ライフサイエンスコーパス: MAP kinase

1 3 MAP kinases (ERK1/2, c-Jun kinase, and p38 MAP kinase).

2 ae Slt2 encoding cell wall integrity-related MAP kinase.

3 r alpha from microglia via activation of p38 MAP kinase.

4 le pockets on the proteins Factor Xa and p38 MAP kinase.

5 y to inhibit both kinases, JNK3 and p38alpha MAP kinase.

6 mak-1 paralogues and two orthologues of p38 MAP kinase.

7 y mediated by increases in activation of p38 MAP kinase.

8 ase 2 is phosphorylated and activated by p38 MAP kinase.

9 pathways interact to converge on Hog1, a p38 MAP kinase.

10 the TGF-beta1-induced phosphorylation of p38 MAP kinase.

11 of the pharmacologically relevant target p38 MAP kinase.

12 nteraction of betaarrs with clathrin and ERK MAP kinase.

13 irming that Ohmm acts downstream of the Hog1 MAP-kinase.

14 non-essential enzymes which are activated by MAP kinases.

15 it mainly facilitates the activation of ERK MAP kinases.

16 e kinase that then activates MKK7 and ERK1/2 MAP kinases.

17 duction is preceded by the activation of ERK MAP kinases.

18 y cytokines through activating NF-kappaB and MAP kinases.

19 /-)mice WAT, including smad, NFAT, NFkB, and MAP kinases.

20 KP5), negatively regulates the activation of MAP kinases.

21 K) 3 and p38alpha mitogen-activated protein (MAP) kinase.

22 eam NF-kappaB and mitogen-activated protein (MAP) kinases.

23 d substitution in MITOGEN-ACTIVATED PROTEIN (MAP) KINASE 12 (MPK12).

24 kinase (HvCERK1) and protein kinases such as MAP kinase 3 (HvMPK3) and MAPK substrate 1 (HvMKS1), and

25 For example, Arabidopsis MAP kinase 4 (MPK4) regulates the expression of a subset

26 ent of the root growth defects observed in a MAP kinase 4 (MPK4) single-mutant line.

27 ed a mutation in the catalytic domain of the MAP kinase 7 orthologue sma-5(kc1) In sma-5(kc1) mutants

28 phosphohistone 2AX followed knockdown of the MAP kinase-activated protein kinase 2 (MK2), a kinase cu

29 protease TNF-alpha-converting enzyme via p38 MAP kinase activation and its concurrent export to the c

30 genous beta2AR in terms of: cAMP generation, MAP kinase activation and receptor internalization.

31 led that both the Fgf8-Fgfr1 pathway and p38 MAP kinase activation are partially affected by the loss

32 positive feedback loop of GhWRKY59-regulated MAP kinase activation in response to drought stress.

33 Inhibiting BDNF's receptor, TrkB, ERK/MAP kinase activation, or NMDA receptors blocks this att

34 l cord white matter display strong Smad3 and MAP kinase activation.

35 f a broad set of GPCRs without affecting ERK MAP kinase activation.

36 ide (NO), and ERK mitogen-activated protein (MAP) kinase activation from macrophages are linked to co

37 n of Grb2 represents a switch that regulates MAP kinase activity and hence controls cancer progressio

38 P production, beta-arrestin interaction, and MAP kinase activity.

39 se that regulates mitogen-activated protein (MAP) kinase activity.

40 y) induced rapid cell death despite enhanced MAP kinase and AKT activation.

41 activation of other pathways, such as Erk1/2 MAP kinase and Akt, were not affected.

42 of downstream signaling pathways, including MAP kinase and Akt.

43 mily function through phosphorylation by p38 MAP kinase and Akt/protein kinase B signaling pathways h

44 ranscription factors activated downstream of MAP kinase and cAMP pathways also conferred resistance,

45 ase 2 upon phosphorylation, thereby bridging MAP kinase and G-Protein-Coupled Receptor signaling.

