-dependent autophagy.

157 ned activation of c-Jun NH2-terminal kinase (JNK)-signaling cascades, pro-inflammatory effectors/cyto

158 inactivation of the c-Jun N-terminal kinase (JNK).

159 g Kinase 1 (ASK1) and Jun-N-terminal Kinase (JNK).

160 metabolism and c-Jun NH(2)-terminal kinase (JNK).

161 cription (Stat92E), c-Jun N-terminal kinase (JNK)/AP-1 signaling, and expression of matrix metallopro

162 AiP via activation of Jun N-terminal kinase (JNK); however, the specific mechanisms of JNK activation

163 pathway, involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase, and intracellular cGMP, ex

164 ng the activation of two signalling kinases, JNK and FAK, and stimulating trophoblast migration.

165 or (SP600125) or knockdown technology (Lenti-JNK-shRNAs) resulted in significantly suppressed cyst br

166 dipocytes, which was sensitive to macrophage JNK inhibition.

167 expression through an Arrestin-mediated MAPK JNK/ERK phosphorylation cascade.

168 ctivation of VAV1 catalytic-dependent (MAPK, JNK) and non-catalytic-dependent (nuclear factor of acti

169 reactive oxygen species (ROS) and p38 MAPK, JNK, ERK1/2, and NFkappaB-dependent pathways.

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

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

172 , but not TLR3, and inhibition of the MAPKs (JNK and p38) or NF-kappaB abolished miR-146a-induced cfB

173 In the DIO mice, JNK inhibition sensitized leptin's anorectic effect, and

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

175 It has been reported that MKK7-JNK signaling plays an important regulatory role in neur

176 Thus, the MKK7-JNK signaling pathway plays important roles in regulatin

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

178 In a TNBC xenograft mouse model, JNK-IN-8 significantly suppressed tumor growth in a dose

179 2 and E2 Activation of ERKs and p38, but not JNKs, by C. albicansacted synergistically with prostagla

180 Notably, JNK inhibitors exerted potent antifungal therapeutic eff

181 K inhibitors, we investigated the actions of JNK in the control of feeding and body weight homeostasi

182 l death through the persistent activation of JNK and accumulation of reactive oxygen species (ROS).

183 We also demonstrate that activation of JNK by subtoxic concentrations of anisomycin induced sel

184 e we show that caspase-induced activation of JNK during AiP depends on an inflammatory response.

185 nd inhibits the post-traumatic activation of JNK in a rodent model of TBI.

186 ), which impaired constitutive activation of JNK in the nervous system.

187 -derived neurons and that this activation of JNK is essential for efficient viral protein expression

188 ic activity and the subsequent activation of JNK.

189 Genetic or chemical blockades of JNK and MMP1 suppressed metastatic dissemination associa

190 atients and in mice with genetic deletion of JNK in hepatocytes.

191 Importantly, disruption of JNK signaling with a specific inhibitor (SP600125) or kn

192 nhibition prevented the repressive effect of JNK activation on insulin action in retinas.

193 V isolate was as sensitive to the effects of JNK inhibition as an acyclovir-sensitive VZV isolate in

194 , but not in SAT, correlated with indexes of JNK signaling activity, IL6, waist-to-hip ratio and hsCR

195 eta1 through ROS production and induction of JNK and the IRE1 pathway.

196 Inhibition of JNK blocked the hypoxic induction of pro-inflammatory cy

197 Inhibition of JNK increased autophagy and exhibited strongly protectiv

198 However, inhibition of JNK signaling leads to aberrantly enhanced localization

199 Inhibition of JNK, which causes DNA damage-induced apoptosis, partiall

200 itochondrial pathway in which interaction of JNK and Sab on the outside of the mitochondria released

201 Knockdown of JNK, CaMKKbeta, AMPK, or ULK1 prevented T. gondii killin

202 e (JNK); however, the specific mechanisms of JNK activation remain unknown.

203 roteomic analyses to determine mechanisms of JNK activity in hepatocytes.

