ライフサイエンスコーパス: JNK1

1 JNK1 ablation in mice confers long-term metabolic protec

2 JNK1 and -2 MAPKs were inhibited by addition of short in

3 JNK1 and, more significantly, JNK2 participated in the i

4 JNK1 deficiency in adipose tissue suppressed high-fat di

5 JNK1 deficiency leads to significantly higher induction

6 JNK1 directly phosphorylates Hes-1 at Ser-263.

7 JNK1 has been implicated in obesity, glucose intolerance

8 JNK1 in hematopoietic cells, especially in Kupffer cells

9 JNK1 increased phosphorylation of the proapoptotic prote

10 JNK1 is also a key mediator of the oxidative stress resp

11 JNK1 is therefore a potential target for therapeutic tre

12 JNK1 plays a role in the hepatotoxicity, mitochondrial d

13 JNK1(-/-) mice fed an HFD for the long term had reduced

14 JNK1-deficient mice had decreased fibrosis after BDL or

15 JNK1-dependent secretion of the inflammatory cytokine in

16 JNK1/2 was not required for breast epithelial cell proli

17 d stress kinase c-Jun NH2-terminal kinase 1 (JNK1) (all P values <0.05).

18 on or deletion of c-jun N-terminal kinase 1 (JNK1) abrogated PUMA induction, hepatocyte death, and co

19 via reduction of c-Jun N-terminal kinase 1 (JNK1) and B-cell lymphoma 2 (Bcl2) phosphorylation.

20 Jun N-terminal kinase 1 (JNK1) and p38alpha also phosphorylated SPF45 in vitro an

21 that mice lacking c-Jun N-terminal kinase 1 (JNK1) exhibit reduced pathological angiogenesis and lowe

22 The cJun N-terminal kinase 1 (JNK1) is implicated in diet-induced obesity.

23 stress kinase c-Jun NH(2)-terminal kinase 1 (JNK1) is required for Hsp-dependent regulation of HIF-1a

24 e content induces c-Jun N-terminal kinase 1 (JNK1) kinase activity, which in turn affects FOXO locali

25 on enhances Jun N-terminal protein kinase 1 (JNK1) phosphorylation in differentiated MNPs but reduces

26 tivity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted

27 activation of c-Jun NH(2)-terminal kinase 1 (JNK1).

28 howed activation of Jun N-terminal kinase-1 (JNK1), and a JNK antagonist ameliorated aortic growth in

29 c-Jun-N-terminal kinase 1/2 (JNK1/2) activation is a causal event in maternal diabete

30 and subsequent c-jun-N-terminal kinase 1/2 (JNK1/2) activation.

31 (MAPK) and c-Jun NH(2)-terminal kinase 1/2 (JNK1/2) by the drug combination was enhanced by radiatio

32 that silencing c-Jun N-terminal kinase 1/2 (JNK1/2) decreased PARP-1 ubiquitination while increasing

33 e for the activation of JNK1/2 signaling, 2) JNK1 contributes to the teratogenicity of hyperglycemia,

34 TWEAK increased the activity of ERK1/2, JNK1, and p38 MAPK.

35 vation also causes the activation of ERK1/2, JNK1/2, and ERK5 MAPKs and AP1 and SP1, which stimulate

36 pathway inhibited activation of the ERK1/2, JNK1/2, and p38 mitogen-activated protein kinases and re

37 cytokine-induced phosphorylation of ERK1/2, JNK1/2, c-Jun and reduced keratinocyte-derived GM-CSF ex

38 hosphorylation of AKT, EGF receptor, ERK1/2, JNK1/2/3, and c-Jun.

39 on sites (K242, 259, 290 and 569R) abolished JNK1 binding and failed to induce apoptosis.

40 Activated JNK1 contributes to this antiapoptotic phenotype of jnk2

41 Activated JNK1 is implicated in the mechanism of obesity-induced i

42 When caspase-3 is activated, JNK1-2 is proteolyzed at Asp-385 increasing the release

43 rotubule acetylation, flubendazole activates JNK1 leading to Bcl-2 phosphorylation, causing release o

44 ice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2.

