ライフサイエンスコーパス: MAPK kinase

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

2 is not phosphorylated by a dual-specificity MAPK kinase.

3 Smk1 is not phosphorylated by a prototypical MAPK kinase.

4 phorylation of a Thr-X-Tyr motif by upstream MAPK kinases.

5 is phosphorylated and activated by upstream MAPK kinases.

6 s are associated with activation of upstream MAPK kinases.

7 JNK MAPKs for docking sites in their cognate MAPK kinases.

8 (MAPK) signaling by proteolytically cleaving MAPK kinases.

9 ide evidence that phosphorylation of S298 of MAPK kinase 1 (MEK1) by p21-activated kinase (PAK) is a

10 In transgenic mice, expression of activated MAPK kinase 1 (MEK1) in the suprabasal, nondividing, dif

11 dermal cells express oncogenically activated MAPK kinase 1 (MEK1).

12 itor of mTOR, and PD0325901, an inhibitor of MAPK kinase 1 (MEK; the kinase directly upstream of ERK)

13 ERK proteins are activated exclusively by MAPK kinase 1 and 2 phosphorylation of threonine and tyr

14 oM) and PD98059 (10 microM), an inhibitor of MAPK kinase 1/2 (MEK1/2), inhibited adenosine-stimulated

15 cells but not in MCF-7Ca cells treated with MAPK kinase 1/2 inhibitors U0126, and PD98059 (IC(50) ap

16 This effect was prevented by MAPK kinase 1/2 inhibitors, suggesting that induction of

17 In contrast, the MAPK kinase 1/2-specific inhibitor PD98059 inhibited MMP

18 ivation of mitogen-activated protein kinase (MAPK) kinase 1 negatively regulated STAT3-Y705 phosphory

19 Constitutively activated MAPK kinase-1 (MEK1) expression in FAK(-/-) and A549 FAK

20 with activated Akt or constitutively active MAPK kinase-1, an upstream activator of MAPK, partially

21 t with the mitogen-activated protein kinase (MAPK) kinase-1 (MEK1) inhibitor.

22 ely active mitogen-activated protein kinase (MAPK) kinase 2 (MEK2), p33(Ringo), or Delta 90 cyclin B.

23 at expresses a constitutively active form of MAPK kinase 3 (Ad-CA-MKK3), an upstream activator of p38

24 study, we provide evidence that the kinases MAPK kinase 3 (Mkk3) and Mkk6 are activated during treat

25 cally inactive mutant of the upstream kinase MAPK kinase 3 (MKK3) increased the calcium induced MMP-9

26 We sought to determine the role of MAPK kinase 3 (MKK3), a kinase of the p38 group, in the

27 Knockout of the p38 MAPK upstream kinase, MAPK kinase 3 (MKK3), did not affect ischemic activation

28 threonine sites, and the three dual kinases, MAPK kinase 3 (MKK3), MKK4, and MKK6, are known to be th

29 ny of the MAPK pathway member-encoding genes MAPK kinase 3 (Mkk3), Mkk6, p38a, or p38b displayed prof

30 n this study, we further sought to determine MAPK kinase 3 (MKK3)-dependent TGF-beta1 responses by ge

31 ctivation is through dual phosphorylation by MAPK kinase 3 (MKK3).

32 active upstream kinases in the pathway (i.e. MAPK kinase 3 (MKK3b(E)) and MAPK kinase 6 (MKK6b(E)).

33 d phosphorylation of p38 MAPK in response to MAPK kinase 3 activation, thereby resulting in decreased

34 ytes, COX-2 was induced by the expression of MAPK kinase 3 EE (MKK3EE), a constitutive activator of p

35 phosphorylation of TAK1 at Thr-187 and MKK3 (MAPK kinase 3).

36 cts of some upstream p38 activators, such as MAPK kinase 3, on Th1 development are not as strong as t

37 dominant-negative RAGE and dominant-negative MAPK kinase 3, we demonstrated that S100A11-induced chon

38 for activating MHV-induced p38 MAPK was the MAPK kinase 3.

