ライフサイエンスコーパス: Jun-N-terminal kinase

1 s underwent apoptosis with the activation of Jun N-terminal kinase.

2 iated by Frizzled3, Dishevelled (Dvl), and c-Jun N-terminal kinase.

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

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

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

6 Jun N-terminal kinase 1 (JNK1) and p38alpha also phospho

7 increased phosphorylation of Akt, p38, and c-Jun N-terminal kinase 1 that was also beta2-integrin dep

8 itogen-activated protein kinase gamma, and c-Jun N-terminal kinase 1), which in turn might be due to

9 quentially by discoidin domain receptor 1, c-Jun N-terminal kinase 1, and phosphorylated JunB, which

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

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

12 ry factor (IRF) 5, and TLR4 and suppressed c-Jun N-terminal kinase 1/2/3, Lyn, STAT-3, and STAT-6 pho

13 c-Jun-N-terminal kinase 1/2 (JNK1/2) activation is a causa

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

15 Jun N-terminal kinase-2, but independent of Jun N-terminal kinase-1, extracellular signal-regulated

16 nal-regulated kinase-1/2, p38alpha kinase, c-Jun N-terminal kinase-1/2, phosphoinositide 3-kinase-gam

17 ent-binding protein 1c, and phosphorylated c-Jun N-terminal kinase 2, which were accompanied by a syn

18 Blocking either TAK1 or Jun N-terminal kinase-2 inhibited EMT.

19 ght-chain-enhancer of activated B cells, and Jun N-terminal kinase-2, but independent of Jun N-termin

20 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 in

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

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

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

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

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

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

28 pases 3 and 7, which resulted from reduced c-Jun N-terminal kinase activation and initiator caspase 8

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

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

31 This is mediated via Jun N-terminal kinase activation of c-Jun, which, in tur

32 XCL10 induced long-term protein kinase B and Jun N-terminal kinase activation, leading to hepatocyte

33 ffect I/R-induced free radical generation, c-Jun N-terminal kinase activation, or depletion of reduce

34 racellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase activation, which contributed to C

35 n supine and regional reduction in p38 and c-jun N-terminal kinase activation.

36 actor-kappaB activation at 4 to 12 weeks and jun N-terminal kinases activation at 4 weeks in the MHC-

37 The evolutionarily conserved JNK/AP-1 (Jun N-terminal kinase/activator protein 1) and BMP (Bone

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

39 re, tumor microvesicles and miR-21 require c-Jun N-terminal kinase activity to regulate this apoptoti

40 (-/-) background enhanced stress-activated c-Jun N-terminal kinase activity while elevating IL-6 expr

41 ecrease in stress-activated protein kinase/c-Jun N-terminal kinase activity.

42 ncreased production of lipid peroxides and c-Jun N-terminal kinase activity.

43 AMP-activated protein kinase signaling with Jun N-terminal kinase and extracellular signal-regulated

44 Inhibition of Jun N-terminal kinase and extracellular signal-regulated

45 uppressor function for KIND1, and identify c-Jun N-terminal kinase and NF-kappaB as potential therape

46 nvolved in T-cell activation, antagonists of Jun N-terminal kinase and nuclear factor kappaB did inhi

47 -activated protein kinases (MAPKs, i.e., the Jun N-terminal kinase and p38 MAPK), and then MAPK-depen

48 cellular signal-regulated kinases 1 and 2, c-Jun N-terminal kinase and p38 mitogen-activated protein

49 Analyses of signaling pathways identified Jun N-terminal kinase and p38 mitogen-activated protein

50 , whereas TNF-alpha-induced phosphorylated c-Jun N-terminal kinase and phosphorylated extracellular s

51 ylation of stress activated protein kinase/c-Jun N-terminal kinase and that other death receptors and

52 lobe epilepsy brain samples, including the c-Jun N-terminal kinase and the protein kinase R-like endo

53 mechanisms involving the activation of the c-Jun N-terminal kinases and the mitogen-activated protein

54 xtracellular signal-regulated kinases 1/2, c-Jun N-terminal kinase, and c-Jun, indicating downregulat

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

56 erons, TNF-alpha, and the three MAPK (p38, c-Jun N-terminal kinase, and extracellular signal regulate

57 ocytes had increased phospho-Akt and phospho-Jun N-terminal kinase, and gene expression analysis of s

58 e, extracellular signal-regulated kinase and Jun N-terminal kinase, and interleukin-8 induction.

