ライフサイエンスコーパス: MAPK

1 MAPK activation depends on Ras and is caused by RasGRP3,

2 MAPKs were involved in ICAM-1-dependent expression of TN

3 racellular signal-regulated kinase (ERK) 1/2 MAPK (upstream activators of MSK1) reduced MOR expressio

4 Specific inhibitors for ERK1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP600125)

5 ulated the phosphorylation of p38 and ERK1/2 MAPKs in BV2 cells, which was required for NO production

6 1R-associated kinase 1 (IRAK-1), p38, ERK1/2 MAPKs, and p65 NF-kappaB, suggesting that the R753Q TLR2

7 lling evidence linking FGFR2 with the ERK1/2-MAPK pathway, which converges with the PI3K/Akt/mTOR (me

8 pro-degenerative factors such as SARM1 and a MAPK signal and pro-survival factors, the most important

9 we assessed 16 mutations reported in MEK1, a MAPK kinase, and provide a robust ranking of these mutat

10 We demonstrated the importance of a MAPK docking domain necessary for protein-protein intera

11 PDTC, an NF-kappaB inhibitor) or SB203580 (a MAPK inhibitor) showed significantly improved potential

12 silon as required and sufficient to activate MAPK in GNAQ mutant melanomas.

13 r 80% of uveal melanomas (UMs) and activates MAPK.

14 (MAPK) kinase kinase (MAP3K) which activates MAPK pathways through either kinase-dependent or -indepe

15 ues driven by recurrent mutations activating MAPK signaling.

16 and newborn ECs that inherit EGFR and active MAPK from fast-dividing progenitors.

17 ion of the receptor and generates additional MAPK/ERK signalling, protecting cancer cells against ant

18 ROS, H2O2, and NO, modulating the PI3K/Akt, MAPK, NFkappaB and Nrf2 pathways and their downstream tr

19 focal adhesion kinase (FAK) sustain AKT and MAPK pathway signaling under continuous EGFR inhibition

20 enzyme was found to activate both Ca(++) and MAPK signalling via PAR2.

21 data was analyzed for HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations from sarcoma TCGA.

22 in kinases such as MAP kinase 3 (HvMPK3) and MAPK substrate 1 (HvMKS1), and transcription factors suc

23 and intracellular signaling by NF-kappaB and MAPK pathways were comparable in oxLDL-loaded Mvarphis,

24 ditionally, we identified that NF-kappaB and MAPK signaling pathways are both involved in the process

25 , which promotes activation of NF-kappaB and MAPK signalling and increases the production of proinfla

26 key regulator of cell death, NF-kappaB, and MAPK signaling.

27 Thus, TTM reduces copper levels and MAPK signaling, thereby inhibiting BRAF(V600E)-driven me

28 mitogen-activated protein kinase (MAPK) and MAPK-activated protein kinase 2 (MK2) stress pathways in

29 rectal cancer tissues, xenograft models, and MAPK reporter constructs, we showed that tumor cells wit

30 ng pathways, including the PI3K/Akt/mTOR and MAPK pathways, and with other receptors, including estro

31 owth, suggesting a combination of mTORC1 and MAPK inhibitors may be of therapeutic value in patients

32 tumor driver that activates both mTORC1 and MAPK to promote tumor growth, suggesting a combination o

33 ced rapid activation of STAT3, NFkappaB, and MAPK signaling in HMVP2 cells, which was again attenuate

34 her inhibition or activation of the PI3K and MAPK pathways.

35 ircuitry including Shh, Wnt, Hippo, PI3K and MAPK pathways.

36 7 on the same residues modulated by PI3K and MAPK signaling.

37 as a target at the intersection of PI3K and MAPK signaling.

38 ll number of genes in the Ras processing and MAPK pathways and pinpoint PREX1 as an AML-specific acti

39 5p and miR-211-5p durably stimulated Ras and MAPK upregulation after vemurafenib exposure.

40 cancer to examine the effect of Jak/STAT and MAPK pathway inhibition in vitro.