46 ow that combining ascorbic acid (AA) and 2i (MAP kinase and GSK inhibitors) increases the efficiency

47 then enhances LPS-induced activation of p38 MAP kinase and the expression of inflammation-related cy

48 bound proteins in the dmPFC that include ERK/MAP kinase and the NMDA receptor subunits, GluN1 and Glu

49 inase previously shown to inhibit NF-kappaB, MAP kinase and Wnt signalling.

50 KP-1 was a pivotal feedback control for both MAP kinases and NF-kappaB pathway in response to S. aure

51 GTP exchange, KRAS-GTP-driven signaling via MAP kinases and PI3 kinases and mitogen-stress-related k

52 downstream of p38 mitogen-activated protein (MAP) kinase and cyclic-AMP-response element binding prot

53 Additionally, we have mapped kinases and phosphatases that are activated upon

54 TRIF pathways and to the activation of PKC, MAP kinase, and NF-kappaB signaling to induce the produc

55 athways and to the activation of PKC-betaII, MAP kinase, and NF-kappaB signaling to induce the produc

56 cription factor 2 (ASCL2), Wnt/beta-catenin, MAP kinase, and Notch signaling.

57 way by inhibiting the activation of the Slt2 MAP kinase, and synergizes with cell wall stressors such

58 nd basic FGF induced phosphorylation of Akt, MAP kinases, and S6 kinase and Fos expression in the abs

59 The Pmk1 and Mps1 MAP kinases are essential for appressorium formation and

60 Unlike most protein kinases, MAP kinases are not commonly activated by autophosphoryl

61 nalysis identified MAPK3, which encodes ERK1 MAP kinase, as the most topologically important hub in p

62 Inactivation of MAP kinase at late pachytene is critical for timely disa

63 ansport function, via the Wallenda (Wnd)/DLK MAP kinase axonal damage signaling pathway.

64 This expression is mediated by ERK MAP kinase but not PI3K signalling.

65 t, FSH stimulated the phosphorylation of p38 MAP kinase but PKA-CQR did not.

66 Activation of p38 mitogen-activated protein (MAP) kinase but not extracellular signal-related kinase

67 CLIC4 is required for the activation of p38 map kinase by TGF-beta, a pathway that signals myofibrob

68 cell lymphomas, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK) are significant

69 urons whereby ApoE activates a non-canonical MAP kinase cascade that enhances APP transcription and a

70 gene cluster and CrMYC2 act downstream of a MAP kinase cascade that includes a previously uncharacte

71 and HAESA-like 2 (HAE/HSL2) that regulate a MAP kinase cascade that is required for abscission.

72 Our study identified a complete MAP kinase cascade that phosphorylates and activates a k

73 ng Receptor Tyrosine Kinases, members of the MAP Kinase cascade, and WEE1.

74 rrents and that this effect is mediated by a MAP kinase cascade, including ASK1 and c-Jun N-terminal

75 ting that a GPI-AP functions upstream of the MAP kinase cascade.

76 downstream of EPF ligands and upstream of a MAP kinase cascade.

77 stress-activated mitogen-activated protein (MAP) kinase cascade consisting of GhMAP3K15-Mitogen-acti

78 Signal transduction via NFkappaB and MAP kinase cascades is a universal response initiated up

79 rine-threonine phosphorelays, exemplified by MAP kinase cascades, are predominant in eukaryotes.

80 ated molecular patterns (PAMPs) and activate MAP kinase cascades, which regulate changes in gene expr

81 e MAPK scaffold (CST5), and the two terminal MAP kinases (CEK1/CEK2).

82 nome-duplication Dig1/Dig2 proteins regulate MAP kinase controlled signalling pathways involved in ma

83 e protein is implicated in the regulation of MAP kinase-controlled processes involved in mating, fila

84 nflammation and impairs pLTF by a spinal p38 MAP kinase-dependent mechanism.

85 nflammation, thereby impairing pLTF by a p38 MAP kinase-dependent mechanism.

86 We show that the p38 MAP kinase-dependent, EGFR tyrosine kinase (TK)-independ

87 termination at the weak intronic PAS of the MAP kinase dlk-1.

88 tumor progression locus 2 (Tpl2/MAP3K8), and MAP kinase ERK is differentially activated by TLRs.

