ライフサイエンスコーパス: JNK

1 JNK activation by U50,488 and dynorphin B also stimulate

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

3 JNK inactivation suppresses osteogenic differentiation,

4 JNK inhibition or NLRP12 overexpression reduced prolifer

5 JNK inhibitors were also effective at stopping high D-gl

6 JNK links to 53BP1, a nuclear protein that negatively re

7 JNK signaling activates a matrix metalloprotease (MMP1)

8 JNK was also required for the proper axonal transport of

9 JNK was suppressed by SP600125 or Jnk siRNA.

10 JNK-mediated inhibition of adiponectin secretion increas

11 JNK/AP-1 signaling commissions chromatin accessibility a

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

13 a-catenin and non-canonical Wnt1/Wnt8-Fzl5/8-JNK signaling.

14 ration strongly blocked GSK-3beta (Serine 9)/JNK phosphorylation in the APAP-induced acute liver inju

15 GSK-3beta (Serine 9)/JNK phosphorylation is mainly involved in APAP-induced l

16 and that dual-specificity phosphatase 16, a JNK-specific phosphatase, functions as an endogenous reg

17 Our experiments identify a JNK-dependent feedback amplification loop between intest

18 and osteoclastogenesis in the presence of a JNK inhibitor (SP600125).

19 a transcriptional signature reminiscent of a JNK-dependent wounding response, while mating-or injecti

20 letion of the risk locus or treatment with a JNK antagonist was sufficient to maintain gap junctions

21 ) at Ser63 and Ser73 after SSL exposure in a JNKs-independent manner.

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

23 normal MN development raising caution about JNK antagonism in this pediatric neuromuscular disease.

24 Accordingly, JNK inhibition is capable of reversing MAP2K7Deltaexon2-

25 Despite retained capacity to activate JNK-c-Jun, we observed no basal increase of p-c-Jun leve

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

27 udies reveal no evidence of stress-activated JNK-c-Jun signaling in MNs of SMA mice or human tissues,

28 ound that cell polarity disruption activates JNK signaling, which in turn upregulate wg expression th

29 ins with exogenous 20E-selectively activates JNK in the same tissue.

30 phosphorylation of ERK1/2 without affecting JNK or p38, and contributed to CXCL1 and TNF production.

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

32 ad, it selectively activated MAPK ERK1/2 and JNK.

33 gulated kinase), AKT (protein kinase B), and JNK (c-Jun N-terminal kinase) pathways.

34 uld promote novel cross talk between CaN and JNK signaling by limiting MKK7gamma phosphorylation and

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

36 or Pyk2 reduced TNF-alpha-stimulated ERK and JNK activation and CAM expression, suggesting that activ

37 that MAP3K19 directly activates the ERK and JNK cascades and highlight a role for this kinase in mai

38 quires FAK/Pyk2 activity to activate ERK and JNK MAPKs leading to inflammatory gene expression.

39 this reduces viability and decreases ERK and JNK pathway activation.

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

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

42 , a pro-death MAPK, without altering ERK and JNK.

43 ase in gene expression by activating ERK and JNK; these changes in gene expression could be mitigated

44 tream signaling molecules p38 MAPK, ERK, and JNK contribute fundamentally to a long-range metaplastic

45 defense, to dampen downstream NF-kappaB and JNK activation and immune responses.

46 ncy, resulting in activation of p38 MAPK and JNK.

47 The apparent balance between p38 MAPK and JNK/ROS signaling has important physiological implicatio

48 d neutrophil death was PI3K-, p38 MAPK-, and JNK-dependent and evoked anti-inflammatory cytokines in

49 bule ends, both phosphomimetic mutations and JNK activation increase the occurrence of CLIP-170 remna

50 ffacement, cell death, and sustained p38 and JNK activation.

51 ory cytokines and exhibited elevated p38 and JNK activities, at least in part, because of lower MAPK

52 kinase (MAPK) family members such as p38 and JNK and induced nuclear factor kappa B (NF-kappaB) pathw

53 man MAP3K4 functions upstream of the p38 and JNK mitogen activated protein kinases (MAPKs).