41 Mechanistically, PRDM15 modulates WNT and MAPK-ERK signaling by directly promoting the expression

42 nscription of upstream regulators of WNT and MAPK-ERK signaling to safeguard naive pluripotency.

43 al network acting downstream of LIF, WNT and MAPK-ERK to stabilize mouse embryonic stem cells (ESCs)

44 redox-sensitive signaling including Akt and MAPKs pathways.

45 TLR4/MyD88 signaling cascades (NF-kappaB and MAPKs) in lipopolysaccharide (LPS)-stimulated macrophage

46 ling to critical downstream pathways such as MAPK.

47 was defective in activating PAK3 as well as MAPK (mitogen-activated protein kinase).

48 cular Mechanisms of Cancer, p53-, TGF-beta-, MAPK- and Wnt-signaling).

49 ion of BIM and achieves immunosuppression by MAPK/NF-kB-dependent activation of PD-L1 gene expression

50 Regulation of NMNAT2 by MAPK signaling does not require SARM1, and so cannot be

51 m, whose development is tightly regulated by MAPK signaling pathways following the activation of upst

52 of DUSP2 is not restricted to the classical MAPK pathways and that DUSP2 can also regulate the atypi

53 of reactive oxygen species, PRP may connect MAPK and oxidative stress signaling.

54 is involved in regulating multiple conserved MAPK pathways.

55 nce developed in the absence of constitutive MAPK pathway activation.

56 an the conserved T-X-Y motif in conventional MAPKs such as ERK1/2.

57 catecholamines, we observed that convergent MAPKs signalling pathways facilitate P-UAEC proliferatio

58 Conversely, MAPKs, which are inhibited by glucocorticoids, provide f

59 Hence, pro-degenerative MAPK signaling functions upstream of SARM1 by limiting t

60 Finally, we demonstrate MAPK-dependent TRBP and Lin28a induction, with physiolog

61 Gbetagamma-metalloproteinase/EGFR-dependent MAPK/ERK signaling cascades.

62 ased activation of VAV1 catalytic-dependent (MAPK, JNK) and non-catalytic-dependent (nuclear factor o

63 in vivo Our results imply that differential MAPK signaling balances EMT, cancer stem cell potential,

64 invasion, and tumor growth by downregulating MAPK pathway activity.

65 tably, increased RAS activity and downstream MAPK signaling was observed in stomachs only when E-cadh

66 Whereas BRAF fusions primarily dysregulate MAPK signaling, the CRAF fusions QKI-RAF1 and SRGAP3-RAF

67 ll quiescence by selective inhibition of EGF/MAPK signaling and define culture conditions that direct

68 eptor/mitogen-activated protein kinase (EGFR/MAPK) signalling triggers Drosophila intestinal stem cel

69 s, we found that Hsp90 inhibition blocks ERK MAPK activation in the periaqueductal gray and caudal br

70 suppresses distal phosphorylation of the Erk MAPK.

71 ERK/MAPK deletion in D1R-MSNs (direct pathway) resulted in d

72 Ns.SIGNIFICANCE STATEMENT Alterations in ERK/MAPK activity are associated with drug abuse, as well as

73 MP C2 cells and attenuated activation of ERK/MAPK and the master transcription factor NF-kappaB in re

74 lineated the cell-type-specific roles of ERK/MAPK signaling due to the reliance on globally administe

75 ur results demonstrate the importance of ERK/MAPK signaling in governing the motor functions of the s

76 on globally administered pharmacological ERK/MAPK inhibitors and the use of genetic models that only

77 The ERK/MAPK intracellular signaling pathway is hypothesized to

78 derscore the potential importance of the ERK/MAPK pathway in human movement disorders.

79 models that only partially reduce total ERK/MAPK activity.

80 Here, we generated mouse models in which ERK/MAPK signaling was completely abolished in each of the t

81 eract with clathrin terminal domain and ERK2 MAPK in vitro.

82 a senescence-like state caused by excessive MAPK signaling.

83 We previously identified a pollen-expressed MAPK (p56) from Papaver rhoeas that was rapidly activate

84 Although several pollen-expressed MAPKs exist, very little is known about their function.

85 Our results indicate that FGF/MAPK blockade may be particularly efficacious against mP

86 riming is prevented by inhibition of the FGF/MAPK signalling pathway.

