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 of the pharmacologically relevant target p38 MAP kinase.

3 nteraction of betaarrs with clathrin and ERK MAP kinase.

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

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

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

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

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

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

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

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

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

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

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

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

16 it mainly facilitates the activation of ERK MAP kinases.

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

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

19 such as Ca(2+), reactive oxygen species, and MAP kinases.

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

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

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

23 e combination of sorafenib and inhibitors of MAP kinase 1 and MAP kinase2 had a synergistic antiproli

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

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

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

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

28 Applying this approach to MAP kinase 6 (MKK6), which activates the p38 subfamily o

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

30 is facilitated by mitogen-activated protein (MAP) kinase-activated protein kinase 2 (MK2) but is inhi

31 n-dependent serine protein kinase) and Madd (MAP kinase-activating death domain).

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

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

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

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

36 endothelial cells via NPR-A binding and p38 MAP kinase activation.

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

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

39 ytes in a manner dependent on NF-kappaB- and MAP kinase-activation, which is further enhanced by hypo

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

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

42 ative stress, along with reduced JNK and p38 MAP kinase activity.

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

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

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

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

47 l autonomously and acts in parallel to DLK-1 MAP kinase and EFA-6 pathways.

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

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

50 eptic mice may result from inhibition of the MAP kinase and NF-kappaB signaling pathways.

51 cantly less or no suppression of LPS-induced MAP kinase and NFkappaB activation was also observed in

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

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

54 e receptor activation of ERK1/2 and p38alpha MAP kinases and is critical for regulating immune respon

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

56 inal kinase (JNK) mitogen-activated protein (MAP) kinase and Fos and Jun transcription factors, may s

57 inal kinase (JNK) mitogen-activated protein (MAP) kinase and the transcription factors Fos and Jun (A

58 by activation of mitogen-activated protein (MAP) kinases and nuclear factor kappa B and decreased my

59 in kinase C (PKC), activates in parallel the MAP-kinase and FAK/Yes-associated protein pathways.

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

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

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

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

64 SRF chromatin occupancy by actin signaling, MAP kinases, and MRTFs.

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

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

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

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

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

70 f the IKKalpha kinase that is induced by the MAP kinases BRAF and TAK1 and promotes tumor growth inde

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

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

73 portant for the stimulation of PKA and Gpmk1 MAP kinase by compounds in wheat spikelets.

74 tress in airway epithelial cells through p38 MAP kinase-c-Jun signaling and drives senescence by inhi

75 kinetics play a crucial role in determining MAP kinase cascade signaling dynamics and cell fate deci

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

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

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

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

80 witches that initiate signalling through the MAP kinase cascade to control cellular proliferation, di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 a significantly decreased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of aff

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

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

100 scWB reports increased phosphorylation of MAP kinases (ERK1/2, p38) under hypertonic conditions.

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

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

103 asurements of the mitogen-activated protein (MAP) kinase ERK2 have shown that activation by dual phos

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

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

106 pha via its canonical receptor CXCR4 and the MAP kinase ERK5.

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

108 al Cell, Nichols et al. (2019) establish the MAP kinase ErkB as a critical component for chemotaxis s

109 orylated at an [S/T]PR motif by the atypical MAP kinase ErkB.

110 inhibition of the mitogen-activated protein (MAP) kinase extracellular signal-regulated kinase (ERK)

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

112 FgSR is phosphorylated by the MAP kinase FgHog1, and the phosphorylated FgSR interacts

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

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

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

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

117 an Msb2-dependent mitogen-activated protein (MAP) kinase (HOG2) and an APSES transcription factor (ST

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

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

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

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

122 via their transmembrane domain, can activate MAP kinases in a ligand-independent manner.

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

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

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

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

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

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

129 MAP kinase inducing activity was dependent on CRAF dimer

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

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

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

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

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

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

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

137 nfected C57BL/6 mice with doramapimod, a p38 MAP-kinase inhibitor, results in reduced inflammation, g

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

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

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

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

142 ighly specific, brain-penetrant inhibitor of MAP kinase-interacting kinases resets the translation of

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

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

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

146 hereas phosphorylation of the upstream MAPKs MAP kinase kinase 3 (MKK3) and MKK6, was virtually undet

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

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

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

150 The frequencies of MAP kinase kinase kinase kinase 3 [also named germinal c

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

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

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

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

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

156 pressors in T cell lymphoma and suggest that MAP-kinase kinase (MEK) inhibitors combined with ALK inh

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

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

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

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

161 The Ras-Map kinase (MAPK) cascade underlies functional decisions

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

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

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

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

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

167 cologic inhibition of BRAF or the downstream MAP kinase MEK is highly effective in treating BRAF-muta

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

169 s approach, as we demonstrate by compiling a MAP kinase model.