89 am effectors, the mitogen-activated protein (MAP) kinase Erk and protein kinase B (Akt).

90 PLC-PKC-PKD1 pathway, NF-kappaB pathway, and MAP kinase (ERK, p38, and JNK) pathways are important fo

91 of extracellular-signal-activated kinase1/2 MAP kinase (ERK-MAPK).

92 RKs through direct action on a novel site in MAP kinase/ERK kinase (MEK).

93 ion of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kinase signaling.

94 We show that the MAP kinases ERK1/2 phosphorylate TC21 and R-Ras on this

95 lpha phosphorylation and activation of all 3 MAP kinases (ERK1/2, c-Jun kinase, and p38 MAP kinase).

96 l contains the MAPK3 gene, which encodes the MAP kinase, ERK1.

97 yet it is efficiently phosphorylated by the MAP kinase ERK2 at a consensus threonine site (T38).

98 onse to activation by phosphorylation of the MAP kinase ERK2.

99 The atypical MAP kinases ERK3 and ERK4 are activated by phosphorylati

100 so inhibit MEK5, which activates the related MAP kinase ERK5.

101 hly conserved ortholog of the human atypical MAP kinase ERK8.

102 activation of the mitogen-activated protein (MAP) kinase (extracellular signal-regulated kinase [ERK]

103 hosphorylation by mitogen-activated protein (MAP) kinases for their transcriptional functions.

104 Furthermore, the loss of Hog1 MAP kinase function aggravates the loss of RNA polymeras

105 ockout mutants of the ortholog of yeast HOG1 MAP kinase gene in U. virens.

106 ir-125b directly represses stress-responsive MAP kinase genes and associated signaling.

107 An enzyme called p38 MAP kinase helps nematodes to adapt to low-oxygen enviro

108 ranscription factor Msn2 with Dot6, Sfp1, or MAP kinase Hog1, revealed both coordinated and decoupled

109 Further studies uncovered defects related to MAP kinase I (Slt2) pathways, and we provide evidence th

110 H-1 increased phosphorylated (activated) p38 MAP kinase immunofluorescence in identified phrenic moto

111 ress-induced cell death by regulating ERK1/2 MAP kinase in intestinal epithelial cells.

112 phosphorylation of the CTD S2 kinase Lsk1 by MAP kinase in response to cellular signalling.

113 gae effector HopAI known to inactivate plant MAP kinases in M. oryzae.

114 First messenger-dependent activation of MAP kinases in neuronal and endocrine cells is critical

115 p38 without simultaneously activating other MAP kinases in neuronal and endocrine cells.

116 ointing to increased activity of one or more MAP kinases in PKA knockout cells.

117 mpk6-2 mutant and plants overexpressing the MAP kinase-inactivating phosphatase, AP2C3.

118 Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enz

119 MAP kinase inducing activity was dependent on CRAF dimer

120 oprofen; 55 +/- 9%; p < 0.001) or spinal p38 MAP kinase inhibition (58 +/- 2%; p < 0.001).

121 Furthermore, it suggests that p38 MAP kinase inhibition may be a useful strategy to inhibi

122 alponin reduction, MCP-1 inhibition, and p38 MAP kinase inhibition than any individual agonist.

123 tant allele frequency were more sensitive to MAP kinase inhibition, and CRISPR-Cas9-mediated replacem

124 A well-validated p38 MAP kinase inhibitor SB203580 (0.5-5muM) cancelled the e

125 on extending the inhibition profile of a p38 MAP kinase inhibitor toward mutant EGFR inhibition.

126 ported 1a (skepinone-L) as a type I p38alpha MAP kinase inhibitor with high potency and excellent sel

127 viously disclosed phase II clinical p38alpha MAP kinase inhibitor, a structurally novel clinical prod

128 Blockade of CCR7, or treatment with a p38 MAP kinase inhibitor, reduced lymphatic dissemination of

129 The best balanced dual JNK3/p38alpha MAP kinase inhibitors are 6m (IC50: JNK3, 18 nM; p38alph

130 kinase-interacting serine-threonine kinases MAP kinase-interacting kinase 1 (Mnk1/2), the eIF4E upst

131 The MAP kinase-interacting kinases (MNK1 and MNK2) are non-e

132 Although the MAP kinase-interacting kinases (MNKs) have been known fo

133 Here we identify MAP kinase-interacting serine/threonine protein kinase 1

134 Our data suggest that the active form of MAP kinase interacts with gamma-tubulin on specific subs

135 d 2 suggested that activation of ERK 1 and 2 MAP kinases is required for BAFF-R to promote B cell sur

136 be important for EGF-dependent signaling to MAP kinases, is overexpressed.

