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 Here, we show that mice lacking c-Jun N-terminal kinase 1 (JNK1) exhibit reduced patholo

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

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

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

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

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

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

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

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

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

17 t mechanically induced signaling through the c-jun N-terminal kinase 2 [JNK2] is elicited via a mecha

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

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

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

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

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

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

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

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

26 c-Jun N-terminal kinase 3alpha1 (JNK3alpha1) is a mitoge

27 aling through a mechanism involving Rac1 and c-Jun N-terminal kinase-activating protein 1-dependent t

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 ry WM cells, as well as of apoptosis through c-Jun N-terminal kinase activation, nuclear factor kappa

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

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

34 allmark features of apoptosis including JNK (c-Jun N-terminal kinase) activation and nuclear fragment

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

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

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

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

41 (chemokine (c-c)ligand-3, phosphorylation of c-jun N-terminal Kinase and mitogen-activated protein ki

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

43 volved in TNFalpha-induced activation of the c-Jun N-terminal kinase and nuclear factor kappaB (NF-ka

44 stic transcription factors and inhibition of c-Jun N-terminal kinase and p38 mitogen-activated protei

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

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

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

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

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

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

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

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

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

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

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

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

65 tif has been implicated in the activation of c-Jun N-terminal kinase, but is not required for the eff

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 r signaling, including P-JNK (phosphorylated c-Jun N-terminal kinase), caspase-8, and p75(NTR) cleava

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

72 roups, insulin-stimulated phosphorylation of c-Jun-N-terminal kinase decreased by 29% +/- 13% and pho

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

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

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

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 y promoting the following: (i) activation of c-Jun N-terminal kinase; (ii) inhibition of calpain and

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

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

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

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

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

84 We show that EGF signaling through Ras and c-Jun N-terminal kinase is responsible for targeting TGa

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

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

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

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

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

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

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

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

93 vestigate the role of Abeta oligomer-induced c-Jun N-terminal kinase (JNK) activation leading to phos

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

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

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

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

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

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

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

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

102 tion requires mixed-lineage kinase (MLK) and c-Jun N-terminal kinase (JNK) activity.

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

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

105 f transcription protein-3 (STAT3) and STAT5, c-Jun N-terminal kinase (JNK) and caspase-3 in imatinib-

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

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

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

111 Phosphorylation of c-Jun N-terminal kinase (JNK) and insulin receptor subst

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 r induced by Myc depletion were inhibited by c-Jun N-terminal kinase (JNK) and p38 inhibitors but not

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

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

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

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

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

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

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

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

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

127 Pharmacological inhibition of c-Jun N-terminal kinase (JNK) did not affect C/EBPbeta d

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

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

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

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

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

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

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

135 Given the importance of c-Jun N-terminal kinase (JNK) in the stress response, we

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

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

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

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

140 ty relationship studies on a novel series of c-Jun N-terminal kinase (JNK) inhibitors.

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

142 c-Jun N-terminal Kinase (JNK) is a key regulator in tumo

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 c-Jun N-terminal kinase (JNK) is activated by multiple p

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

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

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

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

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

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

153 The p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein

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

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

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

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

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

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

160 ortunistic bacterial pathogen, activates the c-Jun N-terminal kinase (JNK) pathway, a hallmark of the

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

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

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

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

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

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

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

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

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

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

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

172 Previously we demonstrated that c-Jun N-terminal kinase (JNK) plays a central role in ac

173 c-Jun N-terminal kinase (JNK) plays a pivotal role in th

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

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

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

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

178 have previously shown that the inhibition of c-Jun N-terminal kinase (JNK) signaling blocks T3D-induc

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

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

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

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

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

184 racellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways.

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

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

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

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

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

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

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

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

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

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

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

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

197 f nuclear factor kappaB inhibitor (IkappaB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated

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

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

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

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

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

212 naling caused spatiotemporal deactivation of c-jun N-terminal kinase (JNK), which reduced the phospho

213 us to suppress persistent phosphorylation of c-Jun N-terminal kinase (JNK), which was induced by the

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 s (FFA) induce hepatocyte lipoapoptosis by a c-Jun N-terminal kinase (JNK)-dependent mechanism.

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

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

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

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

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

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

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

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

226 -747 treatment also increased phosphorylated c-Jun N-terminal kinase (JNK).

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

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

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

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

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

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

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

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

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

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

237 xpression of CtsK via calcineurin/NFATc1 and c-Jun N-terminal kinase (JNK)1/2-dependent signaling.

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

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

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

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

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

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

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

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

246 ody of data supporting an essential role for c-jun-N-terminal kinase (JNK) in neurodegenerative disor

247 Our previous study showed that activation of c-jun-N-terminal kinase (JNK) in spinal astrocytes plays

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

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

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

251 ation of a repressive signaling pathway, the c-Jun-N-terminal kinase (JNK) signaling pathway in PPd10

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

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

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

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

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

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

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

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

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

261 Since the c-Jun N-terminal kinases (JNKs) display both oncogenic a

262 In the adult mouse, signaling through c-Jun N-terminal kinases (JNKs) links exposure to acute

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

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

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

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

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

270 not extracellular signal-regulated kinase or c-Jun N-terminal kinase, mitogen-activated protein kinas

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 activation of nuclear factor kappaB and the c-Jun-N-terminal kinase pathway.

281 ion of ASK1 on Ser83 inhibited ASK1-mediated c-Jun N-terminal kinase phosphorylation as well as p38 k

282 hosphorylation of ASK1 at T838 and increased c-Jun N-terminal kinase phosphorylation, the two biologi

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 in Drosophila and mice, and that its target, c-Jun N-terminal kinase, promoted degeneration locally i

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

287 6 (PRDX6) to the receptor-Galphai complex by c-Jun N-terminal kinase, resulting in Galphai depalmitoy

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

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

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

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

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

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

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

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

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

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

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