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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 (MAPK) signaling by proteolytically cleaving MAPK kinases.
8 JNK MAPKs for docking sites in their cognate 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
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
17 ivation of mitogen-activated protein kinase (MAPK) kinase 1 negatively regulated STAT3-Y705 phosphory
19 with activated Akt or constitutively active MAPK kinase-1, an upstream activator of MAPK, partially
21 ely active mitogen-activated protein kinase (MAPK) kinase 2 (MEK2), p33(Ringo), or Delta 90 cyclin B.
22 at expresses a constitutively active form of MAPK kinase 3 (Ad-CA-MKK3), an upstream activator of p38
23 study, we provide evidence that the kinases MAPK kinase 3 (Mkk3) and Mkk6 are activated during treat
24 cally inactive mutant of the upstream kinase MAPK kinase 3 (MKK3) increased the calcium induced MMP-9
26 Knockout of the p38 MAPK upstream kinase, MAPK kinase 3 (MKK3), did not affect ischemic activation
27 threonine sites, and the three dual kinases, MAPK kinase 3 (MKK3), MKK4, and MKK6, are known to be th
28 ny of the MAPK pathway member-encoding genes MAPK kinase 3 (Mkk3), Mkk6, p38a, or p38b displayed prof
29 n this study, we further sought to determine MAPK kinase 3 (MKK3)-dependent TGF-beta1 responses by ge
31 active upstream kinases in the pathway (i.e. MAPK kinase 3 (MKK3b(E)) and MAPK kinase 6 (MKK6b(E)).
32 d phosphorylation of p38 MAPK in response to MAPK kinase 3 activation, thereby resulting in decreased
33 ytes, COX-2 was induced by the expression of MAPK kinase 3 EE (MKK3EE), a constitutive activator of p
35 cts of some upstream p38 activators, such as MAPK kinase 3, on Th1 development are not as strong as t
36 dominant-negative RAGE and dominant-negative MAPK kinase 3, we demonstrated that S100A11-induced chon
38 ed phosphorylation of upstream MAPK factors (MAPK kinase 3/6 (MKK3/6), MKK4, and MAP/ERK kinase 1 (ME
39 ylation of p38 MAPK, upstream dual activator MAPK kinase 3/6, and downstream transcription factors ac
40 the phosphorylation/activation of p38alpha, MAPK kinase 3/6, and MAPKAP-2 in response to erythropoie
44 ents of the p38-MAPK pathway in these cells (MAPK kinase 3/MAPK kinase 6, p38-MAPK, MAPK-activated pr
45 am kinases in the MAP kinase cascades, i.e., MAPK kinase-3 (MKK3), MKK6 (the immediately upstream act
46 of the apoptosis signal-regulating kinase-1/MAPK kinase-3/p38 MAPK (ASK1/MKK3/p38 MAPK) signalosome,
47 The apoptosis signal-regulating kinase-1/MAPK kinase-3/p38 MAPK signalosome assembled on Rab5a an
48 forms, demonstrated the requirement of Rac1, MAPK kinase 3B, and p38beta for the full expression of N
52 c-Jun NH2-terminal kinases, p38 kinase, and MAPK kinase 4 induced by UVB/12-O-tetradecanoylphorbol-1
53 tion than WT hearts, with increased upstream MAPK kinase 4 phosphorylation, following ischemia/reperf
56 rial targeting of JNK and the upstream MKK4 (MAPK kinase 4), accompanied by striking protection again
57 vels of the downstream signaling components, MAPK kinase 4, MAPK kinase 7, and JNK, suggests that Hsp
58 ) kinase 1/mitogen-activated protein kinase (MAPK) kinase 4 (JNKK1/MKK4) as a prostate cancer metasta
59 namely the mitogen-activated protein kinase (MAPK) kinase 4 (MKK4) and MKK7, constitute a signaling n
60 identified mitogen-activated protein kinase (MAPK) kinase 4/c-Jun NH2-terminal kinase (JNK)-activatin
63 AP-1-dependent activities by p38 activators MAPK kinase 6 (MKK6) and/or arsenite in human breast can
66 ression of a constitutively active mutant of MAPK kinase 6 (MKK6, an upstream activator of p38 MAPK)
68 adenovirus-mediated delivery of recombinant MAPK kinase 6 also activates VDR and sensitizes MCF-7 ce
70 8-MAPK pathway in these cells (MAPK kinase 3/MAPK kinase 6, p38-MAPK, MAPK-activated protein kinase-2
73 d or co-transfected with an active mutant of MAPK kinase-6, and treated either with or without the p3
75 nstream signaling components, MAPK kinase 4, MAPK kinase 7, and JNK, suggests that Hsp90/p50(cdc37) r
76 and T3M4 cells, PD98059 and U0126 inhibited MAPK kinase activation but not EGF-stimulated mitogenesi
78 vo gene transcription, the TGF-beta1-induced MAPK kinase activation that is involved in the regulatio
79 activate Rho family G-proteins that promote MAPK kinase activation via a mechanism inhibited by Clos
81 xtracellular signaling-regulated kinase, and MAPK kinase activities in CD3-activated T cell leukemia.