54 vated protein kinase (MAPK) pathway (p38 and JNK) in mouse hippocampal cultures.

55 sponses involve activation of MAPKs (p38 and JNK).

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

57 SK1 and activation of stress kinases p38 and JNK.

58 Pharmacological inhibition of PDGFRbeta and JNK impaired tumor cell invasion induced by integrin alp

59 f BDNF and FGF2, through the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the bene

60 es in reactive oxygen species production and JNK phosphorylation.

61 e is a multi-step process requiring ROS- and JNK-mediated Mmp2 upregulation and BM damage.

62 n this region, local endogenous JAK-STAT and JNK signaling creates a tissue microenvironment that is

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

64 Strategies to block the TGFB and JNK signaling pathways might be developed for treatment

65 dysplastic BE tissues, we found the TGFB and JNK signaling pathways to be hyperactivated in EACs and

66 onal guidance, inflammation (AMPK, NFKB, APK/JNK signaling), and antioxidant signaling (NRF2, HIF1A).

67 ASK1-JNK signaling promoted phosphorylation of the UPR-associ

68 In axons, JNK and Rab5 were required for retrograde transport and

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

70 cle (GM) by western blotting; IKKalpha/beta, JNK, ERK 1/2, NF-kappaBp65, and NF-kappaBp50 phosphoryla

71 I3, and MAPK3 involved in the WNT, TGF-beta, JNK, HedgeHog and ERK1/2 pathways suggests the regulatio

72 amples we found a direct correlation between JNK activation, NE levels and Bmal1 expression in the li

73 U50,488 and dynorphin B stimulated biphasic JNK activation with an early arrestin-independent phase,

74 e found that in OmpU-treated monocytes, both JNK and p38 activation is linked to the TLR2 activation

75 hibitors stimulate EC proliferation via both JNK activation and the unfolded protein response caused

76 hages, p38 activation is TLR2 dependent, but JNK activation happens through a separate pathway involv

77 by a feed-forward regulatory loop caused by JNK-regulated FGF21 autocrine signaling in adipocytes th

78 ndependent pathways that share modulation by JNK, Fos, and Jun that influence how axons respond to st

79 rol of the regulation of dendrite pruning by JNK signaling.

80 ed cytoprotective pathways, linking calcium, JNK, Nrf2, and Gadd45, that act to both "shield" tissues

81 healing but becomes detrimental upon chronic JNK overstimulation, with important implications for chr

82 provide a conserved mechanism that connects JNK and Wnt signaling in regulating tumor progression.

83 In contrast, JNK activator (anisomycin)-induced autophagy was blocked

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

85 re required for Gp130/JAK/STAT3, but not DLK/JNK, axon-to-soma signaling.

86 was dependent on the neuronal pathway of DLK/JNK activation and included an initial wave of viral gen

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

88 pendent manner and to promote its downstream JNK activation, leading to the production of tenascin C,

89 h marker, Fas, with activation of downstream JNK and p38 MAPK.

90 by impaired peroxisomal import and elevated JNK signaling in aged oenocytes.

91 IL-4-activated macrophages leads to enhanced JNK activation, thereby promoting a phenotypic switch fr

92 ells, which express MKK7gamma mRNA, enhances JNK activation.

93 immunoregulation by blunting the MAPK (ERK, JNK)-mediated priming signal of the NLRP3 inflammasome a

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

95 We examined JNK-c-Jun activity in SMA mouse and human cultured cells

96 tor, Relish, and the stress signaling factor JNK, encoded by the gene basket in Drosophila.

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

98 response to AZA, consistent with a role for JNK in RNase L-induced apoptosis.

