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1 a implicate the neuroligin-3 ectodomain as a mitogen.
2 production in response to TB antigen and/or mitogen.
3 mation, extracellular matrix remodeling, and mitogens.
4 mbryonic zebrafish to identify cardiomyocyte mitogens.
5 mbers, and normal proliferative responses to mitogens.
6 screen identified multiple components of the mitogen activated protein kinase (MAPK) pathway enhancin
8 nical nuclear factor kappa B (NF-kappaB) and mitogen activated protein kinase (MAPK) pathways have be
9 ncers contain genetic alterations within the Mitogen Activated Protein Kinase (MAPK) signaling networ
12 biquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physio
13 -inflammatory pathways such as NF-kappaB and mitogen activated protein kinases (MAPKs), and the subse
15 an ancient and autoactivating member of the mitogen-activated kinase (MAPK) family and its regulatio
16 Disruption or knockdown of an Msb2-dependent mitogen-activated protein (MAP) kinase (HOG2) and an APS
17 ch engages the c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinase and Fos and Jun t
18 t requires the c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinase and the transcrip
19 magnetic resonance (NMR) measurements of the mitogen-activated protein (MAP) kinase ERK2 have shown t
21 e Using this approach, we identified the p38 mitogen-activated protein (MAP) kinase pathway and autop
22 ptosis, and its expression is facilitated by mitogen-activated protein (MAP) kinase-activated protein
23 ive responses characterized by activation of mitogen-activated protein (MAP) kinases and nuclear fact
24 ts in the UPR, such as activation of the JNK mitogen-activated protein (MAP) kinases or the pseudokin
25 KK1 can trigger various responses, including mitogen-activated protein (MAP) kinases, NF-kappaB signa
27 ia extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (ERK1/2 MAPK)-dependent
29 mune signaling, including phosphorylation of mitogen-activated protein kinase (MAPK) 3 (MPK3) and MPK
31 D family members 2, 3, and 4 (SMAD2/3/4) and mitogen-activated protein kinase (MAPK) activities, whic
36 Mutations at both interfaces interfered with mitogen-activated protein kinase (MAPK) and phosphoinosi
37 d proliferative (PRO) phenotypes linked with mitogen-activated protein kinase (MAPK) and signal trans
38 used it to analyze a set of D-motif peptide-mitogen-activated protein kinase (MAPK) associations to
40 idopsis, an extremely functionally redundant mitogen-activated protein kinase (MAPK) cascade is requi
41 reatment identified robust activation of p38 mitogen-activated protein kinase (MAPK) downstream of PK
42 daptors to regulate AT1R internalization and mitogen-activated protein kinase (MAPK) ERK1/2 activatio
43 increased levels of total and phosphorylated mitogen-activated protein kinase (MAPK) family members s
45 Previous studies showed that activation of mitogen-activated protein kinase (MAPK) in diabetes prom
48 ype I priming, or the combination of Src and mitogen-activated protein kinase (MAPK) inhibitors, whic
50 artially rescued by constitutively activated mitogen-activated protein kinase (MAPK) kinase kinase YO
51 Microbial pathogens often target the host mitogen-activated protein kinase (MAPK) network to suppr
52 paired the activity of key components of the mitogen-activated protein kinase (MAPK) pathway (p38 and
53 WASP-deficient lymphoma showed increased mitogen-activated protein kinase (MAPK) pathway activati
54 ling pathway, beta-arrestin recruitment, and mitogen-activated protein kinase (MAPK) pathway activati
55 brane (PM) correlates with activation of the mitogen-activated protein kinase (MAPK) pathway and subs
56 hodiesterase inhibitor and also modifies the mitogen-activated protein kinase (MAPK) pathway by downr
57 ptor protein tyrosine phosphatase within the mitogen-activated protein kinase (MAPK) pathway controll
61 nsition (EMT), mediated, in part, by the p38 mitogen-activated protein kinase (MAPK) pathway respondi
62 that are marked by diverse mutations in the mitogen-activated protein kinase (MAPK) pathway(1,2).
