ライフサイエンスコーパス: SAPK

1 SAPK phosphorylates Bcl-x(L) on threonine 47 (Thr-47) an

2 c for VEGFR-1) led to activation of Erk-1/2, SAPK/JNK, and translocation of the p65 subunit of nuclea

3 RK1/2 and ERK5 activation but also abrogated SAPK/JNK and p38 MAPK signaling in parallel.

4 edback interactions among GFAP accumulation, SAPK/JNK activation, and proteasomal hypofunction cooper

5 Importantly, TNF fails to activate SAPK or NF-kappaB in a human melanoma cell line deficien

6 oes not reflect a global failure to activate SAPKs in the PKR-null background as these kinases are ac

7 litazone also disrupted TGF beta 1-activated SAPK/JNK signaling, leading to decreased Smad2/3 transac

8 to trigger a rapid accumulation of activated SAPK that was then sustained for >120 min.

9 Additionally, ceramide activates SAPK activity, which is blocked with a dominant-negative

10 , the results demonstrate that Lyn activates SAPK by an MKK7-dependent, SEK1-independent mechanism.

11 studies demonstrate that PKCdelta activates SAPK by an MKK7-dependent, SEK1-independent mechanism.

12 Cycloheximide, which activates SAPK, while inhibiting protein synthesis, stabilized end

13 By activating SAPK/JNK signaling, which is normally suppressed during

14 MAPK pathways while reciprocally activating SAPK/JNK in leukemia cells exposed to UCN-01 and, in so

15 Interestingly, expression of AKT, SAPK/JNK, and ERK was not altered by QLQX treatment.

16 to anisomycin, an agonist that activates all SAPKs, including SAPK4/p38delta.

17 fferentiation through activating Smad2/3 and SAPK/JNK MAPK pathways, which in turn stimulates alpha-s

18 Significant activation of p-38 and SAPK was observed in all four brain structures, accompan

19 ated through a complex PKCalpha-MAPK/ERK and SAPK/JNK signaling pathway, which leads to growth stimul

20 relationship between Gene 33 expression and SAPK activation.

21 hibits both TNF- and TRAF2-mediated GCKR and SAPK activation, but has a minimal effect on ASK1 activa

22 /Uev1A is required for TNF-mediated GCKR and SAPK activation, but may not be required for ASK1 activa

23 adaptor proteins, which can lead to GCKR and SAPK activation.

24 topically expressed, CIKS stimulates IKK and SAPK/JNK kinases and it transactivates an NF-kappaB-depe

25 connect upstream signaling events to IKK and SAPK/JNK modules.

26 cular cloning of CIKS (connection to IKK and SAPK/JNK), a previously unknown protein that directly in

27 Furthermore, both NF-kappaB and SAPK activation appear independent of both TNFR1 localiz

28 (MAPK) superfamily, including p38 kinase and SAPK/JNK, play a central role in mediating cellular resp

29 -alpha is mediated through both p38 MAPK and SAPK/JNK, but not p42/44 MAPK or NF-kappaB, pathways.

30 mes activated by HGF/SF through p38 MAPK and SAPK/JNK.

31 ng pathways, including ERK1/2, p38 MAPK, and SAPK as judged from the results of experiments using siR

32 the phosphorylation of ERK1/2, p38 MAPK, and SAPK/ERK kinase-1 (SEK1) of the JNK pathway.

33 As MEKK1 functions upstream to MKK7 and SAPK, the finding that a dominant-negative MEKK1(K-M) mu

34 horylation of ERK44/42 MAPK, but not p38 and SAPK, 1 min after they were added to monocytes.

35 ed mitogen-activated protein kinases p38 and SAPK/JNK.

36 evels of phosphorylation of p44/42, p38, and SAPK/JNK MAP kinase.

37 l well-studied MAP kinases (ERK1/2, p38, and SAPK/JNK).

38 ime-dependent phosphorylation of p44/p42 and SAPK/JNK pathways in C pneumoniae-infected cells.

39 orm a signaling complex with MEKK1, SEK, and SAPK.

