ライフサイエンスコーパス: c-Jun N-terminal kinase

1 ediated by Frizzled3, Dishevelled (Dvl), and c-Jun N-terminal kinase.

2 C (PKC) inhibitor but not by an inhibitor of c-Jun N-terminal kinase.

3 the activities of nuclear factor-kappaB and c-Jun N-terminal kinase.

4 by a MAP kinase cascade, including ASK1 and c-Jun N-terminal kinase.

5 Furthermore, inhibition or deletion of c-jun N-terminal kinase 1 (JNK1) abrogated PUMA inductio

6 ibitory effect on autophagy via reduction of c-Jun N-terminal kinase 1 (JNK1) and B-cell lymphoma 2 (

7 The increased superoxide content induces c-Jun N-terminal kinase 1 (JNK1) kinase activity, which

8 gulated kinase 1/2 (phospho-ERK) and phospho-c-Jun N-terminal kinase 1 (phospho-JNK) in the striatum

9 n increased phosphorylation of Akt, p38, and c-Jun N-terminal kinase 1 that was also beta2-integrin d

10 mitogen-activated protein kinase gamma, and c-Jun N-terminal kinase 1), which in turn might be due t

11 sequentially by discoidin domain receptor 1, c-Jun N-terminal kinase 1, and phosphorylated JunB, whic

12 We also found that silencing c-Jun N-terminal kinase 1/2 (JNK1/2) decreased PARP-1 ub

13 ases (extracellular signal-regulated kinase, c-Jun N-terminal kinase 1/2, and p38).

14 tory factor (IRF) 5, and TLR4 and suppressed c-Jun N-terminal kinase 1/2/3, Lyn, STAT-3, and STAT-6 p

15 c-Jun-N-terminal kinase 1/2 (JNK1/2) activation is a cau

16 ticulum (ER) stress induction and subsequent c-jun-N-terminal kinase 1/2 (JNK1/2) activation.

17 c-Jun N-terminal kinase-1 (JNK-1) is a stress-regulated

18 ignal-regulated kinase-1/2, p38alpha kinase, c-Jun N-terminal kinase-1/2, phosphoinositide 3-kinase-g

19 ement-binding protein 1c, and phosphorylated c-Jun N-terminal kinase 2, which were accompanied by a s

20 h reactivity towards H(2)O(2) that activates c-Jun N-terminal kinase-2alpha2 (JNK2alpha2).

21 The c-jun N-terminal kinase 3 (JNK3) is expressed primarily

22 We target the gatekeeper MET146 of c-Jun N-terminal kinase 3 (JNK3) to exemplify the applic

23 The concept of covalent inhibition of c-Jun N-terminal kinase 3 (JNK3) was successfully transf

24 osphotyrosine-EphrinB2 signalling repressing c-jun N-terminal kinase 3 activity via STAT1.

25 er, MAPK10/JNK3 kinase, and found that JNK3 (c-Jun N-terminal kinase 3) is critical for KLF9's axon-g

26 hibitor of NF-kappaB kinase-beta, NF-kappaB, c-Jun N-terminal kinase 3, and TNF-alpha protein levels

27 amin A, expression of pro-apoptotic proteins c-Jun N-terminal kinase 3, caspase 3, and cytochrome C,

28 aspases 3 and 7, which resulted from reduced c-Jun N-terminal kinase activation and initiator caspase

29 tes to cytokine and UV-induced NF-kappaB and c-Jun N-terminal kinase activation and upregulation of C

30 tion of Bax and cytochrome c release but not c-Jun N-terminal kinase activation during BSIA.

31 affect I/R-induced free radical generation, c-Jun N-terminal kinase activation, or depletion of redu

32 xtracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase activation, which contributed to

33 han supine and regional reduction in p38 and c-jun N-terminal kinase activation.