137 Upon dual phosphorylation by MAP kinase kinase 1, the dynamics of assigned methyls in

138 cell activation, the Jun kinase (JNK) kinase MAP kinase kinase 7 (MKK7) is alternatively spliced to f

139 Also, systemic administration of an MAP kinase kinase inhibitor increased breakpoint ratios,

140 ng the important cellular signaling molecule MAP kinase kinase kinase 2 (MAP3K2), at exactly the same

141 o domains in other proteins that mediate Ras-MAP kinase kinase kinase associations; however, this RBL

142 , a homologue of Mst11, which corresponds to MAP kinase kinase kinase in Magnaporthe oryzae, and urat

143 ddition, a direct PKA site that inhibits the MAP kinase kinase kinase Map3k5 (ASK1) is upstream of JN

144 The MAP kinase kinase kinase TGFbeta-activated kinase 1 (TAK

145 na there are approximately 80 genes encoding MAP kinase kinase kinases (MAP3K), 10 genes encoding MAP

146 n requires a chitin receptor and one or more MAP kinase kinase kinases and MAP kinase kinases.

147 Further, mutants defective in the upstream MAP kinase kinase MKK3 also display hypersensitivity in

148 e that includes a previously uncharacterized MAP kinase kinase, CrMAPKK1.

149 ctivates dual leucine-zipper kinase (DLK), a MAP-kinase kinase kinase that then activates MKK7 and ER

150 se kinase kinases (MAP3K), 10 genes encoding MAP kinase kinases (MAP2K), and 20 genes encoding MAP ki

151 nd one or more MAP kinase kinase kinases and MAP kinase kinases.

152 a single ERK-like mitogen-activated protein (MAP) kinase (MAK-1)-signaling cascade, whereas a second

153 Unlike the MAP kinase (MAPK) cascade that phosphorylates p38 on the

154 phosphorylated and activated by a canonical MAP kinase (MAPK) cascade, represent a point of signalin

155 o the RAGE receptor and activates the p42/44 MAP kinase (MAPK) cascade.

156 uppression of two branches of MAMP-activated MAP kinase (MAPK) cascades.

157 Smk1 is a meiosis-specific MAP kinase (MAPK) in budding yeast that is required for

158 Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pathwa

159 antly, we find that Vegf signaling activates MAP kinase (MAPK)-dependent E26 transformation-specific

160 inase kinases (MAP2K), and 20 genes encoding MAP kinases (MAPK).

161 ivated downstream mitogen-activated protein (MAP) kinase (MAPK) and phosphatidylinositol 3-kinase (PI

162 on of Erk and p38 mitogen-activated protein (MAP) kinases (MAPKs) in neutrophils.

163 ted CCR7 expression in EMT cells through p38 MAP kinase-mediated activation of the JunB transcription

164 memory formation and cognition, such as the MAP kinases, MKPs, CaMKII, CREB, Fyn, and Tau.

165 dual phosphorylation reactions catalyzed by MAP kinase modules are sequential at both levels of the

166 MAP kinase modules propagate diverse extracellular signa

167 MAP kinase (MPK) cascades in Arabidopsis thaliana and ot

168 t PERK signaling is a component of the mouse MAP kinase neuronal stress response controlled by the Du

169 Activation of ERK MAP kinases occurred in these cells by 30 min postchalle

170 MAP kinases of the ERK family are conserved from yeast t

171 ii) prevents activation of the Kss1 and Fus3 MAP kinases of the mating pheromone pathway, which in tu

172 ay, either with direct inhibitors of the p38 MAP kinase or a small-molecule therapeutic that also inh

173 Thus, inhibition of MAP kinase p38 may be an antiviral strategy that protect

174 reas Epac2 is activated for signaling to the MAP kinase p38 to mediate growth arrest.