45 s determined by their efficacy in activating JNK1 and that persistent inactivation of the kappa-recep

46 f not only mTOR complex 1 (mTORC1), but also JNK1/2, following LPS stimulation in macrophages.

47 ctivator Cdc25b phosphatase, Polo-like 1 and JNK1 kinases, and cMyc transcription factor.

48 Here, we show that JNK1-1 and JNK1-2 are activated early by osmostress, and sustained

49 st, we find reduced activation of ERK1/2 and JNK1 in cKit(V558Delta) homozygous PGCs and EGCs.

50 activation and phosphorylation of ERK1/2 and JNK1.

51 NKG2D-mediated phosphorylation of ERK1/2 and JNK1/2 and activation of NF-kappaB and AP1.

52 and prolonged phosphorylation of ERK1/2 and JNK1/2 MAPK, which was associated with time-dependent MK

53 MKK4 variants partially restored Erk1/2 and JNK1/2 signaling in LT-exposed cells, enabling the cells

54 with MEK1/2 and JNK inhibitors or MEK1/2 and JNK1/2 siRNA but not with ERK1/2 inhibitor.

55 uired for the activation of MAPKs ERK1/2 and JNK1/2, which in turn activated the transcription factor

56 olves the phosphorylation of both ERK1/2 and JNK1/2, which play opposing roles in the apoptotic respo

57 ation of PKCdelta-dependent PKD, ERK1/2, and JNK1/2/c-Jun that occurred with decreases in the BH3-onl

58 mediated by a novel Galpha(i)-, MEK1/2-, and JNK1/2-dependent pathway.

59 PKC directly phosphorylated PSD-95 and JNK1 in vitro Inhibiting PKC, JNK, or calcium/calmodulin

60 ) 1/2 or AKT suppressed enhanced killing and JNK1/2 activation.

61 Inhibition of p38 MAPK and JNK1/2 abolished MDA-7/IL-24 toxicity and blocked BAX an

62 by radiation, and signaling by p38 MAPK and JNK1/2 promoted cell killing.

63 limb ischemia led to an increase in MEK1 and JNK1 activation and Fra-1, c-Jun, and MMP-2 expression r

64 e immunity by negative control of mTORC1 and JNK1/2 activation.

65 nses can be inhibited by reducing mTORC1 and JNK1/2 activities with chemical inhibitors or small hair

66 ntrols TLR responses through both mTORC1 and JNK1/2.

67 nduced phosphorylation of MAPKs p38alpha and JNK1/2/3.

68 tate, but not oleate, required AMPK, PKR and JNK1 and involved the activation of the BECN1/PIK3C3 lip

69 ough the simultaneous disruption of Rho- and JNK1-mediated pathways, respectively.

70 eals a reciprocal causation of ER stress and JNK1/2 in mediating the teratogenicity of maternal diabe

71 i- and LPS-induced IL-8 secretion as well as JNK1/2 activation/phosphorylation in CD36-overexpressing

72 o maternal hyperglycemia were used to assess JNK1/2 activation, NTDs, activation of transcription fac

73 However, the relationship between JNK1/2 activation and endoplasmic reticulum (ER) stress

74 teratogenicity of hyperglycemia, and 3) both JNK1 and JNK2 activation cause activation of downstream

75 on of the proapoptotic protein BIM, and both JNK1 and BIM knockdown protected beta-cells against cyto

76 dDAVP decreased phosphorylation of both JNK1/2 (T183/Y185) and ERK1/2 (T183/Y185; T203/Y205), co

77 We further demonstrated that both JNK1 and JNK2 regulated Notch1 transcription via activat

78 d that acetylated FOXO3 preferentially bound JNK1, and a mutant FOXO3 lacking four known acetylation

79 ere we report that phosphorylation of Bad by JNK1 is required for glycolysis through activation of ph

80 atosis, and insulin resistance, conferred by JNK1 ablation, was sustained over a long period and was

81 Inhibition of JNK signaling either by JNK1 RNA interference (RNAi) or the JNK inhibitor suppre

82 We also showed that suppression of JNK1 by JNK1 siRNA increased p53 protein level and decreased PS1

83 P-induced apoptosis is partially mediated by JNK1/2, but it is completely dependent on caspase-9 acti

84 Mouse SIRT1 is phosphorylated by JNK1 at Ser-46 (Ser-47 in human SIRT1), which is one of

85 eta-induced apoptosis, which is prevented by JNK1/2 siRNA and the IP3R inhibitor xestospongin C.