34 On the other hand, inhibition of c-Jun N-terminal kinase activity inhibited PMA-induced i

35 more, tumor microvesicles and miR-21 require c-Jun N-terminal kinase activity to regulate this apopto

36 K2(-/-) background enhanced stress-activated c-Jun N-terminal kinase activity while elevating IL-6 ex

37 decrease in stress-activated protein kinase/c-Jun N-terminal kinase activity.

38 increased production of lipid peroxides and c-Jun N-terminal kinase activity.

39 ast partially controlled through ROS-induced c-Jun N-terminal kinase activity.

40 suppressor function for KIND1, and identify c-Jun N-terminal kinase and NF-kappaB as potential thera

41 racellular signal-regulated kinases 1 and 2, c-Jun N-terminal kinase and p38 mitogen-activated protei

42 ificantly activated Raf1 and ERK1/2, but not c-Jun N-terminal kinase and p38 pathways.

43 tracellular signal-regulated kinase, but not c-Jun N-terminal kinase and p38, pathway activation.

44 ts, whereas TNF-alpha-induced phosphorylated c-Jun N-terminal kinase and phosphorylated extracellular

45 orylation of stress activated protein kinase/c-Jun N-terminal kinase and that other death receptors a

46 l lobe epilepsy brain samples, including the c-Jun N-terminal kinase and the protein kinase R-like en

47 h mechanisms involving the activation of the c-Jun N-terminal kinases and the mitogen-activated prote

48 Rac1 activation is accompanied by JNK (c-Jun N-terminal kinase) and NF-kappaB activation, culmi

49 extracellular signal-regulated kinases 1/2, c-Jun N-terminal kinase, and c-Jun, indicating downregul

50 -signal-regulated kinases 1/2 (p44/42 MAPK), c-Jun N-terminal kinase, and cPLA2alpha also attenuated

51 rferons, TNF-alpha, and the three MAPK (p38, c-Jun N-terminal kinase, and extracellular signal regula

52 wnstream signaling to nuclear factor kappaB, c-Jun N-terminal kinase, and mechanistic target of rapam

53 for antigen receptor signaling to NF-kappaB, c-Jun N-terminal kinase, and mTOR.

54 ellular signal-regulated kinase 1/2, phospho-c-Jun N-terminal kinase, and phospho-cJun, as well as de

55 -regulated kinases, phosphorylation level of c-jun N-terminal kinases, and active caspase-3; reduced

56 of the protein kinases TAK, IKK-alpha/beta, c-Jun N-terminal kinases, and p38alpha mitogen-activated

57 own by decreased expression of P-p38 MAPK, P-c-jun-N-terminal kinase, and P-extracellular signal-regu

58 extracellular signal-regulated kinases, and c-jun N-terminal kinases; and expression of active caspa

59 Our findings indicate p38 and c-Jun N-terminal kinase as intriguing targets for correc

60 xtracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinases, as well as the internalization

61 s the PAR-1/c-Src/Rho GTPases Rac1 and Cdc42/c-Jun N-terminal kinase axis resulting in the activation

62 ions of the E3 ubiquitin ligase highwire and c-Jun N-terminal kinase basket in olfactory receptor neu

63 rs lipid accumulation and lipid uptake, with c-Jun N-terminal kinase being an essential player, where

64 We identified a new NOD2 partner, c-Jun N-terminal kinase-binding protein 1 (JNKBP1), a sc

65 xtracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated pr

66 (apoptosis signal-regulating kinase 1) or of c-Jun N-terminal kinase, but not by an inhibitor of p38

67 ng kinase (ASK1)-dependent activation of the c-Jun N-terminal kinase/c-Jun and p38 pro-death pathways

68 s are mediated by a NADPH oxidase/superoxide/c-Jun N-terminal kinase/c-Jun signalling pathway, involv

69 sient cytoplasmic Ca(2+) rises, resulting in c-Jun N-terminal kinase, Ca(2+)/calmodulin-dependent pro

70 clear factor 1alpha, and inactivation of the c-Jun N-terminal kinase contribute to SULP-induced down-

71 onal kinases, including protein kinase C and c-Jun N-terminal kinase, contribute to desensitization.