99 rrent study, we demonstrate a vital role for JNK signaling at later stages of corticogenesis, when in

100 G2-stalling protects cells from JNK-induced apoptosis, but under chronic conditions, red

101 in their rapid elimination via the TNF/Eiger>JNK signalling pathway, local over-expression of NR2 cau

102 Here we demonstrate that hepatic JNK controls bile acid production.

103 We found that hepatic JNK deficiency alters cholesterol metabolism and bile ac

104 Signaling analyses demonstrated higher JNK activation in Nlrp12(-/-) HCC and cultured hepatocyt

105 Together, these data identify JNK as a potential conduit linking stress responses and

106 Because the Akt-IKK-JNK-MEK-MK2 pathways regulate many important cellular fu

107 No differences were identified in JNK phosphorylation status and DNA methylation in the ev

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

109 Recently, increased JNK-c-Jun signaling was reported in SMA raising the poss

110 lated C3 botulinum toxin substrate 1-induced JNK phosphorylation.

111 not prevent activation of the stress-induced JNK-c-Jun signaling pathway.

112 FGF signaling induces JNK-dependent proteasomal degradation of the insulin rec

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

114 We find that inhibiting JNK signaling or depletion of the microbiome restores ba

115 o the c-Jun N-terminal kinase (JNK) inhibits JNK phosphorylation, which is required for downstream ap

116 criptional regulation of ZEB1, ITGA3, ITGB1, JNK, and ENT1 by ZIP4 using chromatin precipitation and

117 n in raw mutants requires JNK, Fos, and Jun, JNK also promotes axonal degeneration.

118 ROS and the stress kinase JNK mediate the accumulation of matrix metalloproteinase

119 activates the redox-sensitive stress kinase JNK.

120 uces apoptosis in the absence of Jun kinase (JNK) activation, but instead leads to elevated levels of

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

122 s transcriptionally regulated by Jun-Kinase (JNK), which has been previously implicated in progenitor

123 amplified by Jun N-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK) sig

124 ivating the c-Jun N-terminal protein kinase (JNK) and NF-kappaB pathways; however, the precise mechan

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

126 on enhanced p38 and c-Jun N-terminal kinase (JNK) activity and podocyte dysfunction.

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

128 at operates via the c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) sig

129 otein kinase (MAPK) c-Jun N-terminal kinase (JNK) by the G(i/o) protein-coupled kappa opioid receptor

130 kinase 1 (RIP1) and c-Jun N-terminal kinase (JNK) by transcriptional activation.

131 The stress-induced c-Jun N-terminal kinase (JNK) controls microtubule dynamics by enhancing both mic

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

133 E signals through c-Jun NH2-terminal kinase (JNK) inhibiting fibroblast growth factor 21 (FGF21) and

134 strate that p54/p46 c-jun N-terminal kinase (JNK) inhibition suppresses matrix mineralization and OCN

135 P1-1 binding to the c-Jun N-terminal kinase (JNK) inhibits JNK phosphorylation, which is required for

136 ed that the p38 and c-Jun N-terminal kinase (JNK) MAPKs play key roles in the inflammatory response o

137 phosphorylation of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic effects of APAP.

138 , which engages the c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinase and Fos and

139 ), but requires the c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinase and the tran

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

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

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

143 polymerization and c-Jun N-terminal kinase (JNK) phosphorylation in mediating effects of dorsal hipp

144 es, which induced a c-Jun N-terminal kinase (JNK) phosphorylation-based mechanism that impaired gap j

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

146 ctivation of the cJun NH(2)-terminal kinase (JNK) signal transduction pathway.

147 The cJun NH(2)-terminal kinase (JNK) signaling pathway is activated by metabolic stress

148 or-beta (TGFB) and/or Jun N-terminal kinase (JNK) signaling pathways in more than 80% of EAC samples.