87 enchymal reprogramming and independence from MAPK signalling.

88 ion of the mTOR, histone deacetylase (HDAC), MAPK, and ERBB4 pathways.

89 cing strategy, we provide evidence that high MAPK activity marked a progenitor cell compartment of gr

90 tructs, we showed that tumor cells with high MAPK activity resided specifically at the leading tumor

91 ur infiltrating lymphocytes (TILs), however, MAPK activity is required for T cells function.

92 se findings indicate that loss of CL impairs MAPK pathway activation, and decreased activation of the

93 ocarcinoma by inducing a further increase in MAPK signalling that results in oncogenic toxicity; this

94 gnificant dysregulation of genes involved in MAPK/Wnt signalling pathways.

95 g that EVI1 and estradiol signaling merge in MAPK activation.

96 an cancers harboring activating mutations in MAPK signaling.

97 nd increased phosphorylation was observed in MAPK pathways (p38, ERK, JNK) and the NF-kappaB pathway

98 c control of downstream functions, including MAPK signaling.

99 pairs across multiple cell types, including MAPK pathway genes and apoptotic genes.

100 DMP attenuated LPS-induced MAPK activation in BV2 cells, suggesting the MAPK pathwa

101 ciated with modulation of PAK1/2 and ERK/JNK MAPK signaling and F-actin dynamics.

102 1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP600125), or PI3K (LY294002) were used to determi

103 of IkB-alpha activation and reduction in JNK(MAPK) phosphorylation.

104 involving mitogen-activated protein kinase (MAPK) activation and mitogen- and stress-activated prote

105 ulators of mitogen-activated protein kinase (MAPK) activation, including Spry2, thereby causing syner

106 nal kinase mitogen-activated protein kinase (MAPK) activity, which differentially regulated IP-10 exp

107 es the p38 mitogen-activated protein kinase (MAPK) and MAPK-activated protein kinase 2 (MK2) stress p

108 prototypic mitogen-activated protein kinase (MAPK) cascade and triggers a dose-dependent differentiat

109 ion of the mitogen activated protein kinase (MAPK) cascade.

110 n atypical mitogen-activated protein kinase (MAPK) containing an S-E-G activation motif rather than t

111 rotein p38 mitogen-activated protein kinase (MAPK) delta isoform (p38delta) is a poorly studied membe

112 ion of p38 mitogen-activated protein kinase (MAPK) in podocytes.

113 s-specific mitogen-activated protein kinase (MAPK) in Saccharomyces cerevisiae that couples spore mor

114 ial of p38 mitogen-activated protein kinase (MAPK) inhibitors was coincidentally expanded to a dual i

115 MLK3 is a mitogen-activated protein kinase (MAPK) kinase kinase (MAP3K) which activates MAPK pathway

116 Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical respo

117 (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway have led to clinical responses in lung and

118 downstream mitogen-activated protein kinase (MAPK) pathway in cancer cells.

119 decreased mitogen-activated protein kinase (MAPK) pathway signaling and increased phosphoinositol-3-

120 activated mitogen-activated protein kinase (MAPK) pathway signaling.

121 Mitogen-activated protein kinase (MAPK) pathways are conserved from yeast to man and regul

122 Mitogen-activated protein kinase (MAPK) scaffold proteins, such as IQ motif containing GTP

123 tivate the mitogen-activated protein kinase (MAPK) signaling pathway.

124 s and that mitogen-activated protein kinase (MAPK)-dependent phosphorylation of the RNA-silencing fac

125 nd the p38 mitogen-activated protein kinase (MAPK)-MAPK-activated protein kinase 2 (MK2) pathway to p

126 on of MEK (mitogen-activated protein kinase (MAPK)/ERK kinase) after DOX treatment reversed the late

127 through extracellular signal-related kinase/MAPK inactivation.

