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1 rylation by the dual-specificity kinase MEK (MAP kinase kinase).
2 nine, enhancing Raf-1 kinase activity toward MAP kinase kinase.
3 sive necrosis, and a weak phosphorylation of MAP kinase kinase.
4 micromol/L), a specific inhibitor of p42/44 MAP kinase kinase.
5 inhibited by PD098059, an inhibitor of Mek/ MAP kinase kinase.
6 gh a pathway that required activation of the MAP kinase kinase.
7 ation of the upstream ERK regulatory element MAP kinase kinase.
8 s in the TXY motif of the activation loop by MAP kinase kinases.
9 nd one or more MAP kinase kinase kinases and MAP kinase kinases.
14 MNK1 activation is blocked by inhibitors of MAP kinase kinase 1 (Mkk1) and p38, demonstrating that M
15 transfection of constitutively active mutant MAP kinase kinase 1 (MKK1) enhanced endogenous topoisome
18 osphorylation and p90 ribosomal S6 kinase 2, MAP kinase kinase 1, and Raf-1 activities were increased
21 158780 potently inhibited the LPA-stimulated MAP kinase kinase 1/2 (MKK1/2) activation and EGF recept
23 ted protein kinases 1 and 2 (ERK1, ERK2) and MAP kinase kinases 1 and 2 (MKK1, MKK2), is well-known t
25 it, respectively, mitogen-activated protein (MAP) kinase kinase 1 (MEK 1) and calcineurin, to determi
26 We show that both mitogen-activated protein (MAP) kinase kinase 1 (MEK1) and MAP kinase kinase 2 (MEK
27 , an inhibitor of mitogen-activated protein (MAP) kinase kinase 1 and 2 (MEK1/2) that blocks phosphor
31 e and constitutively active mutants of human MAP kinase kinase-1 (MKK1) were analyzed by deuterium ex
34 ted protein (MAP) kinase kinase 1 (MEK1) and MAP kinase kinase 2 (MEK2) are activated by ionizing rad
35 -Pr1 prostate and A427 lung carcinoma lines, Map Kinase Kinase 3 (MAP2K3) on 17q in the NCI-H774 lung
36 with IFNalpha results in activation of both MAP kinase kinase 3 (MKK3) and MAP kinase kinase 6 (MKK6
37 , and c-Jun NH(2)-terminal kinase-1, but not MAP kinase kinase 3 and p38, augmented ARE activation by
40 of p38alpha relies solely on the presence of MAP kinase kinase 3, despite the expression in brown fat
41 a specific upstream activator of the kinase, MAP kinase kinase 3, resulted in diminished proinflammat
42 CL316,243 (CL) stimulates phosphorylation of MAP kinase kinase 3/6 and p38 MAPK in a time- and dose-d
44 ad [FKHR], HSP27, mitogen-activated protein (MAP) kinase kinase-3 and -6 (MKK3/6), the tumor-suppress
45 rs for the p38 kinases, activated mutants of MAP kinase kinase 3b(E) (MKK3bE) and MAP kinase kinase 6
46 ith SERT and a constitutively active form of MAP kinase kinase 3b(E) [MKK3b(E)] increased 5-HT transp
48 ube development, we examined the activity of MAP kinase kinase 4 (MKK4), a signaling intermediate bet
49 d the in vitro activation of JNK3 alpha 1 by MAP kinase kinase 4 (MKK4), MAP kinase kinase 7 (MKK7),