39 ed phosphorylation of upstream MAPK factors (MAPK kinase 3/6 (MKK3/6), MKK4, and MAP/ERK kinase 1 (ME

40 ylation of p38 MAPK, upstream dual activator MAPK kinase 3/6, and downstream transcription factors ac

41 the phosphorylation/activation of p38alpha, MAPK kinase 3/6, and MAPKAP-2 in response to erythropoie

42 nase kinase kinase 1-dependent activation of MAPK kinase 3/6-p38 MAPK pathway.

43 iated with active MAPK kinase 4 but not with MAPK kinase 3/6.

44 ailed to activate the major p38 MAPK kinase, MAPK kinase 3/6.

45 ents of the p38-MAPK pathway in these cells (MAPK kinase 3/MAPK kinase 6, p38-MAPK, MAPK-activated pr

46 am kinases in the MAP kinase cascades, i.e., MAPK kinase-3 (MKK3), MKK6 (the immediately upstream act

47 of the apoptosis signal-regulating kinase-1/MAPK kinase-3/p38 MAPK (ASK1/MKK3/p38 MAPK) signalosome,

48 The apoptosis signal-regulating kinase-1/MAPK kinase-3/p38 MAPK signalosome assembled on Rab5a an

49 forms, demonstrated the requirement of Rac1, MAPK kinase 3B, and p38beta for the full expression of N

50 MAPK kinase 4 (MKK4) is a dual-specificity kinase that a

51 Studies using MAPK kinase 4 (MKK4) small-interfering RNA showed that M

52 osis AMs and PBMCs is associated with active MAPK kinase 4 but not with MAPK kinase 3/6.

53 c-Jun NH2-terminal kinases, p38 kinase, and MAPK kinase 4 induced by UVB/12-O-tetradecanoylphorbol-1

54 tion than WT hearts, with increased upstream MAPK kinase 4 phosphorylation, following ischemia/reperf

55 pond to anti-TNF-alpha Abs by triggering the MAPK kinase 4 signaling pathway.

56 APK, as well as their upstream kinases MKK4 (MAPK kinase 4) and MEKK3 (MAPK kinase kinase 3).

57 rial targeting of JNK and the upstream MKK4 (MAPK kinase 4), accompanied by striking protection again

58 vels of the downstream signaling components, MAPK kinase 4, MAPK kinase 7, and JNK, suggests that Hsp

59 ) kinase 1/mitogen-activated protein kinase (MAPK) kinase 4 (JNKK1/MKK4) as a prostate cancer metasta

60 namely the mitogen-activated protein kinase (MAPK) kinase 4 (MKK4) and MKK7, constitute a signaling n

61 1/2), p38, mitogen-activated protein kinase (MAPK) kinase 4 (MKK4), and MKK3/6.

62 identified mitogen-activated protein kinase (MAPK) kinase 4/c-Jun NH2-terminal kinase (JNK)-activatin

63 MAPK kinase-4, an upstream activator of JNK, was also si

64 In addition to blocking MKK5 (MAPK kinase 5) activation in the MEKK1 (MAPK kinase kina

65 AP-1-dependent activities by p38 activators MAPK kinase 6 (MKK6) and/or arsenite in human breast can

66 We also generated MAPK kinase 6 (MKK6) muscle-specific transgenic mice to

67 Analyses of MAPK kinase 6 (MKK6)-p38 fusion proteins showed that con

68 ression of a constitutively active mutant of MAPK kinase 6 (MKK6, an upstream activator of p38 MAPK)

69 e pathway (i.e. MAPK kinase 3 (MKK3b(E)) and MAPK kinase 6 (MKK6b(E)).

70 adenovirus-mediated delivery of recombinant MAPK kinase 6 also activates VDR and sensitizes MCF-7 ce

71 Activation of p38 and JNK by an active MAPK kinase 6 stimulates VDR promoter activity independe

72 8-MAPK pathway in these cells (MAPK kinase 3/MAPK kinase 6, p38-MAPK, MAPK-activated protein kinase-2

73 -beta1-activated protein kinase-1 (TAK1) and MAPK kinase 6.