72 riven apoptosis and recently a specific JNK (c-Jun N-terminal kinase)-dependent S574 phosphorylated f

73 ion, promoting proliferation, and decreasing c-JUN N-terminal kinase-dependent apoptosis.

74 that fat accumulation in the liver increases c-Jun N-terminal kinase-dependent BCL-2 interacting medi

75 plaque VSMCs and by palmitate in a p38- and c-Jun N-terminal kinase-dependent manner.

76 modulate the expression of FLG and LOR via a c-Jun N-terminal kinase-dependent pathway.

77 In RBP4-Ox, AT macrophages display enhanced c-Jun N-terminal kinase, extracellular signal-related ki

78 itors aimed at blocking protein kinase C and c-Jun N-terminal kinase had no effect on desensitization

79 s of Plin5(LKO) mice exhibited activation of c-Jun N-terminal kinase, impaired insulin signal transdu

80 Increasing activation of c-Jun N-terminal kinase in Nod2-stimulated human monocyt

81 lum stress responses and reduced activity of c-Jun N-terminal kinase in the liver, explaining the enh

82 UFAs act directly on tumor cells to activate c-Jun N-terminal kinase, inhibit proliferation and induc

83 Genetic or pharmacological c-Jun N-terminal kinase inhibition and NF-kappaB inhibit

84 Conversely, the c-Jun N-terminal kinase inhibitor SP600125 and the perox

85 o kinesin-1 involves the scaffolding protein c-Jun N-terminal kinase-interacting protein-1 (JIP1), wh

86 We found that JNK2, but not JNK1 (c-Jun N-terminal kinase isoform 1), increased SERCA2 upt

87 Activation of the c-Jun N-terminal kinase isoform 2 (JNK2) is reported in

88 Furthermore, inhibition of ERK 1/2 and c-Jun N terminal kinase (JNK) signaling attenuated TNFal

89 viral effect of CD40L required activation of c-Jun N terminal kinases (JNK)1/2, but not induction of

90 tions of action that have been attributed to c-Jun N-terminal kinase (JNK) 1 activation in vivo.

91 c-Jun N-terminal kinase (JNK) 1 and JNK2 are expressed i

92 Here we show that c-Jun N-terminal kinase (JNK) 1, but not JNK2, is critic

93 idazoles were designed as dual inhibitors of c-Jun N-terminal kinase (JNK) 3 and p38alpha mitogen-act

94 Sustained c-Jun N-terminal kinase (JNK) activation has been implic

95 udy, viral gene expression and NF-kappaB and c-Jun N-terminal kinase (JNK) activation of a herpes sim

96 ssociated endoplasmic reticulum (ER) stress, c-Jun N-terminal kinase (JNK) activation, and disruption

97 t Dab2 negatively regulates TGF-beta-induced c-Jun N-terminal kinase (JNK) activation, whereas activa

98 hibited endoplasmic reticulum stress-induced c-Jun N-terminal kinase (JNK) activation.

99 that requires TRC105 concentration-dependent c-Jun N-terminal kinase (JNK) activation.

100 tes-induced DUSP4 reduction enhanced p38 and c-Jun N-terminal kinase (JNK) activity and podocyte dysf

101 this response are not fully understood, but c-Jun N-terminal kinase (JNK) activity appears to be cri

102 Both cell polarity and c-Jun N-terminal kinase (JNK) activity are essential to

103 ng can be accounted for by the activation of c-Jun N-terminal kinase (JNK) activity by mechanical str

104 tioxidants, iron chelation, or inhibition of c-Jun N-terminal kinase (JNK) ameliorated heme-induced o

105 We show that ATZ induces activation of c-Jun N-terminal kinase (JNK) and c-Jun and that genetic

106 ion of RNase L coordinates the activation of c-Jun N-terminal kinase (JNK) and double-stranded RNA-de

107 tile cells promote osteogenesis by enhancing c-Jun N-terminal kinase (JNK) and extracellular related