40 eins (ERK1 and 2, MEK1/2 [MAPKK], STAT3, and SAPK/JNK), and decreased levels of phosphorylation of 14

41 idly activates Ras, as well as both ERKs and SAPKs.

42 As SAPKs are implicated in programmed cell death, these obs

43 pose the hypothesis that the balance between SAPK and protein phosphatases affects the duration and m

44 Both SAPK/JNK and p38 mitogen-activated protein kinases (MAPK

45 SAPK, suggesting a feedback loop to control SAPK activity.

46 thway, we investigated whether ATP-dependent SAPK activation involved such proteases.

47 sed interleukin-1beta, but not ATP-dependent SAPK activity.

48 ility of this phosphatase to dephosphorylate SAPK.

49 n inhibitory role with respect to Drosophila SAPK signaling during development as well as under stres

50 hip to functional alterations in stress (eg, SAPK, JNK) and survival (eg, MAPK, ERK) signaling pathwa

51 distinguished by the family of kinases (Erk, SAPK/JNK, or p38) that is ultimately activated.

52 , p42/ p44 ERK, p38, and to a lesser extent, SAPK/JNK mitogen-activated protein kinase phosphorylatio

53 diverse stimuli by revealing a mechanism for SAPK activation specifically by oxidative stress.

54 ly class of viral proteins were required for SAPK activation.

55 accumulation of SAPKs is a pre-requisite for SAPK-dependent gene expression, and reveal that stress-i

56 of virus infection ICP27 was sufficient for SAPK activation and activation of the p38 targets Mnk1 a

57 r activation of the MEK kinase-1 (MEKK-1)--> SAPK pathway.

58 sine kinase activates the MEKK1 --> MKK7 --> SAPK pathway but not through a direct interaction with M

59 gh a Lyn --> PKCdelta --> MEKK1 --> MKK7 --> SAPK signaling cascade in response to DNA damage.

60 s associated with activation of the MEKK-1-->SAPK cascade.

61 induced ROS production and that the MEKK-1-->SAPK pathway is activated by a ROS-mediated mechanism.

62 art by Lyn and that the Lyn-->MEKK1-->MKK7-->SAPK pathway is functional in the induction of apoptosis

63 (MEKK-1), an upstream effector of the SEK1-->SAPK pathway, in the response of cells to genotoxic stre

64 The Hog1 SAPK associates with nuclear pore complex components and

65 The Hog1 SAPK in Candida albicans is robustly phosphorylated in r

66 In yeast, the Hog1 SAPK plays a key role in reprogramming the gene expressi

67 synthesis and export machineries by the Hog1 SAPK.

68 cription factors are new targets of the Hog1 SAPK.

69 shown to be directly controlled by the Hog1 SAPK.

70 RAF2, TRAF5, and TRAF6 but not with TRAF3 in SAPK activation.

71 pressing a dominant-negative kinase inactive SAPK.

72 a correlation between the ability to induce SAPKs and apoptosis by Rho family members.

73 3) ATP-induced SAPK activation could be recapitulated in P2X7 receptor-

74 roteolysis, but had no effect on ATP-induced SAPK activation.

75 without appreciably modulating CD22-induced SAPK activation.

76 DNA damage-induced SAPK activation was attenuated by (i) treatment with rot

77 o demonstrate that inhibition of Lyn-induced SAPK activity abrogates the apoptotic response of cells

78 egative MEKK1(K-M) mutant blocks Lyn-induced SAPK activity supports involvement of the MEKK1-->MKK7 p

79 onstrate that Lyn, but not Lyn(K-R), induces SAPK activity.

80 ction, because deletion of RILPHLYL inhibits SAPK-mediated phosphorylation of M3/6, and deletion of t

81 targeting of TRAF2 also selectively inhibits SAPK activation.

82 least in part through activation of the JNK SAPK pathway.

83 distinguishable from those of the ERK, JNK (SAPK), and BMK (ERK5) kinases.