82 96) abolished CrkL interaction and sustained MAPK kinase activity, a response that is not normally ob
84 KT and ERK mitogen-activated protein kinase (MAPK) kinase activity is necessary for Ang-2 up-regulati
85 hibitor of mitogen-activated protein kinase (MAPK) kinase activity, caused similar inhibitory effects
87 I-1040, a compound that selectively inhibits MAPK kinase, an upstream regulator of MAPK and thus prev
88 s in Ras activity and the phosphorylation of MAPK kinase and cAMP response element-binding protein (C
89 ility of MAPK pathway inhibitors to suppress MAPK kinase and ERK phosphorylation in cell culture and
92 components Ste11 (MAPK kinase kinase), Ste7 (MAPK kinase), and Fus3 (MAPK) to the plasma membrane for
94 we assessed 16 mutations reported in MEK1, a MAPK kinase, and provide a robust ranking of these mutat
95 tein activated directly by cyclic nucleotide/MAPK kinase, another cAMP downstream effector, was not i
96 e splice pattern and resulting expression of MAPK kinase are implicated in mediating the antitumoral
98 We recently identified NtMEK2, a tobacco MAPK kinase, as the upstream kinase of SIPK and WIPK, tw
103 s the expression of anti-oxidant enzymes via MAPK kinase/ERK and AMPK pathways, and suppresses the ex
105 via activation of PI3K/Akt and inhibition of MAPK kinase/ERK pathways, and Ang(1-7)-Mas antagonizes t
106 in's lymphoma cells was mediated through the MAPK kinase/ERK signal transduction pathway and involved
108 f phenformin to enhance the efficacy of BRAF-MAPK kinase-extracellular signal-regulated kinase pathwa
109 a-activated kinase 1 (TAK1), a member of the MAPK kinase family, plays a key role in B-cell growth an
110 P. carinii mitogen-activated protein kinase (MAPK) kinase gene, also implicated in signaling of matin
112 und that LF similarly cleaves the Drosophila MAPK kinases Hemipterous (Hep) and Licorne in vitro.
113 ll migration (such as Mst and Taok family of MAPK kinases in mesenchymal cells) may represent novel t
114 activated TFII-IDelta interacts with Erk1/2 (MAPK) kinase in the cell cytoplasm and imports the Erk1/
115 s is tightly regulated through activation of MAPK kinases, including the MEK/ERK pathway as well as s
117 ce its inhibition combined with anti-BDNF or MAPK kinase inhibitor abolished or greatly reduced the t
119 We investigated the effect of the prototype MAPK kinase inhibitor U0126 on the (31)P-MR spectra of M
121 ntibody or mitogen activated protein kinase (MAPK) kinase inhibitor, attenuated depolarization-suppor
122 PD98059, a mitogen-activated protein kinase (MAPK) kinase inhibitor, decreased insulin-induced VSMC m
123 ition of p44/42 MAPK signaling by use of the MAPK kinase inhibitors PD 98059 or U0126, or by use of a
125 nthrax lethal toxin (LeTx) or small molecule MAPK kinase inhibitors triggers apoptosis in human melan
126 d with the mitogen-activated protein kinase (MAPK) kinase inhibitors PD98059 and U0126, the p38 MAPK
128 stimulates phosphorylation of both beta-cell MAPK kinase isoforms and p38 MAPK, and bromoenol lactone
130 onine protein kinase that is a member of the MAPK kinase kinase (MAP3K) family and activates p38MAPK.
135 activated kinase 1 (TAK1) is a member of the MAPK kinase kinase (MAPKKK) family and can activate JNK
137 lates stomatal development by activating the MAPK kinase kinase (MAPKKK) YDA (also known as YODA).
138 titutive triple response 1 (CTR1, a Raf-like MAPK kinase kinase (MAPKKK)) to activate the positive MK
139 KK5 (MAPK kinase 5) activation in the MEKK1 (MAPK kinase kinase 1)/MEKKs-MKK4/5-MPK3/6 cascade, HopF2
140 e assays and by expressing WT or kinase-dead MAPK kinase kinase 19 (MAP3K19) in the HEK293T cell line
142 We found that phosphorylation of p38alpha, MAPK kinase kinase 3/6 and MAPKAP-2 occurs only upon gro
143 as mitogen-activated protein kinase (MAPK), MAPK kinase kinase and calcium-dependent protein kinase
144 poptosis-regulating-signal kinase (ASK) 1, a MAPK kinase kinase family member capable of activating t
147 have extended that analysis to the possible MAPK kinase kinase kinases (MAP4Ks) in the JNK pathway.