204 The second phase of JNK phosphorylation was dependent on autocrine productio

205 NAs in calcineurin-independent regulation of JNK and p38 MAPKs caused by targeting of MAP3K1.

206 We investigated the role of JNK in drug-induced liver injury (DILI) in liver tissue

207 However, the roles of JNK in regulating cancer stem-like cell (CSC) phenotype

208 Opioid stimulation of JNK also inactivates dopamine D2 receptors in a PRDX6-de

209 induction of autophagy while suppression of JNK.

210 anxiety behaviour, and advocate targeting of JNK as an avenue for novel therapies against affective d

211 fectors of the ischemic cascade, upstream of JNK, caspases, and BIM and BAX activation.

212 A specific upstream activator of JNKs is the mitogen-activated protein kinase kinase 7 (M

213 timuli, with both effects being dependent on JNK activation.

214 enhancing effects of E2 are not dependent on JNK or GPER activation in the DH.

215 lls, as well as IL-10 production, depends on JNK signaling, but not on known PGRN-activated ERK and P

216 orous epithelial cells to activate oncogenic JNK signaling.

217 ntify DLK as a central regulator of not only JNK but also PERK stress signaling in neurons, with both

218 , Kupffer cell depletion, Tnfr1 deletion, or JNK inhibition reduced cholangiocellular pre-neoplastic

219 ished that inhibition of p38, but not ERK or JNK, rescue T cells from undergoing peripheral deletion

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

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

222 downstream signaling molecules: p-MKK4 and p-JNK was observed.

223 Phosphorylated JNK (p-JNK) interacts with the mitochondrial outer membrane SH3

224 n of mitochondrial p-Src and the effect of p-JNK on mitochondria.

225 decrease in IkappaB kinase alpha/beta, p38, JNK, and Erk1/2 kinase phosphorylation and at the nuclea

226 timulating the rapid phosphorylation of p38, JNK and activation of transcription factor NF-kappaB.

227 ream p38 MAPK signaling pathway and the p38, JNK, and ERK pathways, respectively.

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

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

230 diates aspect of the anorectic effect by pan-JNK inhibition.

231 ne triphosphate-competitive irreversible pan-JNK inhibitor, significantly reduced cell proliferation,

232 SR-3306, a brain-penetrant and selective pan-JNK (JNK1/2/3) inhibitor, reduced food intake and body w

233 Phosphorylated JNK (p-JNK) interacts with the mitochondrial outer membr

234 vels of total and activated (phosphorylated) JNK were measured by immunohistochemistry and Western bl

235 ted PSD-95 and JNK1 in vitro Inhibiting PKC, JNK, or calcium/calmodulin-dependent kinase II activity

236 ccumulation of the axonal transport proteins JNK-interacting protein 1 and amyloid beta precursor pro

237 tivation, whereas ARC overexpression reduces JNK, c-Jun phosphorylation, and c-Jun target gene expres

238 ng delays neurodegeneration without reducing JNK signaling.

239 stant to the combined therapy, PAKs regulate JNK and beta-catenin phosphorylation and mTOR pathway ac

240 nflammatory state whose acquisition requires JNK activation.

241 n of PPM1A activity by sanguinarine restored JNK activation, resulting in increased apoptosis of Mtb-

242 hese MAP4Ks blocks stress-induced retrograde JNK signaling and protects from neurodegeneration, sugge

243 rc, leading to Fra-1 activation, whereas Rho/JNK mediated P2Y2R-induced activation of c-Jun and ATF-2

244 renewal and core pluripotency genes via ROR2/JNK signaling and in parallel cisplatin resistance via l

245 MyD88-NF-kappaB and cell death via Wek-Sarm-JNK.

246 ERK1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP600125), or PI3K (LY294002) were used to det

247 Here, by use of novel and highly selective JNK inhibitors, we investigated the actions of JNK in th

248 XO3-driven apoptosis and recently a specific JNK (c-Jun N-terminal kinase)-dependent S574 phosphoryla

249 letely blocked in the presence of a specific JNK inhibitor.