84 erminal kinase-stress-activated kinase (JNK- SAPK) coimmunoprecipitated with Akt from me-v macrophage

85 protein kinase (MAPK) pathways, ERK1/2, JNK/SAPK, and p38 MAPK (p38), have been shown to enhance the

86 p38 MAPK and p42/44 MAPK, but not p46/54 JNK/SAPK, in the cortex and outer and inner medulla.

87 MLKs activate JNK/SAPK in vivo by directly phosphorylating and activating

88 lular signal-regulated kinase), p38, and JNK/SAPK (c-Jun N-terminal protein kinase/stress-activated p

89 IL-1beta and toxin A induced Erk1/2 and JNK/SAPK but not p38 activation in NCM460 cells.

90 in ERK 1/2, p90RSK, Mnk 1, p38 MAPK and JNK/SAPK phosphorylation (P < 0.05) after the exercise bout.

91 ls, sanguinarine caused enhanced ERK and JNK/SAPK phosphorylation.

92 of ERK 1/2, p90RSK, Mnk 1, p38 MAPK and JNK/SAPK proteins versus YM (P < 0.05).

93 nd in whole cells, and activated ERK and JNK/SAPK.

94 s with the selectivity p38 approximately JNK/SAPK >> ERK.

95 a mechanism by which the MEKK1-dependent JNK/SAPK pathway is negatively regulated by PAK through phos

96 -expression of TAO2 activated endogenous JNK/SAPK and p38 but not ERK1/2.

97 tion both require activation of the ERK, JNK/SAPK and PI-3-K pathways.

98 Finally, JNK/SAPK activity was found to increase in response to oxida

99 kinase/stress-activated protein kinase (JNK/SAPK) and ERK1/2 MAP kinase pathways.

100 kinase/stress-activated protein kinase (JNK/SAPK) and p38 MAPK, in different brain regions.

101 kinase/stress-activated protein kinase (JNK/SAPK) cascade, while others have been shown to be activa

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

103 terminal kinase/stress-activated kinase (JNK/SAPK) pathway in A549 human lung carcinoma cells.

104 kinase/stress-activated protein kinase (JNK/SAPK) pathway is activated by numerous cellular stresses

105 kinase/stress-activated protein kinase (JNK/SAPK) pathway was similarly observed in response to STIN

106 kinase-stress-activated protein kinase (JNK/SAPK) pathways upon various cellular stresses.

107 kinase/stress-activated protein kinase (JNK/SAPK), and TRAF2 can also mediate activation of NF-kappa

108 kinase/stress-activated protein kinase (JNK/SAPK).

109 a potent activator of the stress kinase JNK/SAPK, can induce Bcl2 phosphorylation at Ser(70) and tha

110 kinase/stress-activated protein kinases (JNK/SAPK).

111 of the stress-activated protein kinases, JNK/SAPK and p38, in the intestinal epithelial cell line HCT

112 tream mitogen-activated protein kinases, JNK/SAPK and p38.

113 n kinases family (p38 MAPK, p44/42 MAPK, JNK/SAPK), members of cell survival pathways (AKT/PKB), and

114 ERK 1/2, p90RSK, Mnk 1, eIF4E, p38 MAPK, JNK/SAPK, MKP 1) at rest and following exercise, in sedentar

115 n the UV-induced and K+ channel-mediated JNK/SAPK activation.

116 e dominant negative forms of MKK4, MKK7, JNK/SAPK, MKK3, MKK6, or p38alpha did not suppress PMA-stimu

117 iable consequence of ERK and p38 but not JNK/SAPK activation, and MSK1 potentially provides a link to

118 sts paralleled activation of p38 but not JNK/SAPK, consistent with the idea that TAO2 is a physiologi

119 min inhibits TRAF2-induced activation of JNK/SAPK and of NF-kappaB.

120 alysis to examine expression patterns of JNK/SAPK in wild-type and JNK2-/- polymorphonuclear leukocyt

121 The inhibition of JNK/SAPK signaling pathway by JIK was found to occur between

122 ylation of this site inhibits binding of JNK/SAPK to MEKK1.

123 lel pathways, we examined involvement of JNK/SAPK, p38, and MKK1 in promoter regulation.

124 ro or in cells nor did they cause ERK or JNK/SAPK phosphorylation.