74 the immediate upstream p38-activating kinase MAPK kinase 6.

75 d or co-transfected with an active mutant of MAPK kinase-6, and treated either with or without the p3

76 nstream signaling components, MAPK kinase 4, MAPK kinase 7, and JNK, suggests that Hsp90/p50(cdc37) r

77 and T3M4 cells, PD98059 and U0126 inhibited MAPK kinase activation but not EGF-stimulated mitogenesi

78 ntrol both the extent and the specificity of MAPK kinase activation of MAPK.

79 vo gene transcription, the TGF-beta1-induced MAPK kinase activation that is involved in the regulatio

80 activate Rho family G-proteins that promote MAPK kinase activation via a mechanism inhibited by Clos

81 ed p38 activity in the absence of 'upstream' MAPK kinase activation.

82 xtracellular signaling-regulated kinase, and MAPK kinase activities in CD3-activated T cell leukemia.

83 96) abolished CrkL interaction and sustained MAPK kinase activity, a response that is not normally ob

84 ed in the absence of detectable upstream p38 MAPK kinase activity.

85 KT and ERK mitogen-activated protein kinase (MAPK) kinase activity is necessary for Ang-2 up-regulati

86 hibitor of mitogen-activated protein kinase (MAPK) kinase activity, caused similar inhibitory effects

87 Inhibition of the upstream MAPK kinase (also called MEK) by the small molecule UO12

88 I-1040, a compound that selectively inhibits MAPK kinase, an upstream regulator of MAPK and thus prev

89 s in Ras activity and the phosphorylation of MAPK kinase and cAMP response element-binding protein (C

90 s in Ras activity and the phosphorylation of MAPK kinase and cAMP response element-binding protein (C

91 ility of MAPK pathway inhibitors to suppress MAPK kinase and ERK phosphorylation in cell culture and

92 ERK2 activation was mediated through MAPK kinase and required phosphoinositide 3-kinase signa

93 A p38 mitogen-activated protein kinase (MAPK) kinase and a c-Jun N-terminal-like MAPK are both t

94 components Ste11 (MAPK kinase kinase), Ste7 (MAPK kinase), and Fus3 (MAPK) to the plasma membrane for

95 K) pathway: os-4 (MAPK kinase kinase), os-5 (MAPK kinase), and os-2 (MAPK).

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

97 tein activated directly by cyclic nucleotide/MAPK kinase, another cAMP downstream effector, was not i

98 e splice pattern and resulting expression of MAPK kinase are implicated in mediating the antitumoral

99 Strains lacking Spc1 or its activator, Wis1 MAPK kinase, are hypersensitive to these cations.

100 We recently identified NtMEK2, a tobacco MAPK kinase, as the upstream kinase of SIPK and WIPK, tw

101 We conclude that MAPK-docking sites in MAPK kinases bind selectively to their cognate MAPKs.

102 PD98059, an inhibitor of p44/42 MAPK kinase, blocked thrombin-induced upregulation of ac

103 A constitutively active MAPK kinase, called NtMEK2DD, is capable of eliciting an

104 iated by a mitogen-activated protein kinase (MAPK) kinase-dependent mechanism, and this process was b

105 d invasion, and constitutively activated the MAPK kinase/ERK (MEK/ERK) pathway.

106 s the expression of anti-oxidant enzymes via MAPK kinase/ERK and AMPK pathways, and suppresses the ex

107 II-AT1 by inhibiting the AngII-AT1-triggered MAPK kinase/ERK pathway.

108 via activation of PI3K/Akt and inhibition of MAPK kinase/ERK pathways, and Ang(1-7)-Mas antagonizes t

109 in's lymphoma cells was mediated through the MAPK kinase/ERK signal transduction pathway and involved

110 nduces the production of TNF via a PI3K- and MAPK kinase/ERK-dependent pathway.