149 ated kinase (ERK) and JUN N-terminal kinase (JNK) signaling pathways, we defined MAP3K19 as a novel r

150 vation of oncogenic c-Jun N-terminal kinase (JNK) signaling, induced by the latent membrane protein 1

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

152 tein kinase (MAPK), Jun NH2-terminal kinase (JNK), and nuclear factor kappa-light-chain-enhancer of a

153 eta1 signaling, via c-Jun-N-terminal kinase (JNK), inhibited expression of the gemcitabine transporte

154 appaB kinase (IKK), c-jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK)-extracellu

155 ed kinase (ERK) and c-Jun N-terminal kinase (JNK), phosphorylated the Gle1A N-terminal domain, primin

156 inases, including c-Jun NH2-terminal kinase (JNK), play an important role in the development and func

157 (ERK1/2), p38 and Jun amino-terminal kinase (JNK), which consequently potentiates Pi triggered lethal

158 ctedly uncovered five Jun N-terminal kinase (JNK)-JUN family genes as key barriers of DE differentiat

159 onomous activation of Jun N-terminal kinase (JNK).

160 tin is mediated via c-Jun N-terminal kinase (JNK).

161 kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK).

162 s downstream target c-Jun N-terminal kinase (JNK).

163 d immune-responsive c-Jun N-terminal kinase (JNK).

164 pha and activation of JUN N-terminal kinase (JNK).

165 ERK (extracellular signal-regulated kinase), JNK, and p38 mitogen-activated protein kinases as well a

166 g pathways (STAT3, c-jun n-terminal kinases (JNK), EKR1/2, nuclear factor-kappa B (NF-kappaB)) in the

167 e inhibitor of c-Jun NH(2)-terminal kinases (JNKs) also antagonizes RNase L-dependent cell death in r

168 disable specifically Jun N-terminal kinases (JNKs) and p38s that are required for host immune respons

169 uch as p38 and the c-Jun N-terminal kinases (JNKs) are activated during the cellular response to stre

170 The c-Jun NH2-terminal kinases (JNKs) are stress-activated kinases with multiple substra

171 ss kinases such as c-Jun N-terminal kinases (JNKs), are activated.

172 We further linked JNK to RUNX1 through Activator Protein 1 (AP-1) and inve

173 ted against steatosis correlating with lower JNK activation, reduced Bmal1 and increased FGF21 expres

174 ing from predominant activation of the MAPK, JNK, to that of p38.

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

176 of mitogen-activated protein kinases (MAPKs) JNK and p38.

177 ed the enhanced recruitment of the TAK1/MKK7/JNK signalling complex to phagosomes of IL-4-activated m

178 induced subunit cross-linking could modulate JNK apoptotic signaling, further confirming the role of

179 onal injury responses: Raw does not modulate JNK-dependent axonal injury signaling and regenerative r

180 ough intracellular Ca(2+) levels to modulate JNK-mediated Hippo signaling.

181 Moreover, JNK mediated phosphorylation at an evolutionarily more r

182 homeostasis through the regulation of the NE/JNK/Bmal1 axis.

183 alternate binding mode for part of the NFAT4-JNK interaction, and evidence of bidirectional associati

184 s resulted in activation of NFkappaB but not JNK and p38.

185 ings provide evidence that the activation of JNK by p75 in cell bodies and axons is required for inte

186 further reveal that transient activation of JNK enhances the expression of the insulin receptor and

187 uitylation correlated with the activation of JNK signalling in ovarian cancer tissue from human patie

188 TNF-alpha, via activation of JNK, mediated phosphorylation of SP1 that impaired its b

189 aling, tumors lead to aberrant activation of JNK/Mmp2 signaling, followed by intestinal barrier dysfu

190 ernalization of p75 required the activity of JNK, a downstream kinase mediating p75 death signaling i

191 It is established that one consequence of JNK activation is the development of insulin resistance

192 the signaling mechanisms and consequences of JNK activation by KOR agonists remain uncharacterized.

193 However, the long-term consequences of JNK inhibition have not been evaluated.

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

195 lates HCC pathogenesis via downregulation of JNK-dependent inflammation and proliferation of hepatocy

196 med that PPARalpha mediated these effects of JNK in hepatocytes.