128 ase (JNK) mitogen-activated protein kinases (MAPK)] were assessed in response to N-formyl-methionyl-l

129 phorylate mitogen-activated protein kinases (MAPKs) and thereby critically modulate cell proliferatio

130 ctions of mitogen-activated protein kinases (MAPKs) are ultimately accomplished by the substrate prot

131 Mitogen-activated protein kinases (MAPKs) form important signaling modules for a variety of

132 Cellular mitogen-activated protein kinases (MAPKs) have been shown to play a role in VZV infection o

133 icrotubule assembly and dysregulation of KIT-MAPK signaling also feature as recurrently disrupted pat

134 We show that the X-linked MAPK phosphatase DUSP9 is upregulated in female compared

135 p38 mitogen-activated protein kinase (MAPK)-MAPK-activated protein kinase 2 (MK2) pathway to promote

136 IL-1beta induced activation of the p38(MAPK)/MAPK-activated protein kinase 2 (MK2) pathway in hepatoc

137 matory niches counteracts combined BRAF/MEK (MAPK/extracellular signal-regulated kinase kinase) inhib

138 Overall, these findings elucidate an NFAT-MAPK signaling paradigm for induction of isletokine expr

139 lioma that induce constitutive activation of MAPK are transcriptionally linked to master regulators e

140 atase-1 (SHP-1) and limits the activation of MAPK ERK and p38 that are required for assembly of the N

141 2, thereby causing synergistic activation of MAPK signaling by epigenetic silencing.

142 KRAS accompanied by downstream activation of MAPK signaling, which promotes tumor invasion and progre

143 Sustained activation of MAPK/ERK in adult SCs is therefore deleterious to succes

144 npoint PREX1 as an AML-specific activator of MAPK signaling.

145 rd elucidating the cytoplasmic components of MAPK signaling, the key downstream coactivators that coo

146 2 signaling in vivo enhanced the efficacy of MAPK inhibitors.

147 undamental because acute strong induction of MAPK/ERK in adulthood induces demyelination.

148 xes display distinctly different kinetics of MAPK activation in the cumulus cells, much increased cum

149 for the axonal protection caused by loss of MAPK signaling.

150 study therefore defines a novel mechanism of MAPK activation requiring binding of an activator and al

151 e dependent on copper-mediated modulation of MAPK signaling.

152 tic disorders induced by somatic mutation of MAPK pathway genes.

153 udies have demonstrated that reactivation of MAPK signaling via CRAF overexpression and dysregulation

154 n that appears to be linked to activation of MAPKs and Akt in heart.

155 immunofluorescence technology, activation of MAPKs and Akt occurred in left ventricular (LV) CMs, req

156 indispensable for GBS-mediated activation of MAPKs and NF-kappaB and subsequent expression of proinfl

157 rylation of IRAK-1, diminished activation of MAPKs and NF-kappaB, and deficient induction of cytokine

158 onical NF-kappaB signaling and activation of MAPKs.

159 4 was not mediated through the inhibition of MAPKs and NF-kappaB activation but was mediated through

160 sequent formation of covalent cross-links of MAPKs.

161 Furthermore, the convergent signalling of MAPKs involved in catecholoestradiol-, 17beta-oestradiol

162 l function in melanoma cells after oncogenic MAPK inhibition.

163 stimulation, INAVA was required for optimal MAPK and NF-kappaB activation, cytokine secretion, and i

164 s responses mediated through the PI3K/TOR or MAPK signaling cascades, which act to protect the parasi

165 Similar to other MAPKs, Smk1 is controlled by phosphorylation of a threon

166 fferentiation to SCT is prevented with a p38 MAPK signaling inhibitor and epidermal growth factor co-

167 In addition, sunitinib activated p38 MAPK, which resulted in the upregulation/activity of HuR

168 uitment of MKK4 to lysosomes, activating p38 MAPK at lysosomes.

169 y Ang II-induced phosphorylation of Akt, p38 MAPK or ERK1/2.

170 estinal fibrosis by diminishing MRTF and p38 MAPK activation and increasing autophagy in fibroblasts.

171 repressing its expression through NO and p38 MAPK activation.

172 ibition of Syk and rho kinase or Syk and p38 MAPK did not cause additive bronchodilation.

