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 uired for immediate early activation of both SAPK (p38/JNK) and GCN2 signaling pathways.

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

47 Conversely, SAPK signaling favors CAR assembly and integrity in its

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

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

50 ility of this phosphatase to dephosphorylate SAPK.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 The Hog1 SAPK associates with nuclear pore complex components and

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

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

68 synthesis and export machineries by the Hog1 SAPK.

69 cription factors are new targets of the Hog1 SAPK.

70 shown to be directly controlled by the Hog1 SAPK.

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

72 pressing a dominant-negative kinase inactive SAPK.

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

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

75 roteolysis, but had no effect on ATP-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 (GSK-3beta) and c-Jun N-terminal kinase (JNK/SAPK) in beta-cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 previously that MEKK1 binds directly to JNK/SAPK.

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

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

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

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

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

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

132 ctivate the stress-activated protein kinase (SAPK) and GCN2-mediated stress response pathways.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 Activation of SAPK by forced expression of DeltaMEKK1 increased overal

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

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

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

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

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

203 ASK1 can inhibit TNF and TRAF2 activation of SAPK.

204 ination and degradation by the activation of SAPK.

205 expressed DLK was required for activation of SAPK.

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

207 ive stress cellular damage via activation of SAPK/JNK phosphorylation, Nrf2 nuclear translocation and

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

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

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

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

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

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

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

215 98059 and U0126 inhibitors and inhibition of SAPK/JNK pathway did not suppress C pneumoniae-induced I

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 ional kinases that stimulate defined MAPK or SAPK cascades.

233 8 mitogen-activated protein kinase (MAPK) or SAPK/JNK, but not p42/44 MAPK, using either selective ch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 the stress-activated protein kinase pathway (SAPK) and its effector, MAPK Sty1, downregulates CAR ass

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

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

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

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

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

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

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

256 roning protein kinases, does not affect Spc1 SAPK.

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

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

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

260 tion that compromises signaling through Spc1 SAPK.

261 ate stress signaling from Wis1 MAPKK to Spc1 SAPK.

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

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

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

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

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

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

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

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

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

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

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

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

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

275 Accurate control of For3 levels by the SAPK pathway may thus represent a novel regulatory mecha

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

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

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

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

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

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

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

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

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

285 8/RK inhibitor, SB203580, suggested that the SAPK pathway was not involved in potentiation of apoptos

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

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

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

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

290 3 results in the selective activation of the SAPKs.

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

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

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

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

295 f the stress-induced phosphorylation of this SAPK.

296 yofibroblast differentiation pathway through SAPK/JNK signaling.

297 required for signal transduction from DLK to SAPK.

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

299 hrough activation of catalase expression via SAPK/JNK phosphorylation and Nrf2 nuclear translocation.

300 tudy offers insight into mechanisms by which SAPK outputs are tailored to specific stressors.