175 taII isoform, the mitogen-activated protein (MAP) kinases p38 and extracellular signal-regulated kina

176 ing 14-3-3- and WW-binding domains and a p38 MAP kinase (p38 MAPK) consensus site on Ser-538 (S538).

177 In this study, we showed that p38 MAP kinase (p38) is expressed in doublecortin-positive a

178 K3) MoGSK1 in M. oryzae is regulated by Mps1 MAP kinase, particularly under the stressed conditions.

179 (MAK-1)-signaling cascade, whereas a second MAP kinase pathway (MAK-2), which is also involved in ce

180 runculin A treatment also activates the Sty1 MAP kinase pathway and, strikingly, we find that loss of

181 We propose that the conserved MAP kinase pathway coordinates CO designation with the d

182 Toll-like receptor activation of the ERK-1/2 MAP kinase pathway during inflammatory responses, but it

183 eover, these data identify activation of the MAP kinase pathway in microglia as a cause of neurodegen

184 Thus, despite the central importance of the MAP kinase pathway in some aspects of T cell function, M

185 that CBU0388 enhances the activation of this MAP kinase pathway in yeast, while CBU0885 and CBU1676 a

186 that these three effectors modulate the CWI MAP kinase pathway in yeast.

187 es both BRM acetylation and BRM silencing as MAP kinase pathway inhibitors both induced BRM as well a

188 d why this noncanonical configuration of the MAP kinase pathway is adopted by these key immune cells

189 The yeast Hog1 MAP kinase pathway is believed to control the transcript

190 Signaling through RAS/MAP kinase pathway is central to biology.

191 In Magnaporthe oryzae, the Mst11-Mst7-Pmk1 MAP kinase pathway is essential for appressorium formati

192 ctivator of twitchin kinase and that the p38 MAP kinase pathway may be involved in the regulation of

193 T pathway was activated in one subtype while MAP kinase pathway was activated in the other.

194 ase complex, a key negative regulator of the MAP kinase pathway, binds to MAP3K2 and this interaction

195 e metabotropic receptor that, activating the MAP kinase pathway, leads to synaptic and behavioral def

196 n to be hyperactive in PCa including the RAS/MAP kinase pathway, which phosphorylates Runx2 on multip

197 to tumor cells through the activation of the MAP kinase pathway.

198 r mitogenic effect through activation of the MAP kinase pathway.

199 otubules, and depends on a functioning DLK-1 MAP kinase pathway.

200 h antagonizes the mitogen-activated-protein (MAP) kinase pathway downstream of the FGFR3 receptor and

201 so found that the mitogen-activated protein (MAP) kinase pathway regulates both BRM acetylation and B

202 nase (ERK)/mitogen-activated protein kinase (MAP) kinase pathway, and localises to non-compact myelin

203 inases to the Ras/mitogen-activated protein (MAP) kinase pathway, which is implicated in oncogenic ou

204 l integrity (CWI) mitogen-activated protein (MAP) kinase pathway.

205 either PD0325901or MEK162, led to sustained MAP-kinase pathway inhibition and showed a strong synerg

206 The MAP-kinase pathway, consisting of the kinases RAS, RAF,

207 Collectively, our results demonstrate that MAP kinase pathways are most likely targeted by C. burne

208 ther G-protein or arrestin-mediated cAMP and MAP kinase pathways.

209 SK1-3) are apical kinases of the p38 and JNK MAP kinase pathways.

210 (NF-kappaB), and mitogen-activated protein (MAP) kinase pathways and the inflammasome.

