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1 Chemical inhibition of IkappaB kinase (IKK), mitogen-activated protein extracellular signal-regulated
2 regulatory effects of BCL6 on both MEK-ERK (mitogen-activated protein/extracellular signal-regulated
3 screen identified multiple components of the mitogen activated protein kinase (MAPK) pathway enhancin
5 nical nuclear factor kappa B (NF-kappaB) and mitogen activated protein kinase (MAPK) pathways have be
6 ncers contain genetic alterations within the Mitogen Activated Protein Kinase (MAPK) signaling networ
9 uclear cells of sepsis patients, whereas p38 mitogen activated protein kinase messenger RNA was up-re
11 sis factor-alpha-induced protein 3 (A20) and mitogen activated protein kinase phosphatase-1 were dete
12 rhabditis elegans, we implicate the atypical mitogen activated protein kinase, SWIP-13, in DAT regula
14 ia extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (ERK1/2 MAPK)-dependent
16 mune signaling, including phosphorylation of mitogen-activated protein kinase (MAPK) 3 (MPK3) and MPK
18 ls converging at the MOR promoter, involving mitogen-activated protein kinase (MAPK) activation and m
19 D family members 2, 3, and 4 (SMAD2/3/4) and mitogen-activated protein kinase (MAPK) activities, whic
24 Mutations at both interfaces interfered with mitogen-activated protein kinase (MAPK) and phosphoinosi
25 d proliferative (PRO) phenotypes linked with mitogen-activated protein kinase (MAPK) and signal trans
26 used it to analyze a set of D-motif peptide-mitogen-activated protein kinase (MAPK) associations to
28 e to mating pheromone activates a prototypic mitogen-activated protein kinase (MAPK) cascade and trig
29 idopsis, an extremely functionally redundant mitogen-activated protein kinase (MAPK) cascade is requi
30 reatment identified robust activation of p38 mitogen-activated protein kinase (MAPK) downstream of PK
31 daptors to regulate AT1R internalization and mitogen-activated protein kinase (MAPK) ERK1/2 activatio
32 increased levels of total and phosphorylated mitogen-activated protein kinase (MAPK) family members s
34 Previous studies showed that activation of mitogen-activated protein kinase (MAPK) in diabetes prom
35 KO mice with enhanced phosphorylation of p38 mitogen-activated protein kinase (MAPK) in podocytes.
39 ype I priming, or the combination of Src and mitogen-activated protein kinase (MAPK) inhibitors, whic
41 artially rescued by constitutively activated mitogen-activated protein kinase (MAPK) kinase kinase YO
42 Microbial pathogens often target the host mitogen-activated protein kinase (MAPK) network to suppr
43 paired the activity of key components of the mitogen-activated protein kinase (MAPK) pathway (p38 and
44 WASP-deficient lymphoma showed increased mitogen-activated protein kinase (MAPK) pathway activati
45 ling pathway, beta-arrestin recruitment, and mitogen-activated protein kinase (MAPK) pathway activati
46 brane (PM) correlates with activation of the mitogen-activated protein kinase (MAPK) pathway and subs
48 hodiesterase inhibitor and also modifies the mitogen-activated protein kinase (MAPK) pathway by downr
49 ptor protein tyrosine phosphatase within the mitogen-activated protein kinase (MAPK) pathway controll
50 arget the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway have led
51 "paradoxical" upregulation of the downstream mitogen-activated protein kinase (MAPK) pathway in cance
55 nsition (EMT), mediated, in part, by the p38 mitogen-activated protein kinase (MAPK) pathway respondi
57 ic cells (DCs) with constitutively activated mitogen-activated protein kinase (MAPK) pathway signalin
58 that are marked by diverse mutations in the mitogen-activated protein kinase (MAPK) pathway(1,2).