59 stream signaling to nuclear factor kappaB, c-Jun N-terminal kinase, and mechanistic target of rapamyc

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

61 lular signal-regulated kinase 1/2, phospho-c-Jun N-terminal kinase, and phospho-cJun, as well as decr

62 egulated kinases, phosphorylation level of c-jun N-terminal kinases, and active caspase-3; reduced ex

63 n by decreased expression of P-p38 MAPK, P-c-jun-N-terminal kinase, and P-extracellular signal-regula

64 xtracellular signal-regulated kinases, and c-jun N-terminal kinases; and expression of active caspase

65 at extracellular signal-regulated kinase and Jun N-terminal kinase are essential for tBHQ-induced exp

66 Our findings indicate p38 and c-Jun N-terminal kinase as intriguing targets for correcti

67 racellular signal-regulated kinase 1/2 and c-Jun N-terminal kinases, as well as the internalization o

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

69 ns of the E3 ubiquitin ligase highwire and c-Jun N-terminal kinase basket in olfactory receptor neuro

70 lipid accumulation and lipid uptake, with c-Jun N-terminal kinase being an essential player, whereas

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

72 xtracellular signal-regulated kinase 1/2 and Jun N-terminal kinase branches of the mitogen-activated

73 racellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated prot

74 poptosis signal-regulating kinase 1) or of c-Jun N-terminal kinase, but not by an inhibitor of p38 mi

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

76 are mediated by a NADPH oxidase/superoxide/c-Jun N-terminal kinase/c-Jun signalling pathway, involvin

77 ent cytoplasmic Ca(2+) rises, resulting in c-Jun N-terminal kinase, Ca(2+)/calmodulin-dependent prote

78 ear factor 1alpha, and inactivation of the c-Jun N-terminal kinase contribute to SULP-induced down-re

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

80 ven apoptosis and recently a specific JNK (c-Jun N-terminal kinase)-dependent S574 phosphorylated for

81 at fat accumulation in the liver increases c-Jun N-terminal kinase-dependent BCL-2 interacting mediat

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

83 f Par3 deregulates Rac1 activity to activate Jun N-terminal Kinase-dependent proliferation and tumor

84 tein kinase siRNA lessened the activation of Jun N-terminal kinase, extracellular signal-regulated ki

85 n RBP4-Ox, AT macrophages display enhanced c-Jun N-terminal kinase, extracellular signal-related kina

86 ors aimed at blocking protein kinase C and c-Jun N-terminal kinase had no effect on desensitization i

87 of Plin5(LKO) mice exhibited activation of c-Jun N-terminal kinase, impaired insulin signal transduct

88 Increasing activation of c-Jun N-terminal kinase in Nod2-stimulated human monocyte-

89 m stress responses and reduced activity of c-Jun N-terminal kinase in the liver, explaining the enhan

90 As act directly on tumor cells to activate c-Jun N-terminal kinase, inhibit proliferation and induce

91 Genetic or pharmacological c-Jun N-terminal kinase inhibition and NF-kappaB inhibitio

92 Jun N-terminal kinase inhibition decreased SP-induced mi

93 Conversely, the c-Jun N-terminal kinase inhibitor SP600125 and the peroxis

94 kinesin-1 involves the scaffolding protein c-Jun N-terminal kinase-interacting protein-1 (JIP1), whic

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

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

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

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

99 c-Jun N-terminal kinase (JNK) 1 and JNK2 are expressed in

100 azoles were designed as dual inhibitors of c-Jun N-terminal kinase (JNK) 3 and p38alpha mitogen-activ

101 Sustained c-Jun N-terminal kinase (JNK) activation has been implicat

102 ociated endoplasmic reticulum (ER) stress, c-Jun N-terminal kinase (JNK) activation, and disruption o

103 Dab2 negatively regulates TGF-beta-induced c-Jun N-terminal kinase (JNK) activation, whereas activati

104 bited endoplasmic reticulum stress-induced c-Jun N-terminal kinase (JNK) activation.