86 All these events are prevented by JNK1/2 small interfering RNA (siRNA), indicating the med

87 red in JNK1-/- cells but could be rescued by JNK1 reconstitution under hypoxic conditions.

88 sed JNK1/2 activation and can be reversed by JNK1/2 inhibition.

89 uld be phenocopied in other cell settings by JNK1 silencing.

90 n important target of metabolic signaling by JNK1.

91 e of the four potential residues targeted by JNK1.

92 Conclusion: JNK1 and JNK2 both mediate insulin resistance in HFD-fed

93 e findings suggest that JunD counterbalances JNK1 activation and the downstream redox-dependent hepat

94 Decreasing JNK1 expression reduces Elk-1 occupancy at the Brf1 prom

95 Decreasing JNK1 expression reduces the occupancy of TBP at the Bdp1

96 their mRNAs was also inhibited by decreasing JNK1 and JNK2 levels via JNK1/2 DsiRNA transfection of k

97 In the setting of breast cancer development, JNK1/2 deficiency significantly increased tumor formatio

98 he activation of Cdc42 and leads to elevated JNK1 activity in a Cdc42- but not Rac1-dependent fashion

99 also enhanced phosphorylation of endogenous JNK1/2 in intact cells upon expression of upstream kinas

100 genous arrestin-3 interacted with endogenous JNK1/2 in different cell types.

101 te cyclase 6 (AC6), increased cAMP, enhanced JNK1/p38 cascade, suppressed CRBP-I/RARalpha (cellular r

102 established that the ubiquitously expressed JNK1 and JNK2 isoforms regulate energy expenditure and i

103 cific JNK3 and not by ubiquitously expressed JNK1, providing a molecular basis for neuron-specific pa

104 he ZDF diabetic rat islets, Rac1 expression, JNK1/2, and caspase-3 activation were also significantly

105 fferent sites exhibit similar affinities for JNK1, interaction kinetics differ considerably.

106 or ligands and examined their efficacies for JNK1 activation compared with conventional competitive a

107 her, our studies define a novel function for JNK1 in regulating HIF-1alpha turnover by a VHL-independ

108 However, distinct roles for JNK1 and JNK2 in hepatocyte apoptosis are still unresolv

109 se activation by alphavbeta6 is specific for JNK1, with no involvement of p38 or ERK kinase.

110 Moreover, we isolated macrophages from JNK1-, JNK2-, and MKK3-deficient mice to analyze the inv

111 In contrast, nTregs from JNK1(-/-) mice, similar to WT nTregs, were fully effecti

112 Furthermore, JNK1 phosphorylation of Hes-1 stabilized the Hes-1 prote

113 Hence, JNK1 controls mast cell degranulation and FcgammaR-trigg

114 In hepatocytes, JNK1 and JNK2 appear to have combined effects in protect

115 However, JNK1/2 deficiency caused increased branching morphogenes

116 intoxication with GAP domain results in: (i) JNK1/2 activation; (ii) substantial increases in the mit

117 Collectively, the data implicate JNK1-dependent PUMA expression as a mechanism contributi

118 mice given the JNK inhibitor SP600125 and in JNK1- and JNK2-deficient mice following BDL or CCl(4) ad

119 RBP4 effects are markedly attenuated in JNK1-/- JNK2-/- macrophages and TLR4-/- macrophages.

120 Additionally, the decrease in JNK1 phosphorylation observed with Myc knockdown is asso

121 ed the enhanced antifungal response found in JNK1-deficient mice.

122 sion of the Hsp90 acetyltransferase HDAC6 in JNK1-/- cells was associated with reduced Hsp90 chaperon

123 hereas enforced expression of Hsp90/Hsp70 in JNK1-/- cells increased HIF-1alpha stability relative to

124 Stabilization of HIF-1alpha was impaired in JNK1-/- cells but could be rescued by JNK1 reconstitutio

125 levels of endogenous Hsp90/Hsp70 proteins in JNK1-/- cells affected the protective roles of these cha

126 gene expression were dramatically reduced in JNK1-/- cells.