63 tivated kinase Ste20p, Cdc42p also regulates mitogen-activated protein kinase (MAPK) pathways (mating
65 Cellular signaling pathways, including the mitogen-activated protein kinase (MAPK) pathways, are re
66 dependent on the activation of the NF-kB and mitogen-activated protein kinase (MAPK) pathways, which
67 pattern recognition receptors activates the mitogen-activated protein kinase (MAPK) pathways, which
72 ll fusion, is mediated by Gbetagamma and the mitogen-activated protein kinase (MAPK) scaffold protein
74 In the absence of RASA1, dysregulated Ras mitogen-activated protein kinase (MAPK) signal transduct
75 PF included extracellular matrix remodeling, Mitogen-activated protein kinase (MAPK) signaling and AL
76 strains, we show that candidalysin activates mitogen-activated protein kinase (MAPK) signaling and ch
77 AS, and BRAF mutations which activate p44/42 mitogen-activated protein kinase (MAPK) signaling are fo
78 orted that kinase-dead BRAF variants amplify mitogen-activated protein kinase (MAPK) signaling by dim
79 to interact with both survival and apoptotic mitogen-activated protein kinase (MAPK) signaling cascad
80 ated calcium channel Cacophony (Cac) and the mitogen-activated protein kinase (MAPK) signaling cascad
81 ed by PTPN11, plays an essential role in RAS-mitogen-activated protein kinase (MAPK) signaling during
82 PD-L1 blockade with inhibition of oncogenic mitogen-activated protein kinase (MAPK) signaling may re
83 sor that is differentially regulated through mitogen-activated protein kinase (MAPK) signaling or gen
84 4b to act as a negative regulator of the RAS/mitogen-activated protein kinase (MAPK) signaling pathwa
85 S. cerevisiae plays crucial roles in various mitogen-activated protein kinase (MAPK) signaling pathwa
87 tein, VopA, has potent inhibitory effects on mitogen-activated protein kinase (MAPK) signaling pathwa
88 ally, inhibition of the PI3K, but not of the mitogen-activated protein kinase (MAPK) signaling pathwa
89 AF gene fusions that aberrantly activate the mitogen-activated protein kinase (MAPK) signaling pathwa
90 and activator of transcription 3 (STAT3) and mitogen-activated protein kinase (MAPK) signaling pathwa
91 kinase, p38, and c-Jun amino-terminal kinase mitogen-activated protein kinase (MAPK) signaling to eli
93 of RAF proto-oncogene, Ser/Thr kinase (Raf)-mitogen-activated protein kinase (MAPK) signaling, induc
94 c) Homology Phosphatase 2 (Shp2) to activate Mitogen-Activated Protein Kinase (MAPK) signaling, which
98 1 (CK1) sites Cx43(S325A/328Y/330A), and the mitogen-activated protein kinase (MAPK) sites Cx43(S255/
99 gh autophosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) via a non-canoni
100 identified NF-kappaB activator 1 (Act1), p38 mitogen-activated protein kinase (MAPK), Jun NH2-termina
101 ake of bacteria, which required PDK1, and of mitogen-activated protein kinase (MAPK)- and nuclear fac
102 its rapid basal turnover in neurons and that mitogen-activated protein kinase (MAPK)-dependent phosph
103 kinase (IKK), c-jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK)-extracellular re
104 l GTPases, p21-activated kinase, and the p38 mitogen-activated protein kinase (MAPK)-MAPK-activated p
105 of all pathogenic non-Dsg AuAbs involved p38 mitogen-activated protein kinase (MAPK)-mediated phospho
106 which transcription factors are released by mitogen-activated protein kinase (MAPK)-stimulated acety
111 (PI3K)/Akt serine/threonine kinase (Akt) and mitogen-activated protein kinase (MAPK)/extracellular si
113 an extremely potent allosteric inhibitor of mitogen-activated protein kinase (MAPK)/extracellular-si
114 f the JCI, Yokota et al. reveal that the p38 mitogen-activated protein kinase (MAPK)/IRE1alpha/XBP1 a
115 n of oncogenic Ras(V12) activates downstream mitogen-activated protein kinase (MEK-ERK) signaling to
117 Increases in the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and decrease
118 NASH development and the involvement of p38 mitogen-activated protein kinase (p38) activated by neut
119 CyTP genes is mediated by the conserved p38 mitogen-activated protein kinase (p38-MAPK) pathway.
120 Signal transduction pathways mediated by p38 mitogen-activated protein kinase (p38MAPK), extracellula
121 tly driven by genetic alterations in the RAS-mitogen-activated protein kinase (RAS/MAPK) pathway yet
122 hed in synaptic function and converge on Ras/mitogen-activated protein kinase (Ras/MAPK) signaling.