153 rrested Xenopus oocytes to synthesize Mos, a MAPK kinase kinase required for the coordinated activati
155 ble uPA expression is controlled by MEKK1, a MAPK kinase kinase that regulates the ERK1/2 and JNK pat
156 scaffold protein, Ste5, with Ste7 and Ste11 (MAPK kinase kinase) in the cytosol, providing in vivo co
157 tivated protein kinase (MAPK) pathway: os-4 (MAPK kinase kinase), os-5 (MAPK kinase), and os-2 (MAPK)
158 tein kinase (MAPK) cascade components Ste11 (MAPK kinase kinase), Ste7 (MAPK kinase), and Fus3 (MAPK)
164 that the Drosophila homolog of the mammalian MAPK kinase kinase, TAK1 (transforming growth factor bet
166 luding the phorbol ester TPA, anisomycin and MAPK kinase kinase-1 (MEKK1), phosphorylated Nur77 and i
167 ebrates, five MAPK families are regulated by MAPK kinase kinase-MAPK kinase-MAPK (MKKK-MKK-MAPK) phos
169 MLK3 is a mitogen-activated protein kinase (MAPK) kinase kinase (MAP3K) which activates MAPK pathway
170 MEKK1 is a mitogen-activated protein kinase (MAPK) kinase kinase and an ubiquitin ligase that regulat
172 (MEKK2), a mitogen-activated protein kinase (MAPK) kinase kinase for the extracellular signal-regulat
173 ber of the mitogen-activated protein kinase (MAPK) kinase kinase gene family involved in regulating m
174 conserved mitogen-activated protein kinase (MAPK) kinase kinase homologous to dual leucine zipper ki
176 MLK3) is a mitogen-activated protein kinase (MAPK) kinase kinase that activates MAPK pathways, includ
177 (MLK3), a mitogen-activated protein kinase (MAPK) kinase kinase that is required for the proliferati
178 activated mitogen-activated protein kinase (MAPK) kinase kinase YODA (YDA) and MAPK kinase MKK5.
179 nstrate that SERF1 binds to the promoters of MAPK kinase kinase6 (MAP3K6), MAPK5, dehydration-respons
184 inases (MAPKs) via reduced activation of the MAPK-kinase-kinases (MAP3Ks) mixed lineage kinases (MLKs
185 We identified two phylogenetically unrelated MAPK kinases (LeMKK2 and LeMKK4) that when overexpressed
187 families are regulated by MAPK kinase kinase-MAPK kinase-MAPK (MKKK-MKK-MAPK) phosphorelay systems.
190 and pfmap-2, but no clear orthologue of the MAPK kinase (MAPKK) family, raising the question of the
191 vated protein kinase (MAPK) NTF6/NRK1, or an MAPK kinase (MAPKK) MEK1/NQK1, attenuated N-mediated res
192 expressing a panel of constitutively active MAPK kinase (MAPKK) variants in discrete stomatal lineag
193 t two components of the KGB-1 pathway, MEK-1 MAPK kinase (MAPKK), a homolog of mammalian MKK7, and VH
194 ed protein kinases (MAPKs) by their upstream MAPK kinase (MAPKK), NtMEK2 leads to HR-like cell death.
197 s proteins can bind to an overlapping set of MAPK-kinases (MAPKK) in live cells and dictate the local
199 esulting in the LF-dependent cleavage of the MAPK kinases (MAPKKs) and disrupted signaling to downstr
200 are regulated by upstream kinases, including MAPK kinases (MAPKKs) and MAPK kinase kinases (MAP3Ks).