51 vation of Rac1/Cdc42, mixed lineage kinases, MAP kinase kinases 4 and 7, and JNKs plays a required ro
54 hosphorylation of mitogen-activated protein (MAP) kinase kinase 4, p38, extracellular receptor kinase
56 experiments confirm that IL-1beta activates MAP kinase kinase-4 (MKK4)/SEK1, MKK3, and MKK6 in renal
57 l MAPK signaling proteins (MEK-1, MEK-3, and MAP kinase kinase-4) and may indicate activity of anthra
58 dominant negative ERK5 or dominant negative MAP kinase kinase 5 reduced the number of neurons genera
59 strongly stimulated by constitutively active MAP kinase kinase 6 (MKK6), an upstream activator of p38
60 ly in the preferred activation of p38beta by MAP kinase kinase 6 (MKK6), whereas p38 was activated ne
62 MAPK by expression of constitutively active MAP kinase kinase 6 (MKK6Glu) greatly enhances nuclear t
63 tion of the p38-dependent upstream activator MAP kinase kinase 6 as a member of this group identifies
64 by the expression of constitutivelyactivated MAP kinase kinase 6 in transgenic mice caused increased
65 rtantly, expression of a constitutive active MAP kinase kinase 6(Glu) resulted in the phosphorylation
67 of downstream kinases, MAP kinase kinase 4, MAP kinase kinase 6, and c-Jun NH(2)-terminal kinase-1,
69 ycin and ultraviolet radiation (UV) activate MAP kinase kinase-6 (MKK6) [14,15], p38/RK [16] [17,18]
71 ants of MAP kinase kinase 3b(E) (MKK3bE) and MAP kinase kinase 6b(E) (MKK6bE), elicited characteristi
73 cell activation, the Jun kinase (JNK) kinase MAP kinase kinase 7 (MKK7) is alternatively spliced to f
74 JNK3 alpha 1 by MAP kinase kinase 4 (MKK4), MAP kinase kinase 7 (MKK7), and the combination of MKK4
76 minal kinase (JNK) pathway revealed that the MAP kinase kinase 7 (MKK7)-JNK cascade also mediated IFN
77 kinase (IKK), and reduced phosphorylation of MAP kinase kinase 7 and Jun NH2-terminal kinase (JNK).
78 P is critical for mitogen-activated protein (MAP) kinase kinase 7 (MKK7) phosphorylation and recruitm
80 , an inhibitor of mitogen-activated protein (MAP) kinase kinase activation, inhibited IGF-stimulated
81 Mutations in the earlier identified fuz7 MAP kinase kinase also suppress the filamentous phenotyp
84 nic signaling proteins Src, Ras, Raf-1, Mek (MAP kinase kinase), and Erk (MAP kinase) in baculovirus-
86 ration, we used U0126, a potent inhibitor of MAP kinase kinase, and a constitutively active mutant of
88 ies, overexpression of constitutively active MAP kinase kinase, and an in vitro assay with recombinan
90 , which encodes a mitogen-activated protein (MAP) kinase kinase, and nsy-1, which encodes a MAP kinas
92 These dual specificity kinases also known as MAP kinase kinases are constituents of the sequential ki
95 contrast, expression of mutationally active MAP kinase kinase causes activation of MAP kinase leadin
97 more, genes that encode two novel Drosophila MAP kinase kinases, D-MKK3 and D-MKK4, were identified.