105 at requires TRC105 concentration-dependent c-Jun N-terminal kinase (JNK) activation.

106 s-induced DUSP4 reduction enhanced p38 and c-Jun N-terminal kinase (JNK) activity and podocyte dysfun

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

108 can be accounted for by the activation of c-Jun N-terminal kinase (JNK) activity by mechanical strai

109 oxidants, iron chelation, or inhibition of c-Jun N-terminal kinase (JNK) ameliorated heme-induced oxi

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

111 n of RNase L coordinates the activation of c-Jun N-terminal kinase (JNK) and double-stranded RNA-depe

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

113 in signaling through the activation of the c-Jun N-terminal kinase (JNK) and IkappaB kinase (IKK) pat

114 phatase-deficient mutant, dephosphorylates c-JUN N-terminal kinase (JNK) and induces apoptosis in DLB

115 phenotype is associated with upregulation of Jun N-terminal Kinase (JNK) and Janus Kinase (JAK)/Signa

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

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

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

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

120 P-Me activated the cellular stress kinases c-Jun N-terminal kinase (JNK) and p38 mitogen-activated pr

121 tracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and p38, as well as an incre

122 ther with altered levels of phosphorylated c-Jun N-terminal kinase (JNK) and puc-lacZ expression reve

123 rators of cytoskeletal dynamics, including c-Jun N-terminal kinase (Jnk) and RhoGTPase family members

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

125 s, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK) are significantly up-regulat

126 h GITR ligand increased phosphorylation of c-Jun N-terminal kinase (JNK) but not extracellular signal

127 he mitogen-activated protein kinase (MAPK) c-Jun N-terminal kinase (JNK) by the G(i/o) protein-couple

128 or-interacting protein kinase 1 (RIP1) and c-Jun N-terminal kinase (JNK) by transcriptional activatio

129 The stress-induced c-Jun N-terminal kinase (JNK) controls microtubule dynamic

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

131 royl)oxime]was a specific inhibitor of the c-Jun N-terminal kinase (JNK) family, with preference for

132 Moreover, c-Jun N-terminal kinase (JNK) has been implicated in regul

133 The c-Jun N-terminal kinase (JNK) have a dual role in controll

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

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

136 lated kinase (ERK) and, to a smaller degree, Jun N-terminal kinase (JNK) in the liver.

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

138 acellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17

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

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

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

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

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

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

145 c-Jun N-terminal kinase (JNK) is a serine/threonine phosph

146 c-Jun N-terminal kinase (JNK) is a stress signal transduce

147 In vertebrates, Jun N-terminal kinase (JNK) is also required for tissue

148 lar signal-regulated kinase (ERK), p38, or c-Jun N-terminal kinase (JNK) is observed in Map4k4-silenc

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

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

151 5 (also called SAB) and phosphorylation of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic effe

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

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

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

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

156 Jun N-terminal kinase (JNK) often mediates apoptosis in

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

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

159 We have recently identified the Jun N-terminal kinase (JNK) pathway as an important medi

160 ibit protein synthesis and to activate the c-Jun N-terminal kinase (JNK) pathway correlated well with

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

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

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

164 In addition, we report that the jun N-terminal kinase (JNK) pathway upregulates Mmp1 exp

165 totic cells and, through activation of the c-Jun N-terminal kinase (JNK) pathway, is able to propagat