127 mouse and human cells, loss or reduction in JNK1 expression represses RNA pol III transcription.

128 of multiple downstream effectors, including JNK1.

129 Netrin-1 increased JNK1, not JNK2 or JNK3, activity in the presence of dele

130 colipotoxic conditions resulted in increased JNK1/2 phosphorylation and caspase-3 activity; such effe

131 in vivo, which is correlated with increased JNK1/2 activation and can be reversed by JNK1/2 inhibiti

132 upstream activator, blocked Netrin-1-induced JNK1 activation in HEK293 cells.

133 th of them further enhanced Netrin-1-induced JNK1 activity in vitro.

134 z1) selectively suppresses TNF-alpha-induced JNK1 activation and cell death independently of its tran

135 hat specifically regulates TNF-alpha-induced JNK1 activation and cell death.

136 h significantly suppresses TNF-alpha-induced JNK1 activation and inflammation.

137 R costimulation, MEKK1 predominantly induces JNK1 activation, whereas the related kinase MEKK2 regula

138 p38alpha (IC(50) < 10 nm), does not inhibit JNK1 or JNK2.

139 ations at these sites had markedly inhibited JNK1-dependent phosphorylation, virtually no ENaC inhibi

140 l of myeloma cells by binding and inhibiting JNK1.

141 For instance, JNK1 and JNK2 do not appreciably bind to any D-sites oth

142 the two ubiquitously expressed JNK isoforms (JNK1 and JNK2) in hepatocytes does not prevent hepatocel

143 06, a brain-penetrant and selective pan-JNK (JNK1/2/3) inhibitor, reduced food intake and body weight

144 Mice lacking JNK1 (JNK1(-/-)) were fed an obesogenic high-fat diet (HFD) fo

145 Enhanced JunD/JNK1-dependent liver injury correlated with the acute in

146 functions of both proteins, rather than just JNK1, in the onset of toxic liver injury.

147 enic signals to the activation of NF-kappaB, JNK1/2, p38, and ERK5 pathways.

148 ly, PARP14 inhibits the pro-apoptotic kinase JNK1, which results in the activation of PKM2 through ph

149 The mitogen-activated protein kinase JNK1 suppresses interleukin-3 withdrawal-induced cell de

150 The kinase JNK1 has emerged as a promising drug target for the trea

151 inase (MAPK), Jun N-terminal protein kinase (JNK1), IRF3, and IRF7 were activated after contact with

152 ranscription of the c-Jun N-terminal kinase (JNK1) gene in U2OS osteosarcoma cells.

153 uld be regulated by c-Jun N-terminal kinase (JNK1).

154 rylation of the c-Jun amino-terminal kinases JNK1 and JNK2 and activation of AP-1 transcription.

155 ation, DUSP1/MKP-1 knockdown in MEFS lacking JNK1 and -2 does not result in increased cell death.

156 d mouse embryonic fibroblasts (MEFs) lacking JNK1/2 or PKR showed reduced autophagy levels.

157 Mice lacking JNK1 (JNK1(-/-)) were fed an obesogenic high-fat diet (H

158 sion and activity were mediated by Rac1-MEK1-JNK1-dependent activation of AP-1 (Fra-1/c-Jun).

159 ed Fra-1 and c-Jun expression in a Rac1-MEK1-JNK1-dependent manner.

160 gene transcription via inactivation of MKK4-JNK1/2 signaling.

161 , such as focal adhesion kinase (FAK), MKK7, JNK1/2 and c-Jun, which were also activated in the SKOV3

162 In this context, dominant negative JNK1 expression elevated both Nox2 and Nox4 mRNA levels

163 Neither JNK1 activation by IL-1beta or UV nor TNF-alpha-induced

164 In contrast, activation of JNK2 (but not JNK1) phosphorylated and up-regulated the expression of

165 Most importantly, JNK2, but not JNK1, is sufficient to couple with oncogenic Ras to tran

166 function of JNK2, c-Jun, and HSF-1, but not JNK1, led to dramatic inhibition of arsenite-induced Hsp

167 f nTregs and signaling through JNK2, but not JNK1, triggered the loss of regulatory function while co

168 TPA-induced phosphorylation of JNK2, but not JNK1, was reduced by RasGRP1 depletion.

169 JNK2- and MKK3-, but not JNK1-deficient macrophages were resistant to the down-re

170 CYLD via specific activation of JNK2 but not JNK1.

171 We also identified a novel JNK1-Hes-1 signaling pathway that regulates GluR1 expres

172 Thus, genetic co-ablation of JNK1 and JNK2 genes or inhibition of JNK kinase function

173 (JNK) and c-Jun and that genetic ablation of JNK1 or JNK2 decreased ATZ levels in vivo by reducing c-

174 her candidate gene, PTPN2, and activation of JNK1 and BIM.