173 local action of natriuretic peptide and p38 MAPK in podocytes, we generated podocyte-specific (pod)

174 Activation of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta)

175 tenuation of DUSP4 activated the ERK and p38 MAPK pathways, increased stem-like properties, and spawn

176 oblast differentiation through STAT3 and p38 MAPK signaling using in vitro and in vivo bone-specific

177 udy, we examined the interaction between p38 MAPK and GC-A signaling.

178 tion of GSK3beta on Ser(389) mediated by p38 MAPK specifically inactivates nuclear GSK3beta in the co

179 ith Parkinson's disease fully engages ER-p38 MAPK-CMA pathway in the mouse brain and uncoupling it re

180 The administration of FR167653, p38 MAPK inhibitor, reduced systolic blood pressure (SBP), u

181 evel of TAK1 and subsequent reduction in p38 MAPK and NF-kappaBp65 activation, ultimately culminating

182 a ligands, by blocking TGF-beta1-induced p38 MAPK phosphorylation, prevent increases in both total an

183 Inhibiting p38 MAPK or extracellular signal-regulated kinase (ERK) 1/2

184 ic function for ALS-linked FUS involving p38 MAPK activation.

185 es p38 mitogen-activated protein kinase (p38 MAPK) activation and release of tumor necrosis factor-al

186 s dependent on Bruton's tyrosine kinase, p38 MAPK, and TANK-binding kinase 1 (TBK1), as demonstrated

187 ividual use of Bruton's tyrosine kinase, p38 MAPK, and TBK1 inhibitors.

188 Lysosomal p38 MAPK directly phosphorylates the CMA receptor LAMP2A at

189 n of the tumor growth inhibitor molecule p38 MAPK.

190 ylation, whereas a chemical inhibitor of p38 MAPK (SB203580) reduced the phosphorylation of GSK3beta,

191 Downregulation of p38 MAPK activity via RNA interference or small molecule inh

192 etion of PERK causes hyper-activation of p38 MAPK during myogenesis.

193 uscript we have investigated the role of p38 MAPK signalling pathway and have shown a subpopulation-

194 l signal is transduced via activation of p38 MAPK to influence actin remodeling and cell migration vi

195 CORM-401 had no effect on p38 MAPK activation.

196 appaB, AP1, p-STAT3, p-AKT, p-IKKs and p-p38 MAPK were also determined.

197 ic inhibitors for ERK1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP600125), or PI3K (LY294002)

198 verall, no differences in phosphorylated p38 MAPK, ERK1/2, Akt, and p70S6K were observed.

199 ated PKCzeta subsequently phosphorylates p38 MAPK.

200 The p38 MAPK family is composed of four kinases of which p38alph

201 dent manner, including activation of the p38 MAPK-C/EBPbeta signaling pathway as well as the ubiquiti

202 and BMP2 was positively regulated by the p38 MAPK-Creb axis in osteoclasts, with the promoters of PDG

203 which promotes TNF-alpha release through p38 MAPK leading to beta-cell apoptosis, insufficient insuli

204 in cultured corneal fibroblasts through p38 MAPK regulation of canonical Wnt/beta-catenin signaling,

205 th total and active beta-catenin through p38 MAPK-GSK3beta signaling.

206 ession downstream of TLR4 activation via p38 MAPK and SGK1.

207 DUSP2, a known regulator of the ERK and p38 MAPKs, is unique amongst the MKP family in being able to

208 protein assays of lung tissue indicated p38(MAPK)-dependent activation of Elk-1 transcription factor

209 ncentration-dependent phosphorylation of p38(MAPK) and MK2 in primary mouse hepatocytes.

210 Quantification of p38(MAPK) and MK2 revealed that, in hepatocytes, at maximum,

211 demonstrated that the kinase activity of p38(MAPK) determines signal amplitude, whereas phosphatase a

212 at, in hepatocytes, at maximum, 11.3% of p38(MAPK) molecules and 36.5% of MK2 molecules are activated

213 employing phosphatase inhibitors and the p38(MAPK) inhibitor SB203580.