125 f the MAP-kinases (MAPKs) including p38, JNK/SAPK, Mek1/2 and Erk1/2.

126 d TGF-beta-activated kinase 1 and of the JNK/SAPK (c-Jun N-terminal kinase/stress-activated protein k

127 previously that MEKK1 binds directly to JNK/SAPK.

128 mouse neutrophils, a cell type in which JNK/SAPK expression and activity has been given little study

129 Therefore, the activities of both JNKs/SAPKs and ERK1/2 are sensitive to HIF-1-dependent proces

130 RKI/II, without effect on the related kinase SAPK/JNK (stress-activated protein kinase/c-Jun N-termin

131 ubstrate of stress-activated protein kinase (SAPK) 2a/p38.

132 tivation of stress-activated protein kinase (SAPK) and cellular differentiation.

133 ced the p38 stress-activated protein kinase (SAPK) and expression of cyclooxygenase (COX)-2 transcrip

134 inase (JNK)/stress-activated protein kinase (SAPK) and p38 mitogen-activated protein kinase.

135 by the p38/stress-activated protein kinase (SAPK) axis of signaling, the optimal phosphorylation mot

136 nase in the stress-activated protein kinase (SAPK) cascade.

137 tion of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosi

138 tion of the stress-activated protein kinase (SAPK) pathway.

139 Stress-activated protein kinase (SAPK) pathways are evolutionarily conserved eukaryotic s

140 so known as stress-activated protein kinase (SAPK) pathways, are signaling conduits reiteratively use

141 urprisingly stress-activated protein kinase (SAPK) pathways, pathways that are activated by oxidative

142 inase (JNK)/stress-activated protein kinase (SAPK) phosphorylation was stimulated only by sorbitol (s

143 of JNK/p38 stress-activated protein kinase (SAPK) signaling pathways is critical for the cellular re

144 of the p38 stress-activated protein kinase (SAPK), and overexpression of the dominant-negative p38al

145 also called stress-activated protein kinase (SAPK), which has crucial roles in cellular survival unde

146 es the Hog1 stress-activated protein kinase (SAPK), which is a key player in the regulation of gene e

147 of phospho-stress-activated protein kinase (SAPK), wild-type p53, or cleaved caspase 3.

148 se 1 (JNK1)/stress-activated protein kinase (SAPK).

149 ase and the stress-activated protein kinase (SAPK).

150 s-activated c-Jun N-terminal protein kinase (SAPK).

151 tivation of stress-activated protein kinase (SAPK).

152 tivation of stress-activated protein kinase (SAPK).

153 and the p38 stress-activated protein kinase (SAPK).

154 (p-38), and stress-activated protein kinase (SAPK).

155 sphorylated stress-activated protein kinase (SAPK)/c-jun NH(2)-terminal kinase (JNK).

156 tion of the stress-activated protein kinase (SAPK)/JNK pathway in BAC1 murine macrophages stimulated

157 olve p38 or stress-activated protein kinase (SAPK)/Jun N-terminal kinase (JNK) and was not inhibited

158 ng proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulate

159 inase (JNK)/stress-activated protein kinase (SAPK)] as well as serine/threonine kinase AKT.

160 mulates the stress-activated protein kinase (SAPK, also referred to as Jun kinase or JNK) pathway.

161 tion of the stress-activated protein kinase (SAPK/JNK) by genotoxic agents is necessary for induction

162 tion of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosy

163 tion of the stress-activated protein kinase (SAPK/JNK) pathway.

164 ated protein kinase/c-jun N-terminal kinase (SAPK/JNK) and caspase 3 activity.

165 protein kinase/c-Jun NH(2)-terminal kinase (SAPK/JNK) and p38 mitogen-activated protein kinase (MAPK

166 ivated protein kinase/Jun N-terminal kinase (SAPK/JNK) mitogen-activated protein kinases (MAPKs) in D

167 ivated protein kinase/Jun N-terminal kinase (SAPK/JNK) pathway showed that phosphorylated c-Jun prote

168 ated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), p38 mitogen-activated protein kinase (p38 MAP

169 ated protein kinase/c-Jun N-terminal kinase (SAPK/JNK).