108 1) is a Ser/Thr kinase that operates via the c-Jun N-terminal kinase (JNK) and extracellular signal-r

109 ulin signaling through the activation of the c-Jun N-terminal kinase (JNK) and IkappaB kinase (IKK) p

110 osphatase-deficient mutant, dephosphorylates c-JUN N-terminal kinase (JNK) and induces apoptosis in D

111 n 1 (RIP1) play critical roles in activating c-Jun N-terminal kinase (JNK) and inhibitor of kappaB ki

112 y by a mechanism involving the activation of c-jun N-terminal kinase (JNK) and mitochondrial damage.

113 dy, we show that MCPIP1 negatively regulates c-Jun N-terminal kinase (JNK) and NF-kappaB activity by

114 le, including stimulus-dependent patterns of c-Jun N-terminal kinase (JNK) and nuclear factor kappa B

115 Specific inhibitors of c-Jun N-terminal kinase (JNK) and of IkappaB kinase (IKK

116 c-Jun and activation of its upstream kinase c-Jun N-terminal kinase (JNK) and overexpression of C/EB

117 eased activation-specific phosphorylation of c-Jun N-terminal kinase (JNK) and p38 kinase.

118 -AP-Me activated the cellular stress kinases c-Jun N-terminal kinase (JNK) and p38 mitogen-activated

119 extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and p38, as well as an inc

120 gether with altered levels of phosphorylated c-Jun N-terminal kinase (JNK) and puc-lacZ expression re

121 strators of cytoskeletal dynamics, including c-Jun N-terminal kinase (Jnk) and RhoGTPase family membe

122 We have previously shown that c-Jun N-terminal kinase (JNK) and the Fas death receptor

123 mas, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK) are significantly up-regul

124 llular signal-regulated kinase (ERK) and the c-jun N-terminal kinase (JNK) branches of the mitogen-ac

125 ith GITR ligand increased phosphorylation of c-Jun N-terminal kinase (JNK) but not extracellular sign

126 the mitogen-activated protein kinase (MAPK) c-Jun N-terminal kinase (JNK) by the G(i/o) protein-coup

127 ptor-interacting protein kinase 1 (RIP1) and c-Jun N-terminal kinase (JNK) by transcriptional activat

128 The stress-induced c-Jun N-terminal kinase (JNK) controls microtubule dynam

129 llular-signal-related kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) expression.

130 furoyl)oxime]was a specific inhibitor of the c-Jun N-terminal kinase (JNK) family, with preference fo

131 Moreover, c-Jun N-terminal kinase (JNK) has been implicated in reg

132 The c-Jun N-terminal kinase (JNK) have a dual role in contro

133 ociated focal adhesions to the activation of c-jun N-terminal kinase (JNK) in cells attached to defor

134 The role for c-Jun N-terminal Kinase (JNK) in the control of feeding

135 d significantly increased phosphorylation of c-Jun N-terminal kinase (JNK) in the DH.

136 8 was phosphorylated specifically at S409 by c-Jun N-terminal kinase (JNK) in vitro.

137 Here, we demonstrate that p54/p46 c-jun N-terminal kinase (JNK) inhibition suppresses matr

138 r control diet were treated with SP600125; a c-Jun N-terminal kinase (JNK) inhibitor and its effect o

139 Using synchronized cells, we show that the c-Jun N-terminal kinase (JNK) inhibitor, SP600125, preve

140 Here we show that mice lacking Jnk1, or c-Jun N-terminal kinase (JNK) inhibitor-treated mice, di

141 t is well known that GST P1-1 binding to the c-Jun N-terminal kinase (JNK) inhibits JNK phosphorylati

142 The stress-activated protein kinase c-Jun N-terminal kinase (JNK) is a central regulator in

143 c-Jun N-terminal kinase (JNK) is a member of the mitogen

144 c-Jun N-terminal kinase (JNK) is a serine/threonine phos

145 c-Jun N-terminal kinase (JNK) is a stress signal transdu

146 We recently reported that c-Jun N-terminal kinase (JNK) is associated with adheren

147 lular signal-regulated kinase (ERK), p38, or c-Jun N-terminal kinase (JNK) is observed in Map4k4-sile