99 dent phosphorylation of synapsin I, and MEK (MAP kinase kinase)/ERK inhibition selectively decreased
100 Phosphorylation and activation of both the MAP kinase kinase/ERK and PI3K/Akt pathways occur in lat
101 highly sensitive to PD98059, an inhibitor of MAP kinase kinase/ERK kinase 1 (MEK1) that blocks activa
103 eatment caused marked down-regulation of the MAP kinase kinase/extracellular regulatory kinase (MEK/E
104 re we show that JNKK2, a novel member of the MAP kinase kinase family, was phosphorylated and activat
105 lar cloning of a new member of the mammalian MAP kinase kinase group (MKK7) that functions as an acti
107 thway inhibition is mediated at the level of MAP kinase kinase in a Ras- and Raf-independent fashion,
108 more, this nuclear ERK2 is phosphorylated by MAP kinase kinase in response to growth factors and also
109 ressed by preventing ERK activation with the MAP kinase kinase inhibitor 2-(2-diamino-3-methoxyphenyl
111 treatment of extracts with either a specific MAP kinase kinase inhibitor or a MAP kinase phosphatase
112 ompletely abolished by pretreatment with the MAP kinase kinase inhibitor PD 98059 (30 micromol/L, 60
114 and secretion of interleukin-8, whereas the MAP kinase kinase inhibitor PD98059 partially inhibited
116 We synthesized a previously characterized MAP kinase kinase inhibitor to test the effect that bloc
120 AP kinase) in CD34(+) cells, and we used the MAP kinase kinase inhibitor, PD 098059, which at 30 micr
123 and that inhibiting Erk activation with the MAP kinase kinase inhibitor, PD98059, reversibly inhibit
125 R co-immunoprecipitated with MAP kinase; (3) MAP kinase-kinase inhibitor PD98059 attenuated Ang II-in
131 k6, demonstrating that the function of these MAP kinase kinases is required for full activation of th
132 ligases for the dual-leucine-zipper-bearing MAP kinase kinase kinase (DLK MAPKKK) to regulate the si
133 Cot (also known as Tpl2) is a member of the MAP kinase kinase kinase (MAP3K) family that is known to
136 h phenotype yielded mutations in wallenda, a MAP kinase kinase kinase (MAPKKK) homologous to vertebra
137 (VIGS) to study the role of candidate plant MAP kinase kinase kinase (MAPKKK) homologs of human MEKK
138 as a novel protein that interacts with Win1 MAP kinase kinase kinase (MAPKKK) of the stress-activate
140 tosis signal-regulating kinase 1 (ASK1) is a MAP kinase kinase kinase (MAPKKK) that is required for c
142 screen in yeast, we have identified a human MAP kinase kinase kinase (MAPKKK) that shares homology w
143 ptosis-signal regulating kinase 1 (ASK1) and MAP kinase kinase kinase 1 (MEKK1), stimulate c-Jun kina
144 ng the important cellular signaling molecule MAP kinase kinase kinase 2 (MAP3K2), at exactly the same
148 o domains in other proteins that mediate Ras-MAP kinase kinase kinase associations; however, this RBL
149 tion and the Ras-dependent activation of the MAP kinase kinase kinase B-Raf are blocked by inhibition
150 t studies suggest that Rap1 can activate the MAP kinase kinase kinase B-Raf that is either endogenous
154 , a homologue of Mst11, which corresponds to MAP kinase kinase kinase in Magnaporthe oryzae, and urat
155 was phosphorylated and activated by MEKK1, a MAP kinase kinase kinase in the JNK signaling cascade.
158 osomal protein S6 kinase p70(S6K1), plus the MAP kinase kinase kinase kinase MINK, which had not prev
159 ddition, a direct PKA site that inhibits the MAP kinase kinase kinase Map3k5 (ASK1) is upstream of JN
160 slational activation of mRNA encoding Mos, a MAP kinase kinase kinase necessary for the activation of
161 identified it as the Mos protooncoprotein, a MAP kinase kinase kinase present at low levels in mitoti
162 roteasomal degradation of TAK1, the upstream MAP kinase kinase kinase required for JNK activation.
