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

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

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

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

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

10 lated kinase 1/2 (phospho-ERK) and phospho-c-Jun N-terminal kinase 1 (phospho-JNK) in the striatum an

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

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

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

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

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

16 culum (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 ki

18 cient MFS mice uniquely showed activation of Jun N-terminal kinase-1 (JNK1), and a JNK antagonist ame

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 t partially controlled through ROS-induced c-Jun N-terminal kinase activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 f the protein kinases TAK, IKK-alpha/beta, c-Jun N-terminal kinases, and p38alpha mitogen-activated p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 n, promoting proliferation, and decreasing c-JUN N-terminal kinase-dependent apoptosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 y, viral gene expression and NF-kappaB and c-Jun N-terminal kinase (JNK) activation of a herpes simpl

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

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 n and metastasis by inhibiting myosin II and Jun N-terminal kinase (JNK) activity downstream of PP1.

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

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

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

113 le cells promote osteogenesis by enhancing c-Jun N-terminal kinase (JNK) and extracellular related ki

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

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

116 1 (RIP1) play critical roles in activating c-Jun N-terminal kinase (JNK) and inhibitor of kappaB kina

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

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

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

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

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

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

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

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

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

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

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

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

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

130 ular signal-regulated kinase (ERK) and the c-jun N-terminal kinase (JNK) branches of the mitogen-acti

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

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

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

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

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

136 K) and p38 MAPK in RPE cells and ERK/p38 and Jun N-terminal kinase (JNK) in mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

150 MLK3's catalytic activity and signaling to c-jun N-terminal kinase (JNK) is required for migration of

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

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

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

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

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

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

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

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

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

160 In the adult Drosophila midgut, the Jun N-Terminal Kinase (JNK) pathway is activated in dama

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

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

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

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

165 onvergence point for this signal and for the Jun N-terminal kinase (JNK) pathway, which promotes ISC

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 a transcriptional cofactor for c-Jun at the Jun N-terminal kinase (JNK) target genes Jra and chickad

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

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

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

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

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

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

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

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

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

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

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

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

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

208 those of GLH-1, are likely regulated by the Jun N-terminal kinase (JNK), KGB-1.

209 cells and monocytes through activation of c-Jun N-terminal kinase (JNK), NADPH oxidase, and hypoxia-

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

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

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

215 turated FA, but not unsaturated FA, activate Jun N-terminal kinase (JNK), which has been linked to ob

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 47 treatment also increased phosphorylated c-Jun N-terminal kinase (JNK).

231 itogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK).

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

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

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

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

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

237 ctor 2 (TRAF2) regulates activation of the c-Jun N-terminal kinase (JNK)/c-Jun and the inhibitor of k

238 acroautophagy led to overactivation of the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway that

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 The c-Jun N-terminal kinases (JNKs) are members of the mitogen

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

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

263 c-Jun N-terminal kinases (JNKs) represent valuable targets

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

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

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

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

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

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

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

271 APK (mitogen-activated protein kinase), JNK (Jun N-terminal kinase), or JAK2 (Janus kinase 2).

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 ppaB and mitogen-activated protein kinase (c-Jun N-terminal kinase, p-38, p38alpha) activation, enhan

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

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

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

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

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

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

281 ion not only inhibited adiponectin-induced c-Jun-N-terminal kinase phosphorylation, but also blocked

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

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

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

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

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

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

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

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

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