211 s-activated plant mitogen-activated protein (MAP) kinase pathways play roles in growth adaptation to

212 inase (PI3-K) and mitogen-activated protein (MAP) kinase pathways via TpoR, and autonomous growth in

213 vating mutations in the beta-catenin and the MAP-kinase pathways; this characteristic can help in the

214 that the inducible nuclear dual-specificity MAP kinase phosphatase (MKP) DUSP2, a known regulator of

215 Treatment with MAP kinase phosphatase (MKP3, DUSP6) inhibitors increase

216 icity phosphatase 10 (DUSP10), also known as MAP kinase phosphatase 5 (MKP5), negatively regulates th

217 in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiatin

218 We identified mitogen-activated protein (MAP) kinase phosphatase 3 (MKP3) as a downstream target

219 P5), an inducible mitogen-activated protein (MAP) kinase phosphatase, specifically inactivates and an

220 MAP kinase phosphatases (MKPs), such as Arabidopsis (Ara

221 es and delayed induction of dual-specificity MAP kinase phosphatases (MKPs/DUSPs).

222 ther activated the LPS- and TNFalpha-induced MAP kinase phosphorylation and activation of the NFkappa

223 F-beta1 treatment increased the level of p38 MAP kinase phosphorylation in pericytes, and again, the

224 MAP kinase phosphorylation of AGL15 is necessary for ful

225 species (ROS) and mitogen-activated protein (MAP) kinase phosphorylation, but exhibited normal respon

226 sequence-specific down-regulation of the ERK-MAP kinase phosphosignaling cascade in KRAS-driven cance

227 link this pathway to Mg(2+) homeostasis and MAP kinases, pointing to roles for lysosomal Ca(2+) in c

228 hrough RAS-GRF1 occurs via activation of p38 MAP kinase rather than ERK MAP kinase, which has more fr

229 The Hog1 mitogen-activated protein (MAP) kinase regulates environmental stress responses and

230 tein kinase Sty1, a homolog of mammalian p38 MAP kinase, regulates localization of the Cdc42 polarity

231 phorylation of paxillin and activated p42/44-MAP kinase, Rho GTPase, and paxillin/GEF-H1/p42/44-MAPK

232 a plethora of signaling molecules, including MAP kinases, Rho GTPases, and components of the Wnt sign

233 ucer and the Hog1 mitogen-activated protein (MAP) kinase seem to determine the different dose-respons

234 increased kinase activity in vitro, induced MAP kinase signaling and conferred vemurafenib resistanc

235 ifically contributes to sustaining long-term MAP kinase signaling and cytokine production downstream

236 ly GTPase with a well documented role in ERK/MAP kinase signaling and integrin activation.

237 protein signaling accounts for D2R canonical MAP kinase signaling cascade activation, whereas beta-ar

238 described an important link between the ERK MAP kinase signaling cascade and the translational machi

239 ding a miRNA that suppresses a target in the MAP kinase signaling cascade, a central signal transduct

240 Stress-activated MAP kinase signaling cascades that mediate cytokine synt

241 At the root of MAP kinase signaling complexity is the differential use

242 We show that this unusual configuration of MAP kinase signaling contributes substantially to produc

243 ionate-mediated regulation of phospho-ERK1/2 MAP kinase signaling in FFA2-expressing 293 cells, the G

244 Here, we investigate the role of ERK MAP kinase signaling in this process.

245 /2-extracellular-signal regulated kinase 1/2 MAP kinase signaling pathway following Toll-like recepto

246 dy reveals a critical role for the MEK5-ERK5 MAP kinase signaling pathway in BAFF-induced mature B ce

247 T-2, functions through the conserved RAS/ERK MAP kinase signaling pathway in the C. elegans germline

248 e caused by Ang II is mediated by an ERK 1/2 MAP kinase signaling pathway.

249 brane dynamics, the antagonistic activity of MAP kinase signaling pathways, and the role of stress in

250 y and, strikingly, we find that loss of Sty1 MAP kinase signaling prevents latrunculin A-induced disp

251 ty corresponded to the increased endothelial MAP kinase signaling that was required for angiogenic en

252 lates Akt protein dynamics, which determines MAP kinase signaling thresholds necessary drive a morpho

253 otein family, operates downstream of FGF/Erk MAP kinase signaling to regulate pluripotency and cell f

254 FGF/Erk MAP kinase signaling up-regulates Brf1, which disrupts t

255 n of KRAS, resulting in activation of ERK1/2 MAP kinase signaling, leading to enhanced cell prolifera

256 Inhibition of MAP kinase signaling, suppressing c-Myc expression, or i

257 intracellular mechanisms, we focused on p38 MAP kinase signaling, which is one of the major downstre

258 This regulation is mediated through MAP kinase signaling, which we demonstrate can be activa

259 ral different cellular stresses that involve MAP kinase signaling.