163 l cloning and was found to encode a putative MAP kinase kinase kinase similar to CTR1, a negative reg
164 y shown that the conserved actin-interacting MAP kinase kinase kinase Ssk2p/MEKK4, a member of the hi
166 e it binds the osmosensor Sho1, the upstream MAP kinase kinase kinase Ste11, and the downstream MAP k
172 optosis signal-regulating kinase 1 (ASK1), a MAP kinase kinase kinase, is required for TNF-mediated J
173 in neuronal signaling by a conserved axonal MAP kinase kinase kinase, known as Wallenda (Wnd) in Dro
174 studied the activation mechanism of a human MAP kinase kinase kinase, MTK1 (also known as MEKK4), wh
175 ed effector of polarity signaling, encodes a MAP kinase kinase kinase-related protein that stimulates
179 protein kinase cascade: MEKK1, -2, or -4 for MAP kinase kinase kinase; MKK4 and/or MEK1 for MAP kinas
182 ation, as well as mitogen-activated protein (MAP) kinase kinase kinase (MEKK) 1, MAP kinase kinase (M
183 s a member of the mitogen-activated protein (MAP) kinase kinase kinase group that has been implicated
184 to members of the mitogen-activated protein (MAP) kinase kinase kinase subfamily, this protein kinase
185 ation of MEKK2, a mitogen-activated protein (MAP) kinase kinase kinase upstream of ERK5 that is requi
187 ctivates dual leucine-zipper kinase (DLK), a MAP-kinase kinase kinase that then activates MKK7 and ER
189 s recent studies characterizing the specific MAP kinase kinase kinases (MAP 3-kinases) that link MAP
191 na there are approximately 80 genes encoding MAP kinase kinase kinases (MAP3K), 10 genes encoding MAP
192 amino acid (TAO) kinases are Ste20p-related MAP kinase kinase kinases (MAP3Ks) that activate p38 MAP
193 tein kinases: (i) the SSK2, SSK22, and STE11 MAP kinase kinase kinases (MAPKKKs), (ii) the PBS2 MAPKK
194 ase cascade composed of the Ssk2p and Ssk22p MAP kinase kinase kinases (MAPKKKs), the Pbs2p MAPKK, an
196 athway, including the mixed-lineage group of MAP kinase kinase kinases (MLK), the MAP kinase kinase M
198 , depending on the expression pattern of the MAP kinase kinase kinases of the Raf family: Raf-1 and B
201 we show that TPL-2 , which is homologous to MAP-kinase-kinase kinases in its catalytic domain, forms
202 verexpression and expression of an activated MAP-kinase-kinase (MAP-KK), cytochrome c induced apoptos
203 se kinase kinases (MAP3K), 10 genes encoding MAP kinase kinases (MAP2K), and 20 genes encoding MAP ki
205 r this behavior requires the assumption that MAP kinase kinase (MAPKK) carries out its dual phosphory
207 ivation, we introduced constitutively active MAP kinase kinase (MAPKK) into immortalized melanocytes.
208 upstream pathways that converge on the Pbs2 MAP kinase kinase (MAPKK), leading to the activation of
211 on specific tyrosine and threonine sites by MAP kinase kinases (MAPKKs) is thought to be the sole ac
212 In vitro studies previously identified the MAP kinase kinases (MAPKKs) MKK3 and MKK6 as the primary
213 nt of the protein tyrosine kinase c-Src, the MAP kinase kinase MEK 1/2, and the transcription factor
214 protein (MAP) kinase kinase kinase (MEKK) 1, MAP kinase kinase (MEK) 3/6, and p38 MAP kinase activati
217 JNKK2), a subfamily of the dual specificity MAP kinase kinase (MEK) family, through phosphorylation
218 Rottlerin also inhibited the activation of MAP kinase kinase (MEK) in response to activated Raf, bu
219 ascade (wortmannin and LY29004) but not by a MAP kinase kinase (MEK) inhibitor (PD98059) or a protein
220 ine kinase (PTK) inhibitor genistein, by the MAP kinase kinase (MEK) inhibitor PD98059, and by loadin
223 ction was highlighted by the result that the MAP kinase kinase (MEK) inhibitor, PD 98059, blocked Del
225 a1 adrenoceptor antagonist, prazosin, or the MAP kinase kinase (MEK) inhibitor, U0126 (1,4-diamino-2,