111 a-activated kinase 1 (TAK1), a member of the MAPK kinase family, plays a key role in B-cell growth an

112 P. carinii mitogen-activated protein kinase (MAPK) kinase gene, also implicated in signaling of matin

113 When treated with inhibitors of MEK (MAPK kinase), H-Ras-transformed cells lose their growth

114 und that LF similarly cleaves the Drosophila MAPK kinases Hemipterous (Hep) and Licorne in vitro.

115 ll migration (such as Mst and Taok family of MAPK kinases in mesenchymal cells) may represent novel t

116 activated TFII-IDelta interacts with Erk1/2 (MAPK) kinase in the cell cytoplasm and imports the Erk1/

117 ional differences were abolished by MLCK and MAPK kinase inhibition.

118 ce its inhibition combined with anti-BDNF or MAPK kinase inhibitor abolished or greatly reduced the t

119 Treatment of these cells with the MAPK kinase inhibitor PD98059 prior to infection blocked

120 f the interaction between paclitaxel and the MAPK kinase inhibitor U0126 in three cell lines, on the

121 We investigated the effect of the prototype MAPK kinase inhibitor U0126 on the (31)P-MR spectra of M

122 ould be observed even in the presence of the MAPK kinase inhibitor U0126.

123 The mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059 markedly reduces inductio

124 ntibody or mitogen activated protein kinase (MAPK) kinase inhibitor, attenuated depolarization-suppor

125 PD98059, a mitogen-activated protein kinase (MAPK) kinase inhibitor, decreased insulin-induced VSMC m

126 ition of p44/42 MAPK signaling by use of the MAPK kinase inhibitors PD 98059 or U0126, or by use of a

127 ced protection was antagonized by the p42,44 MAPK kinase inhibitors PD98059 and U0125.

128 nthrax lethal toxin (LeTx) or small molecule MAPK kinase inhibitors triggers apoptosis in human melan

129 d with the mitogen-activated protein kinase (MAPK) kinase inhibitors PD98059 and U0126, the p38 MAPK

130 MAPK kinases interact with Trbs and regulate their stead

131 stimulates phosphorylation of both beta-cell MAPK kinase isoforms and p38 MAPK, and bromoenol lactone

132 The coupling of MAPK kinase kinase (MAP3K) --> MAPK kinase (MEK) --> MAP

133 onine protein kinase that is a member of the MAPK kinase kinase (MAP3K) family and activates p38MAPK.

134 Among the MAPK kinase kinase (MAP3K) family, we identified TGF-bet

135 rved Ser/Thr protein kinase belonging to the MAPK kinase kinase (MAP3K) family.

136 The MAPK kinase kinase (MAP3K) mixed-lineage kinase 3 (MLK3)

137 APK kinase, which in turn is activated by an MAPK kinase kinase (MAP3K).

138 activated kinase 1 (TAK1) is a member of the MAPK kinase kinase (MAPKKK) family and can activate JNK

139 Bem4p also interacted with the MAPK kinase kinase (MAPKKK) Ste11p.

140 lates stomatal development by activating the MAPK kinase kinase (MAPKKK) YDA (also known as YODA).

141 titutive triple response 1 (CTR1, a Raf-like MAPK kinase kinase (MAPKKK)) to activate the positive MK

142 KK5 (MAPK kinase 5) activation in the MEKK1 (MAPK kinase kinase 1)/MEKKs-MKK4/5-MPK3/6 cascade, HopF2

143 ream kinases MKK4 (MAPK kinase 4) and MEKK3 (MAPK kinase kinase 3).

144 We found that phosphorylation of p38alpha, MAPK kinase kinase 3/6 and MAPKAP-2 occurs only upon gro

145 as mitogen-activated protein kinase (MAPK), MAPK kinase kinase and calcium-dependent protein kinase

146 poptosis-regulating-signal kinase (ASK) 1, a MAPK kinase kinase family member capable of activating t

147 e recently discovered MRK as a member of the MAPK kinase kinase family that activates p38gamma.

148 nd demonstrated that it was a major upstream MAPK kinase kinase for the JNK cascade in T-cells.