214 The IL-1beta induced activation of the p38(MAPK)/MAPK-activated protein kinase 2 (MK2) pathway in h

215 l for IL-1beta-induced activation of the p38(MAPK)/MK2 pathway in hepatocytes that was calibrated to

216 s by a target hopping approach from p38alpha MAPK inhibitor templates.

217 The kinase p38alpha MAPK (p38alpha) plays a pivotal role in many biological

218 ly expanded to a dual inhibition of p38alpha MAPK and phosphodiesterase 4 (PDE4), and the potential b

219 damage required the activity of the p38alpha MAPK.

220 d the molecular mechanisms by which p38alpha MAPK regulates osteoclastogenesis and coordinates osteoc

221 ing, including downstream AKT-mTOR pathways, MAPK pathway, as well as redox enzymes were downregulate

222 Pharmacological MAPK inhibition restores migration and apoptosis potenti

223 the G-protein complex (STE4), the pheromone MAPK scaffold (CST5), and the two terminal MAP kinases (

224 2 (CDK2), itself a downstream target of PI3K/MAPK signaling, leads to increased phosphorylation of RN

225 y, we interrogate the complexity in cAMP/PKA-MAPK/ERK1&2 crosstalk by using multi-parameter biosensin

226 d function(s), but knowledge regarding plant MAPK substrates is currently still fragmentary.

227 a much lesser degree p38 were the principal MAPKs involved in facilitating diapedesis of CD4(+) lymp

228 tions in BRAF, MAP2K1, and kinases promoting MAPK signaling.

229 nesis by signaling primarily through the Ras-MAPK pathway.

230 Ras/MAPK pathway activation is associated with significantly

231 together, our data suggest that although Ras/MAPK pathway inhibition can increase tumor immunogenicit

232 nimals were more invasive and had higher RAS/MAPK pathway activation.

233 KIT knockdown also increased RAS/MAPK pathway activation in a BRAF(V600E)-mutant human me

234 in signal transduction events involving Ras/MAPK and PI3K/Akt pathways.

235 Aberrant activation of RAS/MAPK signaling is a driver of over one third of all huma

236 f gene expression programs downstream of RAS/MAPK signaling.

237 targets such as Notch1 and SIRT1, and on Ras/MAPK-dependent pathways.

238 of multiple inhibitors targeting the RTK/Ras/MAPK pathway.

239 as human T-ALL carrying mutations in the RAS/MAPK pathway display a genetic signature indicative of C

240 Germ-line mutations in components of the Ras/MAPK pathway result in developmental disorders called RA

241 te gastric adenocarcinoma subtypes where RAS/MAPK pathway activation and E-cadherin attenuation are c

242 Lipin-2 regulates MAPK activation, which mediates synthesis of pro-IL-1bet

243 , TRRAP), immune surveillance (CD58, RFXAP), MAPK signaling (MAP2K1, NF1), NF-kappaB signaling (PRKCB

244 Treatment with inhibitors targeting the RTK/MAPK pathway increased reactive oxygen species (ROS) in

245 atment resistance as a result of a secondary MAPK pathway-activating mutation during BRAF inhibition

246 lish that differential expression of several MAPK factors underlies the epigenetic control of mating

247 r, it is not activated by a dual-specificity MAPK kinase.

248 C differentiation by regulating the JAK/STAT/MAPK and NFkappaB pathways.

249 systems to investigate the role of one such MAPK, the c-Jun N-terminal kinase (JNK), in VZV lytic in

250 effect of PKC inhibitors to durably suppress MAPK in UM.

251 of-function MEK1DD allele produces sustained MAPK/ERK activation in adult SCs, and we determined the

252 in1; this association lasts longer, sustains MAPK/ERK signalling and mitigates p53 activation.

253 first study implicating a function for a TDY MAPK in pollen.

254 her few data relating to the function of TDY MAPKs in plants currently exist.