227 evious studies have shown that activation of MAP kinase kinase (MEK) is insufficient to induce neuron
229 n mouse eggs a constitutively active form of MAP kinase kinase (MEK) whose only known target is p42/p
233 pathways at four levels: mitogen receptors, MAP kinase kinase (MEK)1/2 and ERK1/2, and certain downs
236 c MAP kinase inhibitors, PD98059 (25 microM; MAP kinase kinase (MEK-1) inhibitor) and SB203580 (10 mi
239 on 3 (STAT-3) and mitogen-activated protein (MAP) kinase kinase (MEK) activity, reduced expression of
240 e comprising Raf, mitogen-activated protein (MAP) kinase kinase (MEK) and MAP kinase is a Ras effecto
241 S1P requires both mitogen-activated protein (MAP) kinase kinase (MEK) and p38 MAP kinase, and MEK is
242 and Erk2-specific mitogen-activated protein (MAP) kinase kinase (MEK) are essential and probably func
243 n-fs, whereas the mitogen-activated protein (MAP) kinase kinase (MEK) inhibitor PD98059 blocked phosp
244 ut the use of the mitogen-activated protein (MAP) kinase kinase (MEK) inhibitor PD98059, were perform
245 ition of the microtubule-associated protein (MAP) kinase kinase (MEK) or overexpression of dominant-n
246 of activation of mitogen-activated protein (MAP) kinase kinase (MEK), and FPT inhibitor II, a select
247 , an inhibitor of mitogen-activated protein (MAP) kinase kinase (MEK), had no effect on the m1 recept
248 e inhibitors as protein kinase CK2, not p38, MAP-kinase kinase (MEK)1/2, phosphatidylinositol 3'-kina
249 d Cu chelators all reduce the ability of the MAP kinase kinase Mek1 to phosphorylate the MAP kinase E
252 ERK2, such as the mitogen-activated protein (MAP) kinase kinase MEK1 and MAP kinase phosphatases.
253 e here have investigated this issue by using MAP kinase kinase (MEK1) inhibitor PD098059 and a domina
255 ctor for a constitutively active form of the MAP kinase kinase (MEK1) led to stimulation of PTTG tran
256 enes encoding two mitogen-activated protein (MAP) kinase kinases, MEK1 and MEK2, two MAP kinases, NTF
257 ssion of a constitutively active form of the MAP kinase kinase, MEK2, was sufficient to induce HIF-1
260 describe a constitutively active form of the MAP kinase kinase, MEK5(D), which selectively activates
268 dbrain dopaminergic neurons by knocking down MAP kinase kinases (MKK) significantly reduced the selec
269 active mutants of mitogen-activated protein (MAP) kinase kinase (MKK), resulting in cell adhesion and
271 dominant-negative mitogen-activated protein (MAP) kinase-kinase (MKK1) abrogated both insulin- and TZ
272 Further, mutants defective in the upstream MAP kinase kinase MKK3 also display hypersensitivity in
277 in these cells appears to be mediated by the MAP kinase kinase MKK7 since high levels of MKK7 and low
280 ed Rac1/Cdc42, mixed-lineage kinases (MLKs), MAP kinase kinases (MKKs) 4 and 7, c-Jun N-terminal kina
285 orskolin or rolipram treatment, but not MEK (MAP kinase kinase) or PI3-K (phosphatidylinositol 3-kina
286 ibition of the MAP kinase p38 but not of the MAP kinase kinase p42/44, suggesting that NO modulates e
288 yeast high osmolarity response pathway, the MAP kinase kinase Pbs2 is thought to function as a scaff
289 Moreover, using selective inhibitors for MAP kinase kinase (PD98059) and p38 (SB203580), we show
291 rosine kinases or mitogen-activated protein (MAP) kinase kinase prevented the activation of eNOS by E
295 M. grisea that are homologous with the yeast MAP kinase kinase STE7 and MAP kinase kinase kinase STE1
297 nthrax lethal factor), which cleaves certain MAP kinase kinases, strongly reduces both the rate and e
299 1 in this fraction was able to phosphorylate MAP kinase kinase, whereas cytoplasmic Raf-1 in the same
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