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

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

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

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

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

171 ctivated protein kinases (MAPKs); notably, c-Jun N-terminal kinase (JNK) phosphorylation depends on T

172 mined the role of actin polymerization and c-Jun N-terminal kinase (JNK) phosphorylation in mediating

173 c-Jun N-terminal kinase (JNK) phosphorylation increased si

174 in kinase were markedly activated, whereas c-Jun N-terminal kinase (JNK) phosphorylation remained at

175 orm in R/R cardiomyocytes, which induced a c-Jun N-terminal kinase (JNK) phosphorylation-based mechan

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

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

178 c-Jun N-terminal kinase (JNK) plays a vital role in malign

179 ncreased galectin-7 expression upregulates c-Jun N-terminal kinase (JNK) protein levels, which is req

180 lar neurodegeneration model to investigate c-Jun N-terminal kinase (JNK) signaling and endoplasmic re

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

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

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

184 Jun N-terminal kinase (JNK) signaling has been implicate

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

186 Activation of c-Jun N-terminal kinase (JNK) signaling pathway is a criti

187 ransforming growth factor-beta (TGFB) and/or Jun N-terminal kinase (JNK) signaling pathways in more t

188 racellular signal-regulated kinase (ERK) and JUN N-terminal kinase (JNK) signaling pathways, we defin

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

190 ression of puckered, a negative regulator of Jun N-terminal kinase (JNK) signaling, at the wound site

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

192 Activation of Jun N-terminal kinase (JNK) signaling, which occurs upon

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

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

195 imply that reduced function of the MAP2K7-c-Jun N-terminal kinase (JNK) signalling cascade may under

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

197 tivation of wnt-planar cell polarity (PCP)-c-Jun N-terminal kinase (JNK) signalling leading to the in

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

199 The c-Jun N-terminal kinase (JNK) was potently activated after

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

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

202 targets of antigen receptors, NF-kappaB and Jun N-terminal kinase (JNK), are activated downstream of

203 on of EBV BGLF2 in cells activated p38 and c-Jun N-terminal kinase (JNK), both of which are important

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

205 cluding the rapid activation of NF-kappaB, c-Jun N-terminal kinase (JNK), extracellular signal-regula

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

207 hat Parkin KO mice had decreased activated c-Jun N-terminal kinase (JNK), increased induction of myel

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

209 naling kinases: Akt, IkappaB kinase (IKK), c-jun N-terminal kinase (JNK), mitogen-activated protein k

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

211 llular signal-regulated kinase 1/2 (ERK1/2), Jun N-terminal kinase (JNK), p38 and ERK5 in response to

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

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

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

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

216 We analyzed the c-Jun N-terminal kinase (JNK)-dependent glycogen synthase

217 entiation, which unexpectedly uncovered five Jun N-terminal kinase (JNK)-JUN family genes as key barr

218 The menin-JUND interaction blocks JUN N-terminal kinase (JNK)-mediated JUND phosphorylatio

219 ost-translational modifications, including c-Jun N-terminal kinase (JNK)-mediated phosphorylation, wh

220 ended to determine whether the activation of Jun N-terminal kinase (JNK)-signaling pathway is involve

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

222 nformation of Dvl more effectively activates Jun N-terminal kinase (JNK).

223 ells via acute, non-autonomous activation of Jun N-terminal kinase (JNK).

224 the expression of TNFalpha and activation of JUN N-terminal kinase (JNK).

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

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

227 ition of doxorubicin-induced activation of c-Jun N-terminal kinase (JNK).

228 al dendrites through the activation of the c-Jun N-terminal kinase (JNK).

229 f p38 mitogen-activated protein kinase and c-Jun N-terminal kinase (JNK).

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

231 l intracellular signaling pathways including Jun N-terminal kinase (JNK).

232 ng apoptosis signaling kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK).

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

234 echanism that involves inactivation of the c-Jun N-terminal kinase (JNK).