202 irulence factor that cleaves and inactivates MAPK kinases (MAPKKs) in host cells and has been propose
203 tivated by dual phosphorylation catalyzed by MAPK kinases (MAPKKs), the MAPK p38beta is exceptional a
204 s of function of MPK3/MPK6 or their upstream MAPK kinases (MAPKKs; or MKKs), MKK4/MKK5, resulted in s
206 e coupling of MAPK kinase kinase (MAP3K) --> MAPK kinase (MEK) --> MAPK core pathways to cell surface
207 ARRY-142886), an oral selective inhibitor of MAPK kinase (MEK) 1 and 2, in children who had neurofibr
208 e conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6
210 ting NRAS mutations leading to activation of MAPK kinase (MEK) and extracellular signal-regulated kin
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 gic reagent PD098059 or by dominant-negative MAPK kinase (MEK) expression via vaccinia viral delivery
214 leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and pat
215 after ischemia, and addition of the p42/p44 MAPK kinase (MEK) inhibitor PD98059 during reperfusion a
218 an embryonic kidney (HEK) 293 cells with the MAPK kinase (MEK) inhibitors 1,4-diamino-2,3-dicyano-1,4
220 For example, the combination of ALK and MAPK kinase (MEK) inhibitors was active in an ALK-positi
221 imultaneous inhibition of p38MAPK and either MAPK kinase (MEK) or JNK significantly alleviates the re
222 40L treatment similarly enhanced BCR-induced MAPK kinase (MEK) phosphorylation, and MEK was required
225 collagen-treated cultures, whereas targeting MAPK kinase (MEK), focal adhesion kinase (FAK), or phosp
232 ated Ca2+ release requires activation of the MAPK kinase (MEK)1,2/extracellular signal-regulated kina
234 ibition of mitogen-activated protein kinase (MAPK) kinase (MEK) can induce regression of tumors beari
235 s with the mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor PD-98059 prior to treatment
236 The use of mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitors has become more common in
237 ncrease in mitogen-activated protein kinase (MAPK) kinase (MEK) phosphorylation in resistant cells co
238 3K-AKT and mitogen-activated protein kinase (MAPK) kinase (MEK)-extracellular signal-regulated kinase
239 odulates a mitogen-activated protein kinase (MAPK) kinase (MEK)-mediated signaling pathway that regul
242 126, two structurally distinct inhibitors of MAPK kinase (MEK1), increased both basal and CNTF-induce
244 8, and the mitogen-activated protein kinase (MAPK) kinase (MEK1/2) using inhibitors of Erk1/2 or p38
245 ctive (CA) mitogen-activated protein kinase (MAPK) kinase, MEK1-DD, which is known to cause different
252 s express high levels of the upstream kinase MAPK kinase (MKK) 3 but relatively low levels of the alt
253 C cells, we first examined the expression of MAPK kinase (MKK) and MAPK in clear cell RCC and confirm
259 ous studies demonstrated that the 2 upstream MAPK kinases (MKK-4 and MKK-7) are phosphorylated in RA
260 s the p38alpha MAPK isoform and the upstream MAPK kinase MKK3 to modulate Fas/Fas ligand expression;
263 Previous studies demonstrated that upstream MAPK kinases (MKK3 and MKK6) that regulate p38 are activ
265 was found to be independent of the upstream MAPK kinase, MKK3/6, and instead depends upon transformi
266 and MPK6 by wounding depends on the upstream MAPK kinases MKK4 and MKK5 but is independent of jasmoni
267 olved in BR signaling, can phosphorylate the MAPK kinases MKK4 and MKK5, which are members of the MAP
268 is thaliana, signaling networks that contain MAPK kinases MKK4/5 and MAPKs MPK3/6 function in abiotic
269 protein kinases (MAPKs), and their upstream MAPK kinases, MKK4 and MKK5, are key regulators of stoma
271 eractions between MAPKs and their activating MAPK kinases (MKKs or MEKs) are crucial for efficient an
272 dentified near the N terminus of each of the MAPK kinases (MKKs or MEKs) MEK1, MEK2, MKK3, MKK4, and
273 ays not only by preventing the activation of MAPK kinases (MKKs) but also by inhibiting the activity
274 can be carried out not only by its upstream MAPK kinases (MKKs) but also by p38alpha autophosphoryla
275 s is controlled by disordered domains of the MAPK kinases (MKKs) that specifically bind to their cogn
276 c analyses demonstrate that in stigmas, five MAPK kinases (MKKs), MKK1/2/3/7/9 are required to transm
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 ed UV-induced activation of SEK, an upstream MAPK kinase of JNK, resulting in suppression of both Kv
280 TGF-beta1 and the role of MKK3, an upstream MAPK kinase of p38 MAPK, by examining the effect of targ
281 -stimulated macrophages, suggesting that p38 MAPK kinase pathway controls FN-mediated inductions of M
283 to examine mitogen-activated protein kinase (MAPK) kinase pathways at various ages in mice transgenic
285 demonstrated MKK3 as the immediate upstream MAPK kinase required for selective activation of p38 MAP
286 ts the first example that attenuation of Ras-MAPK kinase signaling pathway is essential for normal le
287 kinases are activated by the common upstream MAPK kinase Ste7 yet generate distinct output responses,
288 rylated protein kinase B, and phosphorylated MAPK kinase), suggesting the complementarity of these tw
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
295 386), a constitutively active mutant of Slt2 MAPK kinase, whereas overexpression of Sdp1 suppressed l
297 dependent on p38 mitogen-activated protein (MAPK) kinase, which was found to be phosphorylated in ti
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