149 The findings identify MEKK4 as the MAPK kinase kinase for TRAF4 regulation of the JNK pathw

150 have extended that analysis to the possible MAPK kinase kinase kinases (MAP4Ks) in the JNK pathway.

151 90/p50(cdc37) regulates JNK signaling at the MAPK kinase kinase level.

152 nt that c-Jun activation is dependent on the MAPK kinase kinase MEKK1.

153 The MAPK kinase kinase MEKK4 is required for neurulation and

154 catenin and mixed lineage kinase 3 (MLK3), a MAPK kinase kinase member.

155 rrested Xenopus oocytes to synthesize Mos, a MAPK kinase kinase required for the coordinated activati

156 MEKK1 is a MAPK kinase kinase that is activated in response to stim

157 ble uPA expression is controlled by MEKK1, a MAPK kinase kinase that regulates the ERK1/2 and JNK pat

158 scaffold protein, Ste5, with Ste7 and Ste11 (MAPK kinase kinase) in the cytosol, providing in vivo co

159 tivated protein kinase (MAPK) pathway: os-4 (MAPK kinase kinase), os-5 (MAPK kinase), and os-2 (MAPK)

160 tein kinase (MAPK) cascade components Ste11 (MAPK kinase kinase), Ste7 (MAPK kinase), and Fus3 (MAPK)

161 m of protein kinase A but upstream of Mos (a MAPK kinase kinase).

162 ly, disrupted expression of MEKK2, a related MAPK kinase kinase, had no effect on uPA activity.

163 sequential phosphorylation and activation of MAPK kinase kinase, MAPK kinase (MKK), and MAPK.

164 main binds the front end basic region of the MAPK kinase kinase, MEKK3.

165 Herein, we define how MEKK1, a MAPK kinase kinase, regulates cell migration.

166 that the Drosophila homolog of the mammalian MAPK kinase kinase, TAK1 (transforming growth factor bet

167 vation of ERK requires both p50/p105 and the MAPK kinase kinase, Tpl-2.

168 luding the phorbol ester TPA, anisomycin and MAPK kinase kinase-1 (MEKK1), phosphorylated Nur77 and i

169 ebrates, five MAPK families are regulated by MAPK kinase kinase-MAPK kinase-MAPK (MKKK-MKK-MAPK) phos

170 r complex is a newly defined function for an MAPK kinase kinase.

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

172 MEKK1 is a mitogen-activated protein kinase (MAPK) kinase kinase and an ubiquitin ligase that regulat

173 ber of the mitogen-activated protein kinase (MAPK) kinase kinase family.

174 (MEKK2), a mitogen-activated protein kinase (MAPK) kinase kinase for the extracellular signal-regulat

175 ber of the mitogen-activated protein kinase (MAPK) kinase kinase gene family involved in regulating m

176 conserved mitogen-activated protein kinase (MAPK) kinase kinase homologous to dual leucine zipper ki

177 e11 is the mitogen-activated protein kinase (MAPK) kinase kinase in the MAPK cascades that mediate ma

178 NEMO), and mitogen-activated protein kinase (MAPK) kinase kinase MEKK1 upon ligation.

179 MLK3) is a mitogen-activated protein kinase (MAPK) kinase kinase that activates MAPK pathways, includ

180 (MLK3), a mitogen-activated protein kinase (MAPK) kinase kinase that is required for the proliferati

181 nstrate that SERF1 binds to the promoters of MAPK kinase kinase6 (MAP3K6), MAPK5, dehydration-respons

182 kinases, including MAPK kinases (MAPKKs) and MAPK kinase kinases (MAP3Ks).

183 Here we showed that the MAPK kinase kinases MEKK2 (encoded by Map3k2) and MEKK3

184 MEKK2 and MEKK3 are MAPK kinase kinases that activate the ERK5 pathway by ph

185 er, activate mixed lineage kinases-2 and -3, MAPK kinase kinases upstream of JNK, and p38.