260 eractions that may provide new insights into MAP kinase signaling.

261 , fatty acid synthesis, mRNA processing, and MAP kinase signaling.

262 am of effector-triggered immunity-associated MAP kinase signaling.

263 y activate canonical Smad3 and non-canonical MAP kinase signaling.

264 ry scaffolding in mammalian stress-activated MAP kinase signaling.

265 sin stimulates AQP2 exocytosis by inhibiting MAP kinase signaling.

266 of single-mutants targeting genes related to MAP kinase signaling.

267 ulated kinase/mitogen-activated protein (ERK/MAP) kinase signaling but not on the immediate early gen

268 iated p38 and JNK mitogen-activated protein (MAP) kinase signaling cascades trigger specific cellular

269 pericytes via p38 mitogen-activated protein (MAP) kinase signaling.

270 st cancer MDA-MB-231 cells via aberration of MAP-kinase signaling and by the inhibition of matrix met

271 beta(1, 3)-glucan leads to increased Erk1/2 MAP-kinase signaling and cAMP response element-binding p

272 o induce the EGFR-mediated activation of the MAP-kinase signaling pathway and consequently the expres

273 re unable to induce sustained suppression of MAP-kinase signaling.

274 ciency, disrupted TNF mediated NF-kappaB and MAP kinase signalling and caused epidermal hyperplasia a

275 AP-1 factors respond to MAP kinase signalling and comprise dimers of FOS, ATF an

276 hat methylation of MAP3K2 by SMYD3 increases MAP kinase signalling and promotes the formation of Ras-

277 s capable of binding to SOS and upregulating MAP kinase signalling and that the dimeric state is inhi

278 arget of HopAI when it is overexpressed, and MAP kinase signalling is important for cell-to-cell move

279 e this, germline potential was maintained by MAP kinase signalling.

280 dermal extracellular-signal-regulated kinase-MAP-kinase signalling results in epidermal inflammation,

281 imulation of the cell wall integrity pathway MAP kinase Slt2 initially phosphorylates cyclin C to tri

282 in C phosphorylation by the stress-activated MAP kinase Slt2p is required for nuclear to cytoplasmic

283 Our results place MAP kinase Sty1 as an important physiological regulator

284 ach is complementary to existing methods for mapping kinase-substrate binding interfaces.

285 In contrast to other MAP kinase substrates, the transcription factor Ets-1 ha

286 Mitogen-activated protein (MAP) kinase substrates are believed to require consensus

287 The MAP kinase TGFbeta-activated kinase (TAK1) plays a cruci

288 capping activity is inhibited by Erk, a key MAP kinase that is activated by oncogenic signaling.

289 d by Magnaporthe oryzae to activate the Pmk1 MAP kinase that is essential for appressorium formation

290 It was the active form of MAP kinase that was enriched with microtubules and follo

291 The principle recognition site of MAP kinases, the common docking (CD) region, forms selec

292 imulating ROS production that signal via p38 MAP kinase to the transcription factor SKN-1/NRF1,2,3 to

293 s and examination of the activity of the CWI MAP kinase transcription factor Rlm1 indicated that CBU0

294 We detected the expected phosphorylation of MAP kinases, translational regulatory proteins, and subu

295 hosphorylation of mitogen-activated protein (MAP) kinases triggering the activation of the matrix-met

296 activated by p38 mitogen-activated protein (MAP) kinase via its downstream substrates, MK2/3.

297 we found increased levels of phosphorylated MAP Kinase when KIT ligand was added to culture.

298 activation of p38 MAP kinase rather than ERK MAP kinase, which has more frequently been linked to LTP

299 s requires Epac2-dependent activation of p38 MAP kinase, which posed the important question of how Ep

300 ce, an effect abrogated by inhibition of p38 MAP kinase with SB203580.