67 tivated kinase Ste20p, Cdc42p also regulates mitogen-activated protein kinase (MAPK) pathways (mating
68 Cellular signaling pathways, including the mitogen-activated protein kinase (MAPK) pathways, are re
69 dependent on the activation of the NF-kB and mitogen-activated protein kinase (MAPK) pathways, which
70 pattern recognition receptors activates the mitogen-activated protein kinase (MAPK) pathways, which
75 ll fusion, is mediated by Gbetagamma and the mitogen-activated protein kinase (MAPK) scaffold protein
76 In the absence of RASA1, dysregulated Ras mitogen-activated protein kinase (MAPK) signal transduct
77 PF included extracellular matrix remodeling, Mitogen-activated protein kinase (MAPK) signaling and AL
78 strains, we show that candidalysin activates mitogen-activated protein kinase (MAPK) signaling and ch
79 AS, and BRAF mutations which activate p44/42 mitogen-activated protein kinase (MAPK) signaling are fo
80 orted that kinase-dead BRAF variants amplify mitogen-activated protein kinase (MAPK) signaling by dim
81 to interact with both survival and apoptotic mitogen-activated protein kinase (MAPK) signaling cascad
82 ated calcium channel Cacophony (Cac) and the mitogen-activated protein kinase (MAPK) signaling cascad
83 ed by PTPN11, plays an essential role in RAS-mitogen-activated protein kinase (MAPK) signaling during
84 PD-L1 blockade with inhibition of oncogenic mitogen-activated protein kinase (MAPK) signaling may re
85 sor that is differentially regulated through mitogen-activated protein kinase (MAPK) signaling or gen
86 4b to act as a negative regulator of the RAS/mitogen-activated protein kinase (MAPK) signaling pathwa
87 S. cerevisiae plays crucial roles in various mitogen-activated protein kinase (MAPK) signaling pathwa
89 tein, VopA, has potent inhibitory effects on mitogen-activated protein kinase (MAPK) signaling pathwa
90 ally, inhibition of the PI3K, but not of the mitogen-activated protein kinase (MAPK) signaling pathwa
91 and activator of transcription 3 (STAT3) and mitogen-activated protein kinase (MAPK) signaling pathwa
92 kinase, p38, and c-Jun amino-terminal kinase mitogen-activated protein kinase (MAPK) signaling to eli
94 of RAF proto-oncogene, Ser/Thr kinase (Raf)-mitogen-activated protein kinase (MAPK) signaling, induc
95 c) Homology Phosphatase 2 (Shp2) to activate Mitogen-Activated Protein Kinase (MAPK) signaling, which
99 1 (CK1) sites Cx43(S325A/328Y/330A), and the mitogen-activated protein kinase (MAPK) sites Cx43(S255/
100 gh autophosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) via a non-canoni
101 identified NF-kappaB activator 1 (Act1), p38 mitogen-activated protein kinase (MAPK), Jun NH2-termina
102 ake of bacteria, which required PDK1, and of mitogen-activated protein kinase (MAPK)- and nuclear fac
103 kinase (IKK), c-jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK)-extracellular re
104 of all pathogenic non-Dsg AuAbs involved p38 mitogen-activated protein kinase (MAPK)-mediated phospho
105 which transcription factors are released by mitogen-activated protein kinase (MAPK)-stimulated acety
109 (PI3K)/Akt serine/threonine kinase (Akt) and mitogen-activated protein kinase (MAPK)/extracellular si
111 an extremely potent allosteric inhibitor of mitogen-activated protein kinase (MAPK)/extracellular-si
112 f the JCI, Yokota et al. reveal that the p38 mitogen-activated protein kinase (MAPK)/IRE1alpha/XBP1 a
113 n of oncogenic Ras(V12) activates downstream mitogen-activated protein kinase (MEK-ERK) signaling to
114 Increases in the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and decrease
115 NASH development and the involvement of p38 mitogen-activated protein kinase (p38) activated by neut
116 CyTP genes is mediated by the conserved p38 mitogen-activated protein kinase (p38-MAPK) pathway.
117 Signal transduction pathways mediated by p38 mitogen-activated protein kinase (p38MAPK), extracellula
118 tly driven by genetic alterations in the RAS-mitogen-activated protein kinase (RAS/MAPK) pathway yet
119 hed in synaptic function and converge on Ras/mitogen-activated protein kinase (Ras/MAPK) signaling.
120 ovo missense variants in MAPK1, encoding the mitogen-activated protein kinase 1 (i.e., extracellular
121 l myenteric plexi and phosphorylation (p) of mitogen-activated protein kinase 1 (MAPK1) in the enteri
122 e P (SP), S100beta, GFAP, and phosphorylated mitogen-activated protein kinase 1 (pERK) were assessed
123 proteins, auxin stabilizes IAA33 protein via MITOGEN-ACTIVATED PROTEIN KINASE 14 (MPK14) and does not
124 e use Nicotiana attenuata plants silenced in mitogen-activated protein kinase 4 (irMPK4) - with low w
126 elated prognostic proteins, particularly the mitogen-activated protein kinase 6, probable protein pho
127 samples and xenograft mouse models revealed mitogen-activated protein kinase 7/matrix metallopeptida
128 beta-arrestin-dependent signaling responses, mitogen-activated protein kinase [i.e., extracellular si
129 nd extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase activation at the human
132 for Ptpn6 in the negative regulation of p38 mitogen-activated protein kinase activation to control t
133 es G protein-coupled calcium ion signals and mitogen-activated protein kinase activity, and that its
134 ntracellular signaling pathways, such as the mitogen-activated protein kinase and AKT signaling casca
136 e ability of pharmacologic inhibition of the mitogen-activated protein kinase and PI3'K pathways to i
137 is revealed significant up-regulation of the mitogen-activated protein kinase and transforming growth
138 ulation in endothelial cells via JNK and p38 mitogen-activated protein kinase but not NF-kappaB.