148 t MLK3's catalytic activity and signaling to c-jun N-terminal kinase (JNK) is required for migration

149 cription; finally, signaling through p38 and c-Jun N-terminal kinase (JNK) MAPK pathways alters gene

150 Our results revealed that the p38 and c-Jun N-terminal kinase (JNK) MAPKs play key roles in th

151 BP5 (also called SAB) and phosphorylation of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic ef

152 c-Jun N-terminal kinase (JNK) mediates cell signaling es

153 pathway regulated by Raw, which engages the c-Jun N-terminal kinase (JNK) mitogen-activated protein

154 tide adenylyl transferase), but requires the c-Jun N-terminal kinase (JNK) mitogen-activated protein

155 extracellular signal-regulated kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein

156 Because islet amyloid increases c-Jun N-terminal kinase (JNK) pathway activation, we inv

157 MKK7 activates the c-Jun N-terminal kinase (JNK) pathway and is the only MK

158 nhibit protein synthesis and to activate the c-Jun N-terminal kinase (JNK) pathway correlated well wi

159 the noise mapping analysis, we find that the c-Jun N-terminal kinase (JNK) pathway generates higher n

160 We find that the c-Jun N-terminal kinase (JNK) pathway is activated by VZ

161 Moreover, we show that the c-Jun N-terminal kinase (JNK) pathway is involved in the

162 of the apoptosis signal-regulating kinase 1/c-Jun N-terminal Kinase (JNK) pathway, a module known to

163 optotic cells and, through activation of the c-Jun N-terminal kinase (JNK) pathway, is able to propag

164 he gamma isoform of MKK7, a component of the c-Jun N-terminal kinase (JNK) pathway.

165 WDR62 is a novel scaffold protein of the c-Jun N-terminal kinase (JNK) pathway.

166 r, the function of Wnt11 was mediated by the c-Jun N-terminal kinase (JNK) pathway.

167 acts as an anti-apoptotic regulator for the c-Jun N-terminal kinase (JNK) pathway.

168 or the nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) pathways, including Ikbkb,

169 -activated protein kinases (MAPKs); notably, c-Jun N-terminal kinase (JNK) phosphorylation depends on

170 xamined the role of actin polymerization and c-Jun N-terminal kinase (JNK) phosphorylation in mediati

171 c-Jun N-terminal kinase (JNK) phosphorylation increased

172 tein kinase were markedly activated, whereas c-Jun N-terminal kinase (JNK) phosphorylation remained a

173 oform in R/R cardiomyocytes, which induced a c-Jun N-terminal kinase (JNK) phosphorylation-based mech

174 recruited to the opioid receptor complex by c-Jun N-terminal kinase (JNK) phosphorylation.

175 f AAT is possibly mediated by suppression of c-Jun N-terminal kinase (JNK) phosphorylation.

176 c-Jun N-terminal kinase (JNK) plays a vital role in mali

177 Increased galectin-7 expression upregulates c-Jun N-terminal kinase (JNK) protein levels, which is r

178 lular neurodegeneration model to investigate c-Jun N-terminal kinase (JNK) signaling and endoplasmic

179 y to neurotrophin deprivation result in both c-Jun N-terminal Kinase (JNK) signaling and the PERK- an

180 cells, and depends on the activation of the c-Jun N-terminal kinase (JNK) signaling cascade.

181 to simultaneously activate the NF-kappaB and c-Jun N-terminal kinase (JNK) signaling cascades.