186 inases (MAPKs) via reduced activation of the MAPK-kinase-kinases (MAP3Ks) mixed lineage kinases (MLKs

187 We identified two phylogenetically unrelated MAPK kinases (LeMKK2 and LeMKK4) that when overexpressed

188 etriggering failed to activate the major p38 MAPK kinase, MAPK kinase 3/6.

189 families are regulated by MAPK kinase kinase-MAPK kinase-MAPK (MKKK-MKK-MAPK) phosphorelay systems.

190 vation including negative regulation via the MAPK kinase/MAPK signaling pathway.

191 PK, Ntf4 and WIPK, and their common upstream MAPK kinase (MAPKK or MEK), NtMEK2.

192 and pfmap-2, but no clear orthologue of the MAPK kinase (MAPKK) family, raising the question of the

193 vated protein kinase (MAPK) NTF6/NRK1, or an MAPK kinase (MAPKK) MEK1/NQK1, attenuated N-mediated res

194 expressing a panel of constitutively active MAPK kinase (MAPKK) variants in discrete stomatal lineag

195 t two components of the KGB-1 pathway, MEK-1 MAPK kinase (MAPKK), a homolog of mammalian MKK7, and VH

196 ed protein kinases (MAPKs) by their upstream MAPK kinase (MAPKK), NtMEK2 leads to HR-like cell death.

197 stress-induced Spc1 phosphorylation by Wis1 MAPK kinase (MAPKK).

198 se by preventing activation of the family of MAPK kinases (MAPKK).

199 s proteins can bind to an overlapping set of MAPK-kinases (MAPKK) in live cells and dictate the local

200 However, the role of MAPK kinases (MAPKKs or MEKs) in cancer is unclear, alth

201 esulting in the LF-dependent cleavage of the MAPK kinases (MAPKKs) and disrupted signaling to downstr

202 are regulated by upstream kinases, including MAPK kinases (MAPKKs) and MAPK kinase kinases (MAP3Ks).

203 Mammalian MEK MAPK kinases (MAPKKs) have in their N termini an MAPK-do

204 irulence factor that cleaves and inactivates MAPK kinases (MAPKKs) in host cells and has been propose

205 tivated by dual phosphorylation catalyzed by MAPK kinases (MAPKKs), the MAPK p38beta is exceptional a

206 s of function of MPK3/MPK6 or their upstream MAPK kinases (MAPKKs; or MKKs), MKK4/MKK5, resulted in s

207 most human mitogen-activated protein kinase (MAPK) kinases (MAPKKs).

208 e coupling of MAPK kinase kinase (MAP3K) --> MAPK kinase (MEK) --> MAPK core pathways to cell surface

209 ARRY-142886), an oral selective inhibitor of MAPK kinase (MEK) 1 and 2, in children who had neurofibr

210 e conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6

211 In particular, costimulatory signaling via MAPK kinase (MEK) and extracellular signal-regulated kin

212 viously documented that IQGAP1 binds ERK and MAPK kinase (MEK) and regulates EGF-stimulated MEK and E

213 ll lines with constitutively activated MAPK, MAPK kinase (MEK) blockade by PD184352 strikingly potent

214 gic reagent PD098059 or by dominant-negative MAPK kinase (MEK) expression via vaccinia viral delivery

215 leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and pat

216 after ischemia, and addition of the p42/p44 MAPK kinase (MEK) inhibitor PD98059 during reperfusion a

217 BRAF inhibitor, and trametinib, a selective MAPK kinase (MEK) inhibitor.

218 in 30 minutes, which was blocked by PD98059 [MAPK kinase (MEK) inhibitor].

219 an embryonic kidney (HEK) 293 cells with the MAPK kinase (MEK) inhibitors 1,4-diamino-2,3-dicyano-1,4

220 The results suggest that 1) MAPK kinase (MEK) inhibitors do not suppress ERK7 kinase

221 For example, the combination of ALK and MAPK kinase (MEK) inhibitors was active in an ALK-positi

222 imultaneous inhibition of p38MAPK and either MAPK kinase (MEK) or JNK significantly alleviates the re

223 40L treatment similarly enhanced BCR-induced MAPK kinase (MEK) phosphorylation, and MEK was required

224 MAPK is exclusively activated by MAPK kinase (MEK), and here, acute application of a MEK-

225 tively activated component of the MAPK path, MAPK kinase (MEK), decreased N-myc levels.