175 eptor to androgen receptor via activation of JNK1 and causes increased nuclear localization and activ

176 f arrestin-3 to facilitate the activation of JNK1 and JNK2 has never been reported.

177 Activation of JNK1 and p38 MAPK, but not ERK1/2 or Akt kinase, was sig

178 The TNF-alpha-induced activation of JNK1 is augmented in Miz1-deficient mouse embryonic fibr

179 mechanistically, by promoting activation of JNK1, the alphavbeta6 integrin causes androgen receptor-

180 as a consequence of persistent activation of JNK1.

181 res ethanol metabolism and the activation of JNK1.

182 amatically inhibit LPS-induced activation of JNK1/2 and ERK1/2 and remarkably disrupted the TLR4 dime

183 ress markers and abolished the activation of JNK1/2 and its downstream transcription factors, caspase

184 in the loss of Tak1-dependent activation of JNK1/2 and Tak1-mediated survival.

185 ion abolished diabetes-induced activation of JNK1/2 and their downstream effectors: phosphorylation o

186 stress is responsible for the activation of JNK1/2 signaling, 2) JNK1 contributes to the teratogenic

187 etion blocked diabetes-induced activation of JNK1/2 signaling, caspases 3 and 8, and apoptosis in Sox

188 TRAF6 mediates the activation of JNK1/2, p38 mitogen-activated protein kinase, adenosine

189 rmacologic and dominant-negative blockade of JNK1/2 activity inhibited viral replication, and this co

190 we demonstrate that selective deficiency of JNK1 in the murine nervous system is sufficient to suppr

191 ation of transcription factors downstream of JNK1/2, caspase cascade, and apoptosis.

192 be a study in which the long-term effects of JNK1 inactivation on glucose homeostasis and oxidative s

193 esity and insulin resistance, the effects of JNK1 or JNK2 ablation were determined in developing and

194 that was dependent on a further elevation of JNK1/2 activity and recruitment of the extrinsic CD95 pa

195 da albicans infection, and the expression of JNK1 in hematopoietic innate immune cells was critical f

196 Expression of JNK1, which regulates the expression of genes important

197 The proinflammatory function of JNK1 requires bone marrow-derived cells, particularly ma

198 Inhibition of JNK1 by NO reduces Bcl-2 phosphorylation and increases t

199 proved cell viability, whereas inhibition of JNK1 prevented early apoptosis.

200 NA interference (RNAi)-mediated knockdown of JNK1 and JNK2, enhanced replication of HCV replicon RNAs

201 Knockdown of JNK1 in ovo caused defects in spinal cord commissural ax

202 We found that knockdown of JNK1 or JNK2 or treatment with JNK-IN-8, an adenosine tr

203 acological inhibition and siRNA knockdown of JNK1/2 normalized IL-12p40 secretion.

204 oaches demonstrate that the combined loss of JNK1 and JNK2 protein kinase function results in rapid s

205 Mice with loss of JNK1/2 expression in hepatocytes exhibited no defects in

206 with control mice, whereas mice with loss of JNK1/2 in the hematopoietic compartment exhibited a prof

207 We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gen

208 e question as to the potential mechanisms of JNK1 activation related to alcoholic liver injury.

209 ity resulted in increased phosphorylation of JNK1.

210 ciency results in reduced phosphorylation of JNK1/2 and activation of NF-kappaB that lead to impaired

211 K2, PSD-95, and decreased phosphorylation of JNK1/2 at T183/Y185 and PSD-95 at S295 in the ACC in sch

212 inhibition of JNK signaling or reduction of JNK1 levels restores proliferation.