170 ium kinase (stress-activated protein kinase [SAPK]alpha), which is related to members of the mixed li

171 rylated form of the stress-activated kinases SAPK/JNK and p38.

172 r stimuli, stress-activated protein kinases (SAPK) modulate gene expression to maximize cell survival

173 of ATF2 by stress-activated protein kinases (SAPK).

174 c-Jun N-terminal kinases (SAPK/JNKs) are activated by inflammatory cytokines, and

175 ivation of stress-activated protein kinases (SAPKs and c-Jun NH(2)-terminal kinases) requires TNF rec

176 Stress-activated protein kinases (SAPKs) are known to regulate transcription factors in re

177 ression by stress-activated protein kinases (SAPKs) is essential for cell adaptation to extracellular

178 ne whether stress-activated protein kinases (SAPKs) mediated the transfer of diabetes-induced stress

179 ion of the stress-activated protein kinases (SAPKs) p38 and JNK.

180 tivate the stress-activated protein kinases (SAPKs) p38 and JNK.

181 ctivity of stress activated protein kinases (SAPKs), including JNK and p38 MAP kinases.

182 es JNKs or stress-activated protein kinases (SAPKs), is dependent on enhanced glucose utilization med

183 Stress-activated protein kinases (SAPKs), members of a mitogen-activated protein kinase (M

184 ivation of stress-activated protein kinases (SAPKs), p38 MAPK, and JNK.

185 KR and the stress-activated protein kinases (SAPKs), such as p38 mitogen-activated protein kinase (MA

186 ulation of stress-activated protein kinases (SAPKs).

187 quires the stress-activated protein kinases (SAPKs)/c-Jun NH(2)-terminal kinases.

188 The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the

189 ediated by stress-activated protein kinases (SAPKs; also named Jun kinases or JNKs).

190 tivate the stress-activated protein kinases (SAPKs; c-jun NH2-terminal kinases or JNKs).

191 APK family member JNK/stress-activated MAPK (SAPK) is involved in extracellular stress and proinflamm

192 and Ang-2 as well as the activation of MAPK, SAPK/JNK, and p38 by the relevant cell types, we conduct

193 also stimulated phosphorylation of p38 MAPK, SAPK/JNK, and ATF-2.

194 oth PD98059 and SB202190, which inhibit MAPK/SAPK signaling pathways, is sufficient to trigger NFATc

195 is study provides evidence that the p38-MAPK/SAPK pathway is necessary, but insufficient, for mediati

196 of Ras, the MAPKKs MKK4 and MEK1, the MAPKs SAPKs and ERKs, and the specific AP-1 proteins Fra-2 and

197 m for TRAF and TANK synergy in GCKR-mediated SAPK activation, which is important in TNF family recept

198 of protein kinase C zeta (PKCzeta) mediates SAPK signal complex formation and subsequent growth supp

199 for protein kinase C, protein kinase A, MEK, SAPK, IKK, and protein kinase R (PKR) were without effec

200 x significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction

201 These findings indicate that activation of SAPK by DNA damage is mediated in part by Lyn and that t

202 Activation of SAPK by forced expression of DeltaMEKK1 increased overal

203 s upstream of MEKK-1-dependent activation of SAPK in the response to genotoxic stress.

204 on the roles and mechanism of activation of SAPK pathways.

205 ansfection we demonstrate that activation of SAPK rapidly stimulated phosphorylation of M3/6.

206 that PKCdelta functions in the activation of SAPK through a Lyn --> PKCdelta --> MEKK1 --> MKK7 --> S

207 de receptors triggers a strong activation of SAPK via a pathway independent of caspase-1- or caspase-

208 ASK1 can inhibit TNF and TRAF2 activation of SAPK.

209 ination and degradation by the activation of SAPK.

210 expressed DLK was required for activation of SAPK.

211 ia/reperfusion resulted in the activation of SAPK/JNK and p38 in HESCs and HEECs and inhibited Ang-1

212 Abl(K-R) inhibits HPK1-induced activation of SAPK/JNK.

213 eal that ceramide induces the association of SAPK with PKCzeta, but not with PKCepsilon.