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

198 Here, we have investigated the function of JNK signaling in dendrite pruning using Drosophila class

199 Pharmacological inhibition of JNK attenuated IL-10 production by MCG, implicating miR-

200 Pharmacological inhibition of JNK signaling in ex vivo slice cultures caused cortical

201 Direct pharmacological inhibition of JNK significantly improves the efficiencies of generatin

202 ortance of controlling the activity level of JNK signaling to maintain epithelial barrier function an

203 ordingly, NleD cleaved the flexible loops of JNK and p38 but not the rigid loop of ERK.

204 Similarly, genetic loss of JNK function led to precocious stream departure ex vivo,

205 We find that loss of JNK or its canonical downstream effectors Jun or Fos led

206 Loss of JNK signaling results in abnormal endochondral bone form

207 from the early arrestin-independent phase of JNK activation, and this ROS response was suppressed by

208 some; and 3) suppress the phosphorylation of JNK, ERK, and p38 MAPK signaling pathways.

209 TNF-alpha-induced phosphorylation of JNK, p38 and NF-kappaB was also attenuated by the inhibi

210 ic injury and the otoprotective potential of JNK inhibitors is being tested in clinical trials.

211 nditions, reduces proliferative potential of JNK-signaling cells while promoting non-autonomous proli

212 Preinhibition of JNK before the onset of differentiation increased the nu

213 sues, but do highlight the important role of JNK-c-Jun activity during normal MN development raising

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

215 Suppression of JNK activation partially reduced CBD-induced cell death

216 s potential consequences of long-term use of JNK inhibitors for the treatment of metabolic syndrome.

217 macologic inhibition and genetic ablation of JNKs, as well as silencing of expression of TRB3, did no

218 nogenesis and memory consolidation depend on JNK and cofilin signaling, supporting a critical role fo

219 sity and cofilin phosphorylation depended on JNK phosphorylation in the DH.

220 e, which was abolished upon MSR1 deletion or JNK inhibition.

221 ession, suggesting that activation of ERK or JNK is specific through FAK and Pyk2.

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

223 macologic inhibition or knockdown of TGFB or JNK signaling components in EAC cells (FLO-1 or EsoAd1)

224 This enzyme directs p-JNK (phospho-c-Jun N-terminal kinase) to the EC membrane

225 on of DUSP4 prevented the activation of p38, JNK, caspase 3/7 activity, and NADPH oxidase 4 expressio

226 a prevented DUSP4 expression decline and p38/JNK activation in the podocytes and renal cortex of diab

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

228 immediate early activation of both SAPK (p38/JNK) and GCN2 signaling pathways.

229 BI-78D3 does not covalently modify p38MAPK, JNK or ERK5.

230 e coordinated by the stress response pathway JNK.

231 by functionally distinct signaling pathways (JNK and p38) through structurally different MAPK binding

232 of pro-tumoral CAFs that exploits PDGFRbeta/JNK signalling axis to promote tumor invasiveness in BC.

233 ial levels of glutathione and phosphorylated JNK; we made similar observations in fasted Stard1(Delta

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

235 use of the expression of a pro-proliferative JNK isoform that results in growth factor elaboration an

236 ound that testosterone activates the protein JNK in mouse and human adipocytes.

237 demonstrate that the activation of the Rac1/JNK signaling axis downstream of Dock10 leads to an incr

238 kers of oxidative stress, along with reduced JNK and p38 MAP kinase activity.

239 These changes were associated with reduced JNK signaling and enhanced expression and activity of PP

240 kappaB) activity and independently regulates JNK activity.

241 Although protection in raw mutants requires JNK, Fos, and Jun, JNK also promotes axonal degeneration

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

243 Mechanistically, Gish restricts JNK activation by phosphorylating and destabilizing a sm

244 onclusion: Our results demonstrate that RIP1/JNK-dependent PUMA induction mediates AILI by promoting

245 idative phosphorylation genes, trigger a ROS-JNK retrograde signaling pathway that drives CCF formati

246 tress cellular damage via activation of SAPK/JNK phosphorylation, Nrf2 nuclear translocation and anti

247 h activation of catalase expression via SAPK/JNK phosphorylation and Nrf2 nuclear translocation.