213 NA (siRNA), indicating the mediating role of JNK1/2 in IL-1beta-induced cellular alteration.

214 This suggests a regulatory role of JNK1/2 in modulating the ER-mitochondrial-Ca(2+) axis by

215 ondrial dysfunction and evaluate the role of JNK1/2.

216 by reduction of the phosphorylation state of JNK1 and the mRNA levels of proinflammatory cytokines.

217 antly decreased the phosphorylation state of JNK1 in both hepatoma H4IIE cells and mouse primary hepa

218 antly, we determine the crystal structure of JNK1 in complex with the second docking site of MKK7, re

219 ach is described using crystal structures of JNK1 and CHK1 in complex with 1 and 2 and of the CHK1-3b

220 We also showed that suppression of JNK1 by JNK1 siRNA increased p53 protein level and decre

221 hus, this work indicates that suppression of JNK1/2 activity by MKP-1 maintains PARP-1 levels and sug

222 revealed that Nedd4-2 serves as a target of JNK1, but not of p38 MAPK or ERK1/2.

223 e kinase kinase Map3k5 (ASK1) is upstream of JNK1 activation.

224 ut these modifications were not dependent on JNK1/2 activation and were not responsible for prolonged

225 the proteasome, relieving its suppression on JNK1 activation.

226 ever, in CD8(+) T cells, POSH regulates only JNK1.

227 in MFS mice, and inhibition of the ERK1/2 or JNK1 pathways is a potential therapeutic strategy for th

228 nd-specific cofactors such as MEK1-ERK1/2 or JNK1/2.

229 Knockdown of either FoxM1 or JNK1 inhibits tumor cell migration, invasion, and anchor

230 Knockdown of either PKC or JNK1 prevented PKC activator-mediated membrane accumulat

231 sferroxamine treatment, whereas PKCdelta- or JNK1-deficient cells exhibit resistance to extended hypo

232 These inhibitors had high selectivity over JNK1 and p38alpha, minimal cytotoxicity, potent inhibiti

233 mulation and induced phosphorylation of p38, JNK1/2, and BCL2, thereby promoting the autophagic flux.

234 d flagellin-induced NFkappaB (p105 and p65), JNK1/2, and ERK1/2 activation compared with control cell

235 Our findings indicate that the PARP14-JNK1-PKM2 regulatory axis is an important determinant fo

236 n partially reduces levels of phosphorylated JNK1.

237 s, which is responsible for the proapoptotic JNK1/2 pathway activation, apoptosis, and NTD induction.

238 phosphorylation of the proapoptotic protein JNK1 by upregulation of mitogen-activated protein kinase

239 fic functions of the two major JNK proteins, JNK1 and JNK2.

240 We found decreased expression of Rap2, JNK1, JNK2, PSD-95, and decreased phosphorylation of JNK

241 TBP expression mimics the effect of reduced JNK1 or JNK2 levels on Bdp1 expression.

242 JNK activity, which is mediated by residual JNK1 and higher than in wild-type or jnk1-/- hepatocytes

243 ce in support of an accelerated Rac1-Nox-ROS-JNK1/2 signaling pathway in the islet beta-cell leading

244 Silencing JNK1 and -2 also prevented the loss of GCL.

245 cell motility, as inhibition using SP600125 (JNK1/2/3 inhibitor) or a JNK2/3-specific inhibitor block

246 damage in both mice with hepatocyte-specific JNK1/2 deficiency and control mice.

247 Liver-specific JNK1/2 deletion led to tumor reduction and enhanced surv

248 However, muscle-specific JNK1-deficient (M(KO)) mice exhibit improved insulin sen

249 ivated protein kinases (MAPKs), specifically JNK1/2 and ERK1/2, activation in intestinal epithelial c

250 Furthermore, STRA6, JAK2, STAT5, JNK1, or p38 siRNA and cAMP-PKA inhibitor reversed the r

251 , activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 com

252 ic embryopathy and that the oxidative stress-JNK1/2-caspase pathway mediates the proapoptotic signals

253 the activity of S-nitrosylation substrates, JNK1 and IKKbeta.