250 pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-kappaB, and PTEN/PI3K/AKT.

251 he key FcepsilonRI signaling proteins Stat5, JNK, and ERK.

252 el Drosophila brain through a Draper/STAT92E/JNK cascade that may be coupled to protein degradation p

253 -AMPK-FOXO-signaling axis over the sustained JNK-elevation and injurious insulin resistance in CHIP(-

254 ated c-Jun activation in TNBC cells and that JNK activation correlated with c-Jun activation in TNBC

255 Cga gene transcriptional start site and that JNK inhibition dramatically reduces H3S10p levels.

256 Taken together, our data demonstrate that JNK regulates TNBC tumorigenesis by promoting CSC phenot

257 Finally, we find that JNK signaling after injury requires DR6, suggesting a li

258 We find that JNK signalling inhibits the growth of losers, while JAK/

259 Here, we found that JNK regulated c-Jun activation in TNBC cells and that JN

260 ng via activation of c-Jun and indicate that JNK/c-Jun/Notch1 signaling is a potential therapeutic ta

261 , and mammosphere formation, indicating that JNK promotes CSC self-renewal and maintenance in TNBC.

262 These data reveal that JNK is a key pathway in the disease pathogenesis and add

263 We further show that JNK signaling is activated inside the tumor and in nearb

264 Collectively, our data suggest that JNK activity promotes positive energy balance, and the t

265 In conclusion, our results suggest that JNK signaling, which is inversely correlated with WNT4,

266 Here, we report that JNKs, but not ERK1/2 or CAK, can be direct CDK4-activati

267 The JNK inhibitors SP600125 and AEG3482 strongly decreased i

268 excessive adipocyte lipolysis activates the JNK/NFkappaB pathway leading to the up-regulation of COX

269 We found that lipolysis activates the JNK/NFkappaB signaling pathway and inhibition of the JNK

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

271 Overall, the results identify the JNK/S6K1 axis as a key molecular mechanism whereby a hig

272 ubjects carrying common polymorphisms in the JNK or the MC4R gene to be more susceptible to HI.

273 s well as by physiological regulators of the JNK cascade and may function as a signaling checkpoint t

274 Moreover, DH infusion of the JNK inhibitor SP600125 prevented G-1 from enhancing obje

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

276 0 and this synergized with inhibition of the JNK pathway for limiting IL-27p28.

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

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

279 d subsequent retrograde translocation of the JNK signaling complex to the nucleus.

280 ppaB signaling pathway and inhibition of the JNK/NFkappaB axis abrogated the lipolysis-stimulated COX

281 -lineage family of kinases that regulate the JNK, p38, and ERK kinase signaling pathways.

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

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

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

285 Thus, we hypothesized that the JNK/c-Jun signaling pathway contributes to TNBC tumorige

286 ription via activation of c-Jun and that the JNK/c-Jun signaling pathway promoted CSC phenotype throu

287 Therefore, JNKs could be activating kinases for cyclin D1-CDK4 boun

288 ase reverse transcriptase inhibition through JNK activation.

289 Targeting the ROS/Tnf/JNK axis may provide opportunities for ICC therapy.

290 link in TNF signaling pathway that leads to JNK activation and cell death.

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

292 necessary for engaging the ISR subsequent to JNK-mediated retrograde injury signaling.

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

294 icrotubule stability as the initial trigger, JNK signalling as the central mediator, and kinesin-3 me

295 ell-autonomous activation of the tumorigenic JNK stress-activated pathway drives the expression of se

296 ng mechanism in hepatocytes that can act via JNK and subsequent phosphorylation of the histone varian

297 regulate inflammation in tendon healing via JNK and STAT3 signaling.

298 knockdown of JNK1 or JNK2 or treatment with JNK-IN-8, an adenosine triphosphate-competitive irrevers

299 expression levels of sFRP1/5 antagonize Wnt/JNK signaling.

300 sFRP1/5 act additively to potentiate the Wnt/JNK signaling pathway governing the positioning of the A