182 we illustrate a novel and essential role for c-Jun N-terminal kinase (JNK) signaling in guiding the p

183 Activation of c-Jun N-terminal kinase (JNK) signaling pathway is a cri

184 The c-Jun N-terminal kinase (JNK) signaling pathway is essen

185 Although alterations to c-Jun N-terminal kinase (JNK) signaling were apparent in

186 o-factor NEMO in the activation of oncogenic c-Jun N-terminal kinase (JNK) signaling, induced by the

187 nts virus-induced activation of proapoptotic c-Jun N-terminal kinase (JNK) signaling.

188 l survival and death, insulin secretion, and c-Jun N-terminal kinase (JNK) signaling.

189 ts imply that reduced function of the MAP2K7-c-Jun N-terminal kinase (JNK) signalling cascade may und

190 n (MSN) act downstream of Draper to activate c-Jun N-terminal kinase (JNK) signalling in glia, result

191 activation of wnt-planar cell polarity (PCP)-c-Jun N-terminal kinase (JNK) signalling leading to the

192 g phosphorylation of FOXO3 at S-574, a novel c-Jun N-terminal kinase (JNK) site, which promoted nucle

193 er critical inflammatory kinases such as the c-Jun N-terminal kinase (JNK) to regulate insulin action

194 The c-Jun N-terminal kinase (JNK) was potently activated aft

195 -induced Bcl-2 phosphorylation was caused by c-Jun N-terminal kinase (JNK), and AITC activates JNK.

196 m regulator of both IkappaB kinase (IKK) and c-Jun N-terminal kinase (JNK), and an important mediator

197 extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor kappaB

198 extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38.

199 tes the phosphorylation of ERK, p38MAPK, and c-Jun N-terminal kinase (JNK), and p38MAPK inhibition wa

200 re made of basal levels of the pro-apoptotic c-jun N-terminal kinase (JNK), Bax, and the 14-3-3 ancho

201 sion of EBV BGLF2 in cells activated p38 and c-Jun N-terminal kinase (JNK), both of which are importa

202 t a neuronal pathway involving activation of c-Jun N-terminal kinase (JNK), common to many stress res

203 including the rapid activation of NF-kappaB, c-Jun N-terminal kinase (JNK), extracellular signal-regu

204 o investigate the role of one such MAPK, the c-Jun N-terminal kinase (JNK), in VZV lytic infection an

205 that Parkin KO mice had decreased activated c-Jun N-terminal kinase (JNK), increased induction of my

206 Draper, cell death abnormality (Ced)-12, and c-Jun N-terminal kinase (JNK), is essential for the deat

207 ignaling kinases: Akt, IkappaB kinase (IKK), c-jun N-terminal kinase (JNK), mitogen-activated protein

208 al cells and monocytes through activation of c-Jun N-terminal kinase (JNK), NADPH oxidase, and hypoxi

209 -), inhibitor kappaB kinase beta (IKK-beta), c-Jun N-terminal kinase (JNK), or phospho-JNK protein co

210 racellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), phosphorylated the Gle1A

211 n of multiple off-target kinases upstream of c-Jun N-terminal kinase (JNK), principally ZAK.

212 -regulated kinase 1 and 2 (ERK1/2), p38, and c-Jun N-terminal kinase (JNK), results in stimulation of

213 retion, which leads to activation in turn of c-Jun N-terminal kinase (JNK), the Axl receptor tyrosine

214 In addition, mmLDL induced c-Jun N-terminal kinase (JNK)-dependent derepression of

215 We analyzed the c-Jun N-terminal kinase (JNK)-dependent glycogen synthas

216 (ROS) mount a hypersumoylation response in a c-Jun N-terminal kinase (JNK)-dependent manner.

217 post-translational modifications, including c-Jun N-terminal kinase (JNK)-mediated phosphorylation,

218 gulated by the stress- and immune-responsive c-Jun N-terminal kinase (JNK).

219 ession of desmin or vimentin is mediated via c-Jun N-terminal kinase (JNK).

220 activated the Rac1 and Cdc42 Rho GTPases and c-Jun N-terminal kinase (JNK).

221 ibition of doxorubicin-induced activation of c-Jun N-terminal kinase (JNK).