123 ovo missense variants in MAPK1, encoding the mitogen-activated protein kinase 1 (i.e., extracellular
124 l myenteric plexi and phosphorylation (p) of mitogen-activated protein kinase 1 (MAPK1) in the enteri
125 e P (SP), S100beta, GFAP, and phosphorylated mitogen-activated protein kinase 1 (pERK) were assessed
126 proteins, auxin stabilizes IAA33 protein via MITOGEN-ACTIVATED PROTEIN KINASE 14 (MPK14) and does not
128 e use Nicotiana attenuata plants silenced in mitogen-activated protein kinase 4 (irMPK4) - with low w
130 Previously, we demonstrated that Arabidopsis mitogen-activated protein kinase 6 (MPK6) and MPK3 play
131 elated prognostic proteins, particularly the mitogen-activated protein kinase 6, probable protein pho
132 samples and xenograft mouse models revealed mitogen-activated protein kinase 7/matrix metallopeptida
133 beta-arrestin-dependent signaling responses, mitogen-activated protein kinase [i.e., extracellular si
134 g22, PLC2-silenced plants maintain wild-type mitogen-activated protein kinase activation and PHI1, WR
135 nd extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase activation at the human
138 for Ptpn6 in the negative regulation of p38 mitogen-activated protein kinase activation to control t
139 es G protein-coupled calcium ion signals and mitogen-activated protein kinase activity, and that its
140 ntracellular signaling pathways, such as the mitogen-activated protein kinase and AKT signaling casca
142 h levels of reactive oxygen species in a p38 mitogen-activated protein kinase and phosphatidylinosito
143 e ability of pharmacologic inhibition of the mitogen-activated protein kinase and PI3'K pathways to i
144 via the gp130 signaling receptor, activating mitogen-activated protein kinase and signal transducer a
145 is revealed significant up-regulation of the mitogen-activated protein kinase and transforming growth
146 ulation in endothelial cells via JNK and p38 mitogen-activated protein kinase but not NF-kappaB.
147 identified OsPT8 as an interactor of a rice mitogen-activated protein kinase BWMK1, which is a regul
148 -X-C motif chemokine ligand 12 activates the mitogen-activated protein kinase extracellular-signal-re
149 n N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and controls var
151 preceded by decreased phosphorylation of p38 mitogen-activated protein kinase in HMuSC treated with C
152 eased proliferation and dysregulation of p38 mitogen-activated protein kinase in satellite cells comm
154 ed by the accumulation of phosphorylated p38 mitogen-activated protein kinase in the nucleus, which d
156 vides a rationale for combining pan-ERBB and mitogen-activated protein kinase inhibitors as a therape
157 c target of rapamycin complex 1 (mTORC1) and mitogen-activated protein kinase interacting kinase (MNK
159 tion of lipid A limits the activation of the mitogen-activated protein kinase Jun N-terminal protein
160 tor of transcription (STAT) (ruxolitinib) or mitogen-activated protein kinase kinase (MEK) (trametini
161 ines had IC(50) values less than 7 nM to the mitogen-activated protein kinase kinase (MEK) 1/2 inhibi
162 mutational status, and response to B-Raf and mitogen-activated protein kinase kinase (MEK) inhibition
165 therapy with B-Raf proto-oncogene (BRAF) and mitogen-activated protein kinase kinase (MEK) inhibitors
166 e/threonine-specific protein kinases (pRAF), mitogen-activated protein kinase kinase (pMEK), protein
169 ffector PI3K but instead require active MEK (mitogen-activated protein kinase kinase 1) signaling.