255 P. rhoeas threonine-aspartate-tyrosine (TDY) MAPK, PrMPK9-1 Rather few data relating to the function

256 of the MAPK and PI3K pathways, we found that MAPK and PI3K regulate dental epithelial stem cell activ

257 Collectively, our results indicate that MAPK tightly suppresses DC migration and augments DC sur

258 Here, we report that MAPK signaling shows strong intratumoral heterogeneity a

259 binding of an activator and also shows that MAPKs can be diversified to recognize unique phosphoryla

260 The MAPK pathway is activated in the majority of melanomas a

261 The MAPK pathway is responsible for cell proliferation and p

262 The MAPK/ERK pathway has a critical role in PNS development.

263 47L, whose expression robustly activated the MAPK pathway and sensitized cells to BRAF and MEK inhibi

264 and SRGAP3-RAF1 aberrantly activate both the MAPK and phosphoinositide-3 kinase/mammalian target of r

265 addition, as CRAF fusions activate both the MAPK and PI3K/mTOR signaling pathways, we identify combi

266 de evidence that Atf1 phosphorylation by the MAPK Sty1 is required for oxidative stress responses in

267 integrity pathway and its core element, the MAPK Pmk1.

268 man cancers with activating mutations in the MAPK cascade, rendered resistant to targeted therapies,

269 167/442)], followed by genes involved in the MAPK pathway [31.2% (138/442)], PI3K signaling [18.1% (8

270 a substrate of MEK, a central kinase in the MAPK/ERK signaling pathway.

271 s dysregulation as well as inhibitors of the MAPK and PI3K pathways, we found that MAPK and PI3K regu

272 lso appears to modify the specificity of the MAPK by suppressing Y kinase and enhancing S/T kinase ac

273 Thus, all three members of the MAPK family mediate the mitogenic effects of catecholoes

274 (p38delta) is a poorly studied member of the MAPK family.

275 Pharmacological inhibition of the MAPK pathway abrogates the stimulus-dependent recruitmen

276 ns indicate that the signal intensity of the MAPK pathway is a critical determinant not only in tumou

277 Stimulation of the MAPK pathway results in mitogen- and stress-activated pr

278 binds to IQGAP1, a hub for activation of the MAPK pathway, and impedes IQGAP1-dependent phosphorylati

279 Activity of the MAPK pathway, as well as other factors, such as HIF1alph

280 ctivity after constitutive activation of the MAPK pathway, commonly through Ras mutations.

281 Activation of the MAPK Slt2p was defective in crd1Delta cells, and up-regu

282 helial cells, we find that activation of the MAPK/ERK pathway mirrors the rapid and dynamic induction

283 we identify combinatorial inhibition of the MAPK/mTOR pathway as a potential therapeutic strategy fo

284 of treatment response and regulators of the MAPK/Wnt systems.

285 get reinnervation.SIGNIFICANCE STATEMENT The MAPK/ERK pathway promotes developmental myelination and

286 ssion of which would otherwise stimulate the MAPK/ERK pathway to promote NE differentiation of prosta

287 MAPK activation in BV2 cells, suggesting the MAPK pathway as the signaling mechanism underlying the e

288 ulation-level analysis has revealed that the MAPK Fus3 plays an important role in mediating this diff

289 ith inhibitors and siRNAs, we found that the MAPK-JNK pathway was involved in TAK1-mediated HBV suppr

290 this response is driven by signaling via the MAPK Sty1.

291 ndicated that Mst50 is involved in all three MAPK pathways in M. oryzae although its functions differ

292 ency or simultaneous inhibition of all three MAPKs enhanced vaccine responsiveness in old mice.

293 All three MAPKs were activated by ICAM-1 engagement, either throug

294 variants exhibiting loss of function toward MAPK activation in a manner correlated with loss of PAK3

295 cer cells was induced by hypoxia, triggering MAPK signaling in endothelial cells to promote tube form

296 distinct active conformation, which triggers MAPK recruitment and receptor internalization.

297 impact of dehydration on the fate of the two MAPKs.

298 Notably, MDSC restoration relied upon MAPK pathway reactivation and downstream production of t

299 tory cytokines like TNFalpha cooperated with MAPK signaling through the c-Jun/AP-1 transcription fact

300 ces of rat ventral tegmental area (VTA) with MAPK activation and two additional cell signaling pathwa

301 cessary for protein-protein interaction with MAPKs and consequently also for phosphorylation.