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

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

250 Here, we show that upon cell stress, JNK directly phosphorylates the microtubule rescue facto

251 Consistently, sustained JNK activation in the cytosol and mitochondria from hepa

252 Here we demonstrate that JNK signaling in adipocytes causes an increased circulat

253 We demonstrate that JNK signaling induces a dose-dependent extension of G2 i

254 s OPN but not OCN (OPN-OBs), indicating that JNK affects OPN secretory phenotype at the early stage o

255 reported in SMA raising the possibility that JNK inhibitors could be a novel treatment for this disea

256 EcRB1 in c4da neurons, but also reveals that JNK and Ecdysone signaling coordinate to promote dendrit

257 Interestingly, our data show that JNK activity in c4da neurons remains constant from larva

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

259 interneurons in vivo These data suggest that JNK signaling facilitates the tangential migration and l

260 he development of steatosis, suggesting that JNK inhibition represents a possible treatment for this

261 The JNK-JUN pathway does not act through directly inhibiting

262 that IL-22 decreases GJIC by activating the JNK signaling pathway, which down-regulates Cx43 express

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

264 in GJIC can be significantly blocked by the JNK inhibitor SP600125 and by the overexpression of IL-2

265 egulation of Cx43 expression mediated by the JNK signaling pathway was confirmed in a mouse model of

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

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

268 ivator Protein 1 (AP-1) and investigated the JNK-AP-1-RUNX1 regulatory feedback loop, which can be mo

269 odulate the spatiotemporal activation of the JNK and NF-kappaB pathways.

270 JNK2alpha2, a relatively rare member of the JNK family of mitogen-activated protein kinases (MAPK),

271 ch can be reversed by over-expression of the JNK kinase kinase Wnd.

272 events in the UPR, such as activation of the JNK mitogen-activated protein (MAP) kinases or the pseud

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

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

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

276 ary keratinocytes through attenuation of the JNK pathway.

277 with the kinase MEKK1, and activation of the JNK/p38/NFkappaB pathway.

278 les, whereas JNK activation by silencing the JNK phosphatase puckered induces egg laying in virgins.

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

280 Mechanistically, we find that the JNK>PDK signalling axis in 'loser' cells reprograms thei

281 Collectively, these results suggest that the JNK-Id4 signaling axis is crucial in the control of OPN

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

283 Therefore, the JNK-JUN pathway safeguards pluripotency from precocious

284 ein-protein interactions associated with the JNK apoptotic pathway, associations between lung develop

285 1 was regulated by the KRAS oncogene through JNK, and loss of Id1 resulted in downregulation of eleme

286 ted RANKL-induced osteoclastogenesis through JNK activation and CCL2 secretion.

287 her, we identified that MSR1 signals through JNK via K63 polyubiquitylation and provides evidence for

288 ays an important role in inhibiting TNFalpha/JNK-induced necrosome signaling and resultant cytotoxici

289 es ER Ca(2+) level and subsequently leads to JNK activation and Hippo inactivation.

290 e the phosphoswitch differently sensitive to JNK and p38 in vertebrates.

291 kers that predict enhanced susceptibility to JNK inhibition.

292 The IKK2-TPL2-JNK axis is specific for LMP1 and differs from TNFalpha,

293 se is induced by LMP1 via IKK2 and transmits JNK activation signals downstream of IKK2.

294 R-Ras upregulation in endothelial cells via JNK and p38 mitogen-activated protein kinase but not NF-

295 zes with Ras(V12) to induce tumor growth via JNK-mediated Hippo signaling.

296 NF-alpha-induced RUNX1 expression occurs via JNK activation, while NF-kappaB and p38/MAPK inhibition

297 ncreased stem/progenitor-like properties via JNK activation.

298 rease in integrin alpha3beta1 signaling, via JNK, inhibits expression of the gemcitabine transporter

299 hibits oviposition in mated females, whereas JNK activation by silencing the JNK phosphatase puckered

300 hat bridges cytosolic Ca(2+) alteration with JNK activation and Hippo-mediated tumor growth.