171 ivated protein kinase kinase kinase 3)-MEK5 (mitogen-activated protein kinase kinase 5)-ERK5 (extrace
172 found REX1 to bind to the promoter region of mitogen-activated protein kinase kinase 6 (MKK6), thereb
174 gamma) intraperitoneally for 3 d or with the mitogen-activated protein kinase kinase inhibitor selume
175 2 depletion in ECs elicited increased MEKK3 (mitogen-activated protein kinase kinase kinase 3)-MEK5 (
176 restingly, we observed that knockdown of the mitogen-activated protein kinase kinase kinase 4 (MAP3K4
177 Among the differentially expressed kinases, mitogen-activated protein kinase kinase kinase kinase 4
180 r their mechanisms of action using selective mitogen-activated protein kinase kinase MEK1/2, MEK5, an
181 s pyruvate dehydrogenase kinase 1, Akt, Raf, mitogen-activated protein kinase kinase, and ERK1/2.
182 particular, we report synergistic effects of mitogen-activated protein kinase kinase, ribosomal S6 ki
185 -in-class von Hippel-Lindau (VHL)-recruiting mitogen-activated protein kinase kinases 1 and 2 (MEK1/2
188 icity phosphatase 1, impairs the activity of mitogen-activated protein kinase p38, increases the acti
189 rticularly, we found that alterations of the mitogen-activated protein kinase pathway (KRAS and NRAS
191 ward beta-arrestin recruitment and increased mitogen-activated protein kinase pathway activation.
192 llular signal-regulated protein kinase (ERK) mitogen-activated protein kinase pathway and that ERK in
193 ted, at least in part, via activation of the mitogen-activated protein kinase pathway following calci
194 M) in 60%, and phosphatidylinositol 3-kinase/mitogen-activated protein kinase pathway genes (eg, ERBB
195 breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-mutant c
196 phosphorylation of focal adhesion kinase and mitogen-activated protein kinase pathway leading to enha
197 th the extracellular signal-regulated kinase mitogen-activated protein kinase pathway that provides a
198 ectively, these findings demonstrate the ERK mitogen-activated protein kinase pathway to be integrall
199 ibed the paradoxical triggering of the human mitogen-activated protein kinase pathway when a small-mo
200 extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase pathway, consistent wit
201 ransducer and activator of transcription and mitogen-activated protein kinase pathways to regulate ce
204 ofin (ARN), an antirheumatic drug, to induce mitogen-activated protein kinase phosphatase (MKP)-1 exp
205 bacterium tuberculosis (Mtb) by facilitating mitogen-activated protein kinase phosphatase 1 (MKP-1)-d
206 ed with a pharmacological agent that induces mitogen-activated protein kinase phosphatase have potent
207 past several years has elucidated a role for mitogen-activated protein kinase phosphatase to regulate
210 otein kinase C, cyclin-dependent kinase, and mitogen-activated protein kinase showed increased phosph
211 nger NHFs, PDAC cells exhibited increases in mitogen-activated protein kinase signaling and cellular
213 folded protein response, glycolysis, and the mitogen-activated protein kinase signaling cascade.
214 d causal link between LZTR1 dysfunction, RAS-mitogen-activated protein kinase signaling hyperactivity
215 e renin-angiotensin system in the kidney and mitogen-activated protein kinase signaling in the heart.
216 terations in genes whose products are in the mitogen-activated protein kinase signaling pathway and a
217 g mechanism is a gain-of-function of the RAS-mitogen-activated protein kinase signaling pathway.
218 roteins in receptor tyrosine kinase, RAS, or mitogen-activated protein kinase signaling pathways.