235 ced SphK1 up-regulation is mediated by the c-Jun N-terminal kinase (JNK)/activating protein-1 signali

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

237 and activator of transcription (Stat92E), c-Jun N-terminal kinase (JNK)/AP-1 signaling, and expressi

238 Inhibition of c-Jun N-terminal kinase (JNK)/Jun phosphorylation and sile

239 ortholog Dronc drives AiP via activation of Jun N-terminal kinase (JNK); however, the specific mecha

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

241 ivation of the signalling pathways (STAT3, c-jun n-terminal kinases (JNK), EKR1/2, nuclear factor-kap

242 crotubules into short pieces and activated c-Jun N-terminal kinases (JNK).

243 o severe TBI elicits neuroinflammation and c-Jun-N-terminal kinase (JNK) activation, which is associa

244 gainst APAP cytotoxicity despite sustained c-jun-N-terminal kinase (JNK) activation.

245 ing the mitogen-activated protein kinases, c-Jun-N-terminal kinase (JNK) and p38, in a TLR4-dependent

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

247 c-Jun-N-terminal kinase (JNK) is a mitogen-activated prote

248 mosquito immune responses, and show that the Jun-N-terminal kinase (JNK) pathway is a key mediator of

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

250 ochondria-associated P-JNK levels, but the c-jun-N-terminal kinase (JNK) signaling inhibitor SP600125

251 The c-Jun-N-terminal kinase (JNK) signaling pathway regulates

252 equent integrin alpha3beta1 signaling, via c-Jun-N-terminal kinase (JNK), inhibited expression of the

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

254 ellular signal-regulated kinase (ERK)- and c-Jun-N-terminal kinase (JNK)-specific phosphorylations we

255 ptosis Signal-regulating Kinase 1 (ASK1) and Jun-N-terminal Kinase (JNK).

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

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

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

259 These NleDs disable specifically Jun N-terminal kinases (JNKs) and p38s that are required

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

261 The c-Jun N-terminal kinases (JNKs) are members of MAPK family

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

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

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

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

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

267 h p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylat

268 n-mediated export of glutathione (GSH) and c-Jun N-terminal kinase-mediated increased intracellular G

269 erase with the IP-10 gene required p38 and c-Jun N-terminal kinase mitogen-activated protein kinase (

270 ced the phosphorylation of p38 and JNK MAPK (Jun N-terminal kinase mitogen-activated protein kinase)

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

272 al-regulated kinase 1/2, protein kinase C, c-Jun N-terminal kinase, or GRK5 did not inhibit the Cmpd1

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

274 The c-Jun N-terminal kinase pathway is activated in both forms

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

276 nterface during interphase and activates the Jun N-terminal kinase pathway to increase the ability of

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

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

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

280 ducer and activator of transcription 3 and c-Jun N-terminal kinase pathways and reduced nuclear facto

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

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

283 ced FAS upregulation through activation of c-jun-N-terminal kinase resulted in FADD phosphorylation,

284 (PRDX6) to the receptor-Galphai complex by c-Jun N-terminal kinase, resulting in Galphai depalmitoyla

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

286 measuring stress-activated protein kinase/c-jun N-terminal kinase (SAPK/JNK) and caspase 3 activity.

287 P44/42, and stress-activated protein kinase/Jun N-terminal kinase (SAPK/JNK) mitogen-activated prote

288 okine expression, and phosphorylated p38 and Jun N-terminal kinase signaling in primary microglia.

289 llular signal-regulated kinases 1 and 2, and Jun N-terminal kinase signaling pathways, leading to mye

290 nt ATP7B mutant, H1069Q, activates p38 and c-Jun N-terminal kinase signaling pathways, which favor th

291 trinsic apoptotic pathway with the help of c-Jun N-terminal kinase signaling.

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

293 of ligands, and the consequent activation of Jun N-terminal kinase signalling, which in turn triggers

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

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

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

297 e, extracellular signal-regulated kinase and Jun N-terminal kinase (two mitogen-activated protein kin

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

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

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