214 n of SAPK to mitochondria and association of SAPK with the anti-apoptotic Bcl-x(L) protein.

215 nvestigate whether the rapid deactivation of SAPK results from dephosphorylation by dual-specificity

216 tion that is necessary for the expression of SAPK-dependent stress-protective genes.

217 t of HPK1 blocks c-Abl-mediated induction of SAPK/JNK.

218 Furthermore, inhibition of SAPK signaling and inhibition of net K(+) efflux abrogat

219 98059 and U0126 inhibitors and inhibition of SAPK/JNK pathway did not suppress C pneumoniae-induced I

220 downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice.

221 inhibited PMA-stimulated phosphorylation of SAPK, suggesting a feedback loop to control SAPK activit

222 Hypoxia also induced the phosphorylation of SAPK/JNK and p38 in both cultured HESCs and HEECs.

223 d p38MAPK, but offset the phosphorylation of SAPK/JNK that was activated by perifosine treatment alon

224 th activation and mitochondrial targeting of SAPK in the ara-C response.

225 radiation exposure induces translocation of SAPK to mitochondria and association of SAPK with the an

226 hese findings indicate that translocation of SAPK to mitochondria is functionally important for inter

227 th ara-C is associated with translocation of SAPK to mitochondria.

228 lenge the dogma that nuclear accumulation of SAPKs is a pre-requisite for SAPK-dependent gene express

229 d a requirement for PKR in the activation of SAPKs by double-stranded RNA, lipopolysaccharide (LPS) a

230 d SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation

231 A 6-h pulse of SB 203580, an inhibitor of SAPKs, reset the circadian rhythm of melatonin in a phas

232 we provide new insight into the response of SAPKs to diverse stimuli by revealing a mechanism for SA

233 Thus, we characterized axonal transport of SAPKs in peripheral nerve, studied any alteration in str

234 ease (P<0.01) while having greater effect on SAPK/JNK phosphorylation.

235 The c-Jun N-terminal kinase or SAPK/JNK, which responds to stress signaling and is the

236 ional kinases that stimulate defined MAPK or SAPK cascades.

237 8 mitogen-activated protein kinase (MAPK) or SAPK/JNK, but not p42/44 MAPK, using either selective ch

238 tivate c-Jun amino-terminal kinases (JNKs or SAPKs).

239 e motif for MAPKAP kinase-2, but not for p38 SAPK, closely matches the 14-3-3 binding site on Cdc25B/

240 own of ANP32A expression further induced p38 SAPK and COX-2.

241 Inhibition of p38 SAPK reduced CBP HAT activity and its recruitment to the

242 ggesting that signal transduction by the p38 SAPK pathway is required for COX-2 mRNA stability.

243 of Rac or its effector kinases, MLK and p38(SAPK), each increased the velocity of Rab6 positive exoc

244 ular signal-regulated kinase (ERK)(MAPK)/p38(SAPK) activity ratio predicts whether the cells will pro

245 vesicles dependent upon the activity of p38(SAPK) kinase.

246 ies, we review the novel contribution of p38(SAPK), c-Jun NH2-terminal kinase and PKR-like endoplasmi

247 cyclin D1 protein was independent of the p38(SAPK) and phosphatidylinositol 3-kinase pathways, which

248 imilar rate of apoptosis in vivo and the p38(SAPK) or PI3K-Akt signaling pathways were unaffected by

249 s increased basal activation of ERK1/2, p38, SAPK/JNK, and AKT in both regions.

250 role of stress-activated p38 MAP kinase (p38/SAPK-2) signaling in delayed preconditioning of the hear

251 phosphorylation motifs of mammalian p38alpha SAPK and MAPKAP kinase-2 were determined.

252 under hypoxia occurs independent of phospho-SAPK and caspase 3, and the p53 response is an obligator

253 ion-induced increase in the level of phospho-SAPK.