226 collagen-treated cultures, whereas targeting MAPK kinase (MEK), focal adhesion kinase (FAK), or phosp

227 Treatment with PD98059, an inhibitor of MAPK kinase (MEK), restored myogenin expression but did

228 Using an inhibitor of MAPK kinase (MEK), we demonstrated that activated MAPK i

229 MAPK kinase (MEK)/ERK activation is regulated by interac

230 Inhibiting both MAPK kinase (MEK)/ERK and PKA pathways by a combination

231 The MAPK kinase (MEK)/extracellular signal-regulated kinase

232 To explore the importance of the c-Raf/MAPK kinase (MEK)/MAPK pathway, we stimulated adult feli

233 ated Ca2+ release requires activation of the MAPK kinase (MEK)1,2/extracellular signal-regulated kina

234 -mediated pathway that could be inhibited by MAPK kinase (MEK)1/2 antagonists.

235 ibition of mitogen-activated protein kinase (MAPK) kinase (MEK) can induce regression of tumors beari

236 s with the mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor PD-98059 prior to treatment

237 The use of mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitors has become more common in

238 ivated the mitogen-activated protein kinase (MAPK) kinase (MEK) pathway in DiFi cells.

239 ncrease in mitogen-activated protein kinase (MAPK) kinase (MEK) phosphorylation in resistant cells co

240 3K-AKT and mitogen-activated protein kinase (MAPK) kinase (MEK)-extracellular signal-regulated kinase

241 odulates a mitogen-activated protein kinase (MAPK) kinase (MEK)-mediated signaling pathway that regul

242 o known as mitogen-activated protein kinase [MAPK] kinase, MEK, or MKK).

243 binding to ERK1 and ERK2, as well as to the MAPK kinases MEK1 and MEK2.

244 126, two structurally distinct inhibitors of MAPK kinase (MEK1), increased both basal and CNTF-induce

245 blocked by U0126, an inhibitor of the ERK1/2 MAPK kinase (MEK1/2).

246 8, and the mitogen-activated protein kinase (MAPK) kinase (MEK1/2) using inhibitors of Erk1/2 or p38

247 ctive (CA) mitogen-activated protein kinase (MAPK) kinase, MEK1-DD, which is known to cause different

248 B1 domain of atypical protein kinases C, the MAPK kinase, MEK5, and the NBR1 protein.

249 athway by phosphorylating and activating the MAPK kinase, MEK5.

250 sfer downstream of MEKK1 may involve several MAPK kinases (MEKs), it is important to evaluate the reg

251 ir activation loop's TEY motif, catalyzed by MAPK kinases (MEKs).

252 vating the mitogen-activated protein kinase (MAPK) kinases (MEKs).

253 The MAPK kinases MKK-3 and MKK-6 regulate p38 MAPK activatio

254 s in arthritis and is, in turn, regulated by MAPK kinase (MKK) 3 and MKK6.

255 s express high levels of the upstream kinase MAPK kinase (MKK) 3 but relatively low levels of the alt

256 C cells, we first examined the expression of MAPK kinase (MKK) and MAPK in clear cell RCC and confirm

257 ted through a module consisting of a MAPK, a MAPK kinase (MKK), and a MKK kinase (MAP3K).

258 lation and activation of MAPK kinase kinase, MAPK kinase (MKK), and MAPK.

259 ylation of the key MAPKKs that activate JNK (MAPK kinase (MKK)4 and MKK7).

260 Examination of upstream MAPK kinases (MKK) 3, 4, and 6 that function as p38 MAPK

261 pends on a linear binding motif found in all MAPK kinases (MKK).