219 se 4 (MAP3K4) gene, which contributes to p38 mitogen-activated protein kinase signaling, sensitized c
220 ed with wild-type mice, along with decreased mitogen-activated protein kinase signaling, tumor angiog
224 ignalling, cell cycle regulatory signalling, mitogen-activated protein kinase signalling and pathways
225 nsducer and activator of transcription 3 and mitogen-activated protein kinase signalling in an inocul
226 diverse modes of injury converge on p38alpha mitogen-activated protein kinase within the fibroblast t
228 of BRD4 is controlled, in part, by p38 MAPK (mitogen-activated protein kinase) and provide evidence o
229 K (RAS-extracellular signal-regulated kinase/mitogen-activated protein kinase) pathway integrates gro
230 ion of 101 gene transcripts, including MAPK (mitogen-activated protein kinase) signaling targets, HOP
232 s extracellular signal-regulated kinase 1/2, mitogen-activated protein kinase, and Src, shown by immu
235 eltaPMN) neutrophils displayed increased p38 mitogen-activated protein kinase-dependent Ripk1-indepen
236 al-related kinase 1/2 (pERK1/2), a marker of mitogen-activated protein kinase-ERK signal transduction
241 otein expression that was attenuated by MEK (mitogen-activated protein kinase/extracellular signal-re
242 al growth factor receptor (EGFR), as EGFR or mitogen-activated protein kinase/extracellular signal-re
244 with the BRAF inhibitor vemurafenib and the mitogen-activated protein kinase/extracellular signal-re
245 ed that the rapidly accelerated fibrosarcoma/mitogen-activated protein kinase/extracellular signal-re
246 al stem-like (MSL) lineage downregulates the mitogen-activated protein kinase/extracellular signal-re
248 biquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physio
249 -inflammatory pathways such as NF-kappaB and mitogen activated protein kinases (MAPKs), and the subse
251 ciated protein kinase 70 (ZAP-70), and three mitogen-activated protein kinases (extracellular signal-
252 cular chondrocytes via the inhibition of p38 mitogen-activated protein kinases (MAPK) and increasing
253 transcription factors are phosphorylated by mitogen-activated protein kinases (MAPK) in their transa
256 ar signal-regulated kinase 1 and 2 (ERK1/2), mitogen-activated protein kinases (MAPK), leading to unc
257 relatively rare member of the JNK family of mitogen-activated protein kinases (MAPK), phosphorylates
258 d kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)] were assessed
259 ral detail on docking interactions involving mitogen-activated protein kinases (MAPKs) and their subs
262 s diverse kinase pathways, which include the mitogen-activated protein kinases (MAPKs) ERK and p38, t
266 t/MKP-1 pathway results in the inhibition of mitogen-activated protein kinases (MAPKs) JNK and p38.
268 we show that the rapid activation of clade-A mitogen-activated protein kinases (MAPKs) MPK3 and MPK6
272 (DUSP1), an endogenous negative regulator of mitogen-activated protein kinases (MAPKs), resulting in
274 nd ROS signals compromised the activation of mitogen-activated protein kinases (MPKs) 1/2 in leaves.
275 sion of sequestosome 1 (p62) and phospho-p38 mitogen-activated protein kinases (p-p38) showed a signi
276 , oxidative stress, early phosphorylation of mitogen-activated protein kinases and Akt, and upregulat
277 were not affected in PAMP/DAMP activation of mitogen-activated protein kinases and expression of the
280 lular signal-regulated kinase), JNK, and p38 mitogen-activated protein kinases as well as NFkappaB (n
282 st transdifferentiation by activation of p38 mitogen-activated protein kinases resulting in upregulat
283 ptation and stress tolerance, and in several mitogen-activated protein kinases signaling pathways inc
284 of reactive oxygen species and activation of mitogen-activated protein kinases upon exposure to flg22
285 ing a dual-specificity phosphatase targeting mitogen-activated protein kinases, as a type 2 diabetes
287 HAI1 or by HAI1-regulated kinases including mitogen-activated protein kinases, sucrose non-fermentin
289 Disruption or knockdown of an Msb2-dependent mitogen-activated protein (MAP) kinase (HOG2) and an APS
290 ch engages the c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinase and Fos and Jun t
291 t requires the c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinase and the transcrip
292 magnetic resonance (NMR) measurements of the mitogen-activated protein (MAP) kinase ERK2 have shown t
294 e Using this approach, we identified the p38 mitogen-activated protein (MAP) kinase pathway and autop
295 duction of reactive oxygen species (ROS) and mitogen-activated protein (MAP) kinase phosphorylation,
296 ptosis, and its expression is facilitated by mitogen-activated protein (MAP) kinase-activated protein
297 ive responses characterized by activation of mitogen-activated protein (MAP) kinases and nuclear fact
298 ts in the UPR, such as activation of the JNK mitogen-activated protein (MAP) kinases or the pseudokin
299 KK1 can trigger various responses, including mitogen-activated protein (MAP) kinases, NF-kappaB signa