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

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

172 ponses, including mitogen-activated protein (MAP) kinases, NF-kappaB signaling, or cell migration.

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

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

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

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

177 vation of the JNK mitogen-activated protein (MAP) kinases or the pseudokinase TRB3 by the ER stress s

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

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

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

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

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

183 For MAP kinase pathway activation in KRAS-mutant cells, the

184 The discovery of BRAF mutations and of other MAP kinase pathway alterations, as well as the co-occurr

185 ophila, where chemical inhibition of the p38 MAP kinase pathway and autophagy factor depletion failed

186 Dicer is phosphorylated by the ERK-MAP kinase pathway and because this pathway is activated

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

188 ocyte growth factor receptor (c-MET) and the MAP kinase pathway component B-Raf, providing a proof of

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

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

191 Recurrent mutational activation of the MAP kinase pathway in plasma cell myeloma implicates gro

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

193 ogy, who would benefit from treatment with a MAP kinase pathway inhibitor.

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

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

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

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

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

199 s can be up-regulated due to activation of a MAP kinase pathway or inactivation of the tumor suppress

200 to show that dual inhibition of JAK and the MAP kinase pathway provided enhanced therapeutic efficac

201 This dysregulation of the MAP kinase pathway results in increased CTNNB1, increase

202 increases phosphorylation of the downstream MAP kinase pathway targets, MAPK11, MAP3K and MAPK1.

203 olarity of the embryo and is controlled by a MAP kinase pathway that includes the MAPKKK YODA (YDA).

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

205 aces G(s) and induces signalling through the MAP kinase pathway(2).

206 itogenic signaling pathways, like the ERK1/2 MAP kinase pathway, and innate immune signaling.

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

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

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

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

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

212 s that were over-represented in genes of the MAP kinase pathway.

213 t in the presence of an inhibitor of the p38 MAP kinase pathway.

214 dentified the p38 mitogen-activated protein (MAP) kinase pathway and autophagy machinery as both a li

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

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

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

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

219 ics screen suggest that intersections of the MAP kinase pathways and autophagy machinery are critical

220 The cAMP-PKA and MAP kinase pathways are essential for plant infection in

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

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

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

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

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

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

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

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

229 ntly, these inhibitors differentially affect MAP kinase phosphatase activity toward 2P-ERK2.

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

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

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

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

234 Specifically, B. neotomae induced p38 MAP kinase phosphorylation and autophagy in a type IV se

235 MAP kinase phosphorylation of AGL15 is necessary for ful

236 et expression, early NF-kappaB, and late p38 MAP kinase phosphorylation, with the latter being indisp

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

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

239 We find that the p38 MAP kinase PMK-3, which is required for the differentiat

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

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

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

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

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

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

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

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

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

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

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

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

252 vious in vitro studies revealed that the p38 MAP kinase signaling pathway coordinates several inflamm

253 /2-extracellular-signal regulated kinase 1/2 MAP kinase signaling pathway following Toll-like recepto

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

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

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

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

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

259 tate tumorigenesis while increasing bFGF-p38 MAP kinase signaling, beta-catenin-HIF-1alpha expression

260 istiocytosis patients, caused hyperactivated MAP kinase signaling, conferred IL-3 hypersensitivity an

261 rectly activating autophagy and MAP3K5 (ASK)-MAP kinase signaling, E2F1 governs a distinct transcript

262 ways, including adhesion, cell wall-mediated MAP kinase signaling, hypersensitivity to host-derived o

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

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

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

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

267 sin stimulates AQP2 exocytosis by inhibiting MAP kinase signaling.

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

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

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

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

272 by a combined activation of beta-catenin and MAP kinase signaling.

273 ral different cellular stresses that involve MAP kinase signaling.

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

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

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

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

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

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

280 nitiate pMF by a mechanism that requires ERK-MAP kinase signalling and new BDNF protein synthesis (Q

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

282 lammatory cytokines, and is regulated by p38 MAP kinase signalling in vitro.

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

284 n and metastasis genes and (v) regulation of MAP Kinase Signalling Pathway.

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

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

287 Both p38 MAP kinase stimulation and an intact autophagy machinery

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

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

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

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

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

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

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

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

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

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

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

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

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