262 ous studies demonstrated that the 2 upstream MAPK kinases (MKK-4 and MKK-7) are phosphorylated in RA

263 s the p38alpha MAPK isoform and the upstream MAPK kinase MKK3 to modulate Fas/Fas ligand expression;

264 The MAPK kinase MKK3 was also shown to activate Mirk as a pr

265 Mirk co-immunoprecipitated with the MAPK kinase MKK3, an upstream activator of p38.

266 Previous studies demonstrated that upstream MAPK kinases (MKK3 and MKK6) that regulate p38 are activ

267 ion factor, MYC2, and is phosphorylated by a MAPK kinase, MKK3.

268 was found to be independent of the upstream MAPK kinase, MKK3/6, and instead depends upon transformi

269 olved in BR signaling, can phosphorylate the MAPK kinases MKK4 and MKK5, which are members of the MAP

270 is thaliana, signaling networks that contain MAPK kinases MKK4/5 and MAPKs MPK3/6 function in abiotic

271 protein kinases (MAPKs), and their upstream MAPK kinases, MKK4 and MKK5, are key regulators of stoma

272 eractions between MAPKs and their activating MAPK kinases (MKKs or MEKs) are crucial for efficient an

273 dentified near the N terminus of each of the MAPK kinases (MKKs or MEKs) MEK1, MEK2, MKK3, MKK4, and

274 ays not only by preventing the activation of MAPK kinases (MKKs) but also by inhibiting the activity

275 can be carried out not only by its upstream MAPK kinases (MKKs) but also by p38alpha autophosphoryla

276 s is controlled by disordered domains of the MAPK kinases (MKKs) that specifically bind to their cogn

277 at when rendered constitutively active, four MAPK kinases (MKKs), MKK4/5/7/9, are capable of perturbi

278 tein kinase (MAPK) signaling, the ability of MAPK kinases (MKKs, or MEKs) to recognize their cognate

279 tension of mitogen-activated protein kinase (MAPK) kinases (MKKs) that activate p38 MAPKs.

280 ed UV-induced activation of SEK, an upstream MAPK kinase of JNK, resulting in suppression of both Kv

281 TGF-beta1 and the role of MKK3, an upstream MAPK kinase of p38 MAPK, by examining the effect of targ

282 -stimulated macrophages, suggesting that p38 MAPK kinase pathway controls FN-mediated inductions of M

283 tidylinositol 3-kinase (PI 3-kinase) and Ras/MAPK kinase pathways have been the subject of considerab

284 to examine mitogen-activated protein kinase (MAPK) kinase pathways at various ages in mice transgenic

285 ration, and these mutations are sensitive to MAPK kinase, PKC, and AKT inhibitors.

286 demonstrated MKK3 as the immediate upstream MAPK kinase required for selective activation of p38 MAP

287 ts the first example that attenuation of Ras-MAPK kinase signaling pathway is essential for normal le

288 kinases are activated by the common upstream MAPK kinase Ste7 yet generate distinct output responses,

289 of a constitutively active mutant of MKK6, a MAPK kinase that specifically activates p38.

290 38 MAPKs are typically activated by upstream MAPK kinases that phosphorylate a Thr-X-Tyr motif in the

291 /TOPK as a mitogen-activated protein kinase (MAPK) kinase that phosphorylated P38 MAPK but with no kn

292 f their binding partners, including the Ste7 MAPK kinase, the Ste5 adaptor/scaffold protein, and the

293 Here we analyze hypoxic signaling through MAPK kinases to AP-1/c-Jun in the HT29 colon adenocarcin

294 Using constitutively active MAPK kinases, we found that both constitutively active M

295 386), a constitutively active mutant of Slt2 MAPK kinase, whereas overexpression of Sdp1 suppressed l

296 An MAPK is activated by an MAPK kinase, which in turn is activated by an MAPK kinas

297 dependent on p38 mitogen-activated protein (MAPK) kinase, which was found to be phosphorylated in ti

298 Mating factor activates the Fus3/MAPK kinase, whose substrates induce gene expression, ce

299 ich shares high homology and common upstream MAPK kinases with MPK6, is also capable of phosphorylati

300 ein pairs observed the interactions of Ste7 (MAPK kinase) with the MAPKs, Fus3 or Kss1, and of the sc