222 asal dendrites through the activation of the c-Jun N-terminal kinase (JNK).

223 of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase (JNK).

224 tivates BCL2 and BCLxL through activation of c-Jun N-terminal kinase (JNK).

225 ogen-activated protein (MAP) kinases p38 and c-Jun N-terminal kinase (JNK).

226 gen-activated protein kinase (MAPK), Akt, or c-Jun N-terminal kinase (JNK).

227 -747 treatment also increased phosphorylated c-Jun N-terminal kinase (JNK).

228 ving apoptosis signaling kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK).

229 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK).

230 racellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK).

231 uronal cell bodies via its downstream target c-Jun N-terminal kinase (JNK).

232 mechanism that involves inactivation of the c-Jun N-terminal kinase (JNK).

233 duced SphK1 up-regulation is mediated by the c-Jun N-terminal kinase (JNK)/activating protein-1 signa

234 In Rab8 mutant synapses, c-Jun N-terminal kinase (JNK)/activator protein-1 and TG

235 er and activator of transcription (Stat92E), c-Jun N-terminal kinase (JNK)/AP-1 signaling, and expres

236 factor 2 (TRAF2) regulates activation of the c-Jun N-terminal kinase (JNK)/c-Jun and the inhibitor of

237 macroautophagy led to overactivation of the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway th

238 trols neurogenesis by antagonizing Notch and c-Jun N-terminal kinase (JNK)/c-Jun signaling.

239 Inhibition of c-Jun N-terminal kinase (JNK)/Jun phosphorylation and si

240 ycogen synthase kinase-3beta (GSK-3beta) and c-Jun N-terminal kinase (JNK/SAPK) in beta-cells.

241 This Ser 68 is phosphorylated by p38, c-Jun N-terminal kinases (JNK), and extracellular signal

242 ctivation of the signalling pathways (STAT3, c-jun n-terminal kinases (JNK), EKR1/2, nuclear factor-k

243 microtubules into short pieces and activated c-Jun N-terminal kinases (JNK).

244 to severe TBI elicits neuroinflammation and c-Jun-N-terminal kinase (JNK) activation, which is assoc

245 against APAP cytotoxicity despite sustained c-jun-N-terminal kinase (JNK) activation.

246 Adiponectin increased phosphorylation of c-Jun-N-terminal kinase (JNK) and inhibition of c-Jun-N-

247 ating the mitogen-activated protein kinases, c-Jun-N-terminal kinase (JNK) and p38, in a TLR4-depende

248 In Drosophila, ROS triggers c-Jun-N-terminal Kinase (JNK) and Sterol Regulatory Elem

249 c-Jun-N-terminal kinase (JNK) is a mitogen-activated pro

250 The dual leucine zipper kinase (DLK)/c-Jun-N-terminal kinase (JNK) pathway represents a conse

251 itochondria-associated P-JNK levels, but the c-jun-N-terminal kinase (JNK) signaling inhibitor SP6001

252 The c-Jun-N-terminal kinase (JNK) signaling pathway regulate

253 bsequent integrin alpha3beta1 signaling, via c-Jun-N-terminal kinase (JNK), inhibited expression of t

254 enuate GaIN/LPS and ConA-induced ALF through c-jun-N-terminal kinase (JNK)-dependent autophagy.

255 acellular signal-regulated kinase (ERK)- and c-Jun-N-terminal kinase (JNK)-specific phosphorylations

256 appaB (NF-kappaB) and stress kinase (p38 and c-Jun N-terminal kinase [JNK]) pathways in response to m

257 also found that Hes-1 could be regulated by c-Jun N-terminal kinase (JNK1).