254 tions resulted in an increase in the phospho-SAPK signal, whereas hypoxia suppressed the irradiation-

255 Phosphorylated SAPK/JNK increased 36-fold (200 muM CoCl2 concentration)

256 st that central Ang II activates the AT(1)R, SAPK/JNK pathway.

257 he demonstration that this complex regulates SAPK/JNK activation.

258 iated phosphorylation and activation of SEK1-SAPK in coupled kinase assays.

259 roning protein kinases, does not affect Spc1 SAPK.

260 c chaperone, is a positive regulator of Spc1 SAPK in the fission yeast Schizosaccharomyces pombe.

261 We propose that Spc1 SAPK and Hal4 kinase cooperatively function to protect c

262 These results suggest that Spc1 SAPK is a novel client protein for the Cdc37 chaperone,

263 tion that compromises signaling through Spc1 SAPK.

264 ate stress signaling from Wis1 MAPKK to Spc1 SAPK.

265 physiological role of the fission yeast Spc1 SAPK in cellular resistance to certain cations, such as

266 t shock regulation of the fission yeast Spc1 SAPK, a homolog of human p38 and budding yeast Hog1p.

267 s including ZAP70, p27, STAT1, STAT3, STAT6, SAPK, ERK, and JNK were not significantly affected.

268 of TGF-beta on lipopolysaccharide-stimulated SAPK/JNK phosphorylation along with a demonstrated inhib

269 We determined that SAPK/JNK signaling acts in a positive feedback loop to m

270 These findings demonstrate that SAPKs can mediate cell cycle arrest through post-transla

271 Studies of yeasts demonstrated that SAPKs play pivotal roles in survival responses to high o

272 of the known ability of CrkL to activate the SAPK pathway by a catalytically inactive form of GCKR or

273 Stress signals activate the SAPK/JNK and p38 MAPK classes of protein kinases, which

274 he mechanism by which ceramide activates the SAPK signaling pathway in human embryonic kidney cells (

275 stress-induced phosphorylation activates the SAPK, and promotes its nuclear accumulation that is nece

276 e, we report that TNF activates GCKR and the SAPK pathway in a manner that depends upon TRAF2 and Ubc

277 tic interplay between the proteasome and the SAPK/JNK pathway in the context of GFAP accumulation.

278 upstream of the protein kinase MEKK1 in the SAPK pathway.

279 erine/threonine kinases that function in the SAPK signaling cascade.

280 B203580, a dominant negative p38 mutant, the SAPK/JNK inhibitor JNK-interacting protein-1 (JIP-1), or

281 itogen-activated protein kinases but not the SAPK/JNK pathway; pharmacological inhibition of ERK1/2,

282 high osmolarity results in activation of the SAPK Hog1, which associates with transcription factors b

283 have been implicated in the induction of the SAPK pathway, we investigated whether ATP-dependent SAPK

284 hosphorylated SEK and MEKK1, elements of the SAPK signaling complex.

285 Wortmannin-mediated activation of the SAPK/JNK and p38 MAPK pathways also resulted in the mobi

286 ce in hepatocytes through suppression of the SAPK/JNK stress signaling that impairs the insulin signa

287 8/RK inhibitor, SB203580, suggested that the SAPK pathway was not involved in potentiation of apoptos

288 interactions may couple TNF receptors to the SAPK/JNK family of MAPKs; however, a molecular mechanism

289 ) has also been shown to act upstream to the SAPK/JNK signaling pathway.

290 LPHLYL, shares significant homology with the SAPK binding site of the c-Jun protein, called the delta

291 inase kinase (MAP3K) that activates both the SAPKs and p38s in vivo.

292 3 results in the selective activation of the SAPKs.

293 se proteins might collaborate to recruit the SAPKs/JNKs has remained elusive.

294 an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can intera

295 n the present study, we examined whether the SAPKs play a role in the circadian system in cultured Xe

296 et K(+) efflux inhibited activation of these SAPKs by APOL1 G1 or G2.

297 f the stress-induced phosphorylation of this SAPK.

298 yofibroblast differentiation pathway through SAPK/JNK signaling.

299 required for signal transduction from DLK to SAPK.

300 is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as