254 myeloma cells and constitutively suppresses JNK1-mediated apoptosis by affecting expression of poly(

255 Suppressing JNK1/2 activation by either jnk1 or jnk2 gene deletion p

256 ction prevents the effects of nervous system JNK1 deficiency on body mass.

257 We conclude that compounds targeting JNK1 activity in brain and adipose tissue, which do not

258 These data demonstrate that JNK1 in muscle contributes to peripheral insulin resista

259 Together, our findings demonstrate that JNK1-mediated multisite phosphorylation of Bcl-2 stimula

260 We previously demonstrated that JNK1 phosphorylation by TGFbeta1 is also critical for TG

261 These results provide direct evidence that JNK1/PUMA-dependent apoptosis promotes chemical hepatoca

262 Here we found that JNK1 activation suppresses antifungal immunity in mice.

263 s infected with C. albicans, indicating that JNK1 may be a therapeutic target for treating fungal inf

264 small interfering RNA (siRNA) revealed that JNK1 but not JNK2 was required for productive gene trans

265 Our study reveals that JNK1 is important in the coordination of DCC and DSCAM i

266 Our results show that JNK1 and JNK2 are equally involved in diabetic embryopat

267 Here, we show that JNK1-1 and JNK1-2 are activated early by osmostress, and

268 We showed that JNK1-deficient mice had a significantly higher survival

269 In earlier work we showed that JNK1/2 activation is initiated before ER stress and apop

270 These results strongly suggest that JNK1 plays a key role in retinal neoangiogenesis and tha

271 The JNK1-SIRT1 pathway provides a new molecular mechanism fo

272 n of Bim-associated apoptosis as well as the JNK1/2/c-Jun pathway to the induction of apoptosis.

273 Blocking the JNK1 pathway by a chemical inhibitor and siRNA reduces t

274 -JNK-ir were not seen in animals lacking the JNK1 isoform.

275 ed by activation of the p38alpha but not the JNK1 or JNK2 MAPK pathways.

276 egulatory (Treg) cells by suppression of the JNK1 and p38 pathway.

277 evels and was blocked by inactivation of the JNK1/2 signaling pathway.

278 which depends on the overstimulation of the JNK1/c-Jun pathway by saturated fatty acids.

279 roliferation and differentiation through the JNK1-miR-203-p63 pathway.

280 rs autophagosome formation primarily via the JNK1-Bcl-2 pathway.

281 Moreover, this JNK1-mediated signaling pathway was found to inhibit AMP

282 ting PSD-95 phosphorylation directly through JNK1 and calcium/calmodulin-dependent kinase II and also

283 play a role in tumor cell invasion, through JNK1-independent and -dependent mechanisms in U2OS cells

284 Thus, JNK1 activation in adipose tissue can cause insulin resi

285 ation and protein degradation in response to JNK1 activation in obese mice.

286 estin-3 modulates the activity of ubiquitous JNK1 and JNK2 in non-neuronal cells, impacting the signa

287 heart, and testes, in contrast to ubiquitous JNK1 and JNK2.

288 bited by decreasing JNK1 and JNK2 levels via JNK1/2 DsiRNA transfection of keratocytes before their a

289 Palmitate induction of PUMA was JNK1-dependent in primary murine hepatocytes.

290 The degradation disappears in obesity when JNK1 is inactivated in mice.

291 he aim of this study was to evaluate whether JNK1 or JNK2 plays a role in this potentiated hepatotoxi

292 provide a novel molecular mechanism by which JNK1 promotes glycolysis for cell survival.

293 While JNK1 positively regulates TBP expression, the RNA pol II

294 ss-induced deficit of contextual fear, while JNK1 mainly regulates baseline learning in this behavior

295 blish that galectin-7 can be associated with JNK1 and protect it from ubiquitination and degradation.

296 itment domain (CARD) directly interacts with JNK1 and JNK2, which correlates with decreased JNK activ

297 n promotes VSMC survival by interfering with JNK1 and p53 phosphorylation cascades involved in apopto

298 ve distinct effects on steatohepatitis, with JNK1 promoting steatosis and hepatitis and JNK2 inhibiti

299 periments, keratocytes were transfected with JNK1/2 Dicer-substrate RNA (DsiRNA) and then activated w

300 Without JNK1, mast cells fail to degranulate efficiently and rel