258 ne-expanded huntingtin-induced activation of c-Jun N-terminal kinases (JNKs) and p38 MAPKs, whereas e

259 d protein kinases (MAPK) such as p38 and the c-Jun N-terminal kinases (JNKs) are activated during the

260 The c-Jun N-terminal kinases (JNKs) are members of MAPK fami

261 The c-Jun N-terminal kinases (JNKs) are members of the mitog

262 The c-Jun N-terminal kinases (JNKs) are serine/threonine kin

263 ce it is phosphorylated at the N-terminus by c-Jun N-terminal kinases (JNKs) or other protein kinases

264 c-Jun N-terminal kinases (JNKs) represent valuable targe

265 In ischemic tissues, stress kinases such as c-Jun N-terminal kinases (JNKs), are activated.

266 e length of DLK underwent phosphorylation by c-Jun N-terminal kinases (JNKs), which have been shown t

267 The CB1R-HCN pathway, involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase,

268 oth p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphoryl

269 ein-mediated export of glutathione (GSH) and c-Jun N-terminal kinase-mediated increased intracellular

270 sferase with the IP-10 gene required p38 and c-Jun N-terminal kinase mitogen-activated protein kinase

271 rt, with no change in the phosphorylation of c-Jun N-terminal kinases or extracellular signal-regulat

272 gnal-regulated kinase 1/2, protein kinase C, c-Jun N-terminal kinase, or GRK5 did not inhibit the Cmp

273 ncubated with TGF-beta did not activate p38, c-Jun N-terminal kinase, or nuclear factor-kappaB; conve

274 kappaB and mitogen-activated protein kinase (c-Jun N-terminal kinase, p-38, p38alpha) activation, enh

275 The c-Jun N-terminal kinase pathway is activated in both for

276 Furthermore, the c-Jun N-terminal kinase pathway promotes regeneration by

277 activity and cell motility by ROS-activated c-Jun N-terminal kinase pathway, and thus contributed to

278 autophagic and antioxidant responses and the c-jun N-terminal kinase pathway, at the transcriptional

279 ctivation of Rac1 and its downstream p65 and c-Jun N-terminal kinase pathway.

280 nsducer and activator of transcription 3 and c-Jun N-terminal kinase pathways and reduced nuclear fac

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

282 manner dependent on actin polymerization and c-Jun N-terminal kinase phosphorylation.

283 ation not only inhibited adiponectin-induced c-Jun-N-terminal kinase phosphorylation, but also blocke

284 un-N-terminal kinase (JNK) and inhibition of c-Jun-N-terminal kinase-phosphorylation inhibited adipon

285 duced FAS upregulation through activation of c-jun-N-terminal kinase resulted in FADD phosphorylation

286 6 (PRDX6) to the receptor-Galphai complex by c-Jun N-terminal kinase, resulting in Galphai depalmitoy

287 ROS-activated protein kinase C delta and c-jun N-terminal kinases, resulting in the mitochondrial

288 by measuring stress-activated protein kinase/c-jun N-terminal kinase (SAPK/JNK) and caspase 3 activit

289 GTPases activate two distinct MAPK pathways: c-Jun N-terminal kinase signaling (required for cell inv

290 s that was associated with activation of the c-Jun N-terminal kinase signaling pathway.

291 uent ATP7B mutant, H1069Q, activates p38 and c-Jun N-terminal kinase signaling pathways, which favor

292 extrinsic apoptotic pathway with the help of c-Jun N-terminal kinase signaling.

293 , enhanced caspase-3 activity, and activated c-jun-N-terminal-kinase signaling, leading to cyclin D1

294 Inhibition of c-Jun N-terminal kinase/stress-activated protein kinase

295 and this effect was attributed to increased c-Jun N-terminal kinase, thereby inhibiting peroxisome p

296 r factor kappa B p52 and decreased levels of c-Jun N-terminal kinase; this provides a possible mechan

297 This enzyme directs p-JNK (phospho-c-Jun N-terminal kinase) to the EC membrane, where it st

298 traction, whereas simultaneous inhibition of c-Jun N-terminal kinase was required to block TNF-alpha-

299 cal stress stimulation, whereas p38 MAPK and c-Jun N-terminal kinases were mostly unaffected.

300 production of IL-17s required activation of c-Jun-N-terminal kinase, which was antagonized by both c