139 identified OsPT8 as an interactor of a rice mitogen-activated protein kinase BWMK1, which is a regul
140 -X-C motif chemokine ligand 12 activates the mitogen-activated protein kinase extracellular-signal-re
141 preceded by decreased phosphorylation of p38 mitogen-activated protein kinase in HMuSC treated with C
142 eased proliferation and dysregulation of p38 mitogen-activated protein kinase in satellite cells comm
144 ed by the accumulation of phosphorylated p38 mitogen-activated protein kinase in the nucleus, which d
146 vides a rationale for combining pan-ERBB and mitogen-activated protein kinase inhibitors as a therape
147 c target of rapamycin complex 1 (mTORC1) and mitogen-activated protein kinase interacting kinase (MNK
149 tion of lipid A limits the activation of the mitogen-activated protein kinase Jun N-terminal protein
150 tor of transcription (STAT) (ruxolitinib) or mitogen-activated protein kinase kinase (MEK) (trametini
151 ines had IC(50) values less than 7 nM to the mitogen-activated protein kinase kinase (MEK) 1/2 inhibi
152 mutational status, and response to B-Raf and mitogen-activated protein kinase kinase (MEK) inhibition
155 therapy with B-Raf proto-oncogene (BRAF) and mitogen-activated protein kinase kinase (MEK) inhibitors
156 e/threonine-specific protein kinases (pRAF), mitogen-activated protein kinase kinase (pMEK), protein
159 ffector PI3K but instead require active MEK (mitogen-activated protein kinase kinase 1) signaling.
161 ivated protein kinase kinase kinase 3)-MEK5 (mitogen-activated protein kinase kinase 5)-ERK5 (extrace
162 found REX1 to bind to the promoter region of mitogen-activated protein kinase kinase 6 (MKK6), thereb
164 gamma) intraperitoneally for 3 d or with the mitogen-activated protein kinase kinase inhibitor selume
165 2 depletion in ECs elicited increased MEKK3 (mitogen-activated protein kinase kinase kinase 3)-MEK5 (
166 restingly, we observed that knockdown of the mitogen-activated protein kinase kinase kinase 4 (MAP3K4
167 Among the differentially expressed kinases, mitogen-activated protein kinase kinase kinase kinase 4
170 r their mechanisms of action using selective mitogen-activated protein kinase kinase MEK1/2, MEK5, an
171 s pyruvate dehydrogenase kinase 1, Akt, Raf, mitogen-activated protein kinase kinase, and ERK1/2.
174 -in-class von Hippel-Lindau (VHL)-recruiting mitogen-activated protein kinase kinases 1 and 2 (MEK1/2
177 rticularly, we found that alterations of the mitogen-activated protein kinase pathway (KRAS and NRAS
179 ward beta-arrestin recruitment and increased mitogen-activated protein kinase pathway activation.
180 llular signal-regulated protein kinase (ERK) mitogen-activated protein kinase pathway and that ERK in
181 ted, at least in part, via activation of the mitogen-activated protein kinase pathway following calci
182 M) in 60%, and phosphatidylinositol 3-kinase/mitogen-activated protein kinase pathway genes (eg, ERBB
183 phosphorylation of focal adhesion kinase and mitogen-activated protein kinase pathway leading to enha
184 th the extracellular signal-regulated kinase mitogen-activated protein kinase pathway that provides a
185 ectively, these findings demonstrate the ERK mitogen-activated protein kinase pathway to be integrall
186 ibed the paradoxical triggering of the human mitogen-activated protein kinase pathway when a small-mo
187 extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase pathway, consistent wit
188 ransducer and activator of transcription and mitogen-activated protein kinase pathways to regulate ce
191 ofin (ARN), an antirheumatic drug, to induce mitogen-activated protein kinase phosphatase (MKP)-1 exp
192 bacterium tuberculosis (Mtb) by facilitating mitogen-activated protein kinase phosphatase 1 (MKP-1)-d
193 ed with a pharmacological agent that induces mitogen-activated protein kinase phosphatase have potent
194 past several years has elucidated a role for mitogen-activated protein kinase phosphatase to regulate
197 otein kinase C, cyclin-dependent kinase, and mitogen-activated protein kinase showed increased phosph
198 nger NHFs, PDAC cells exhibited increases in mitogen-activated protein kinase signaling and cellular
200 folded protein response, glycolysis, and the mitogen-activated protein kinase signaling cascade.
201 d causal link between LZTR1 dysfunction, RAS-mitogen-activated protein kinase signaling hyperactivity
202 terations in genes whose products are in the mitogen-activated protein kinase signaling pathway and a
203 g mechanism is a gain-of-function of the RAS-mitogen-activated protein kinase signaling pathway.
204 roteins in receptor tyrosine kinase, RAS, or mitogen-activated protein kinase signaling pathways.
205 se 4 (MAP3K4) gene, which contributes to p38 mitogen-activated protein kinase signaling, sensitized c
209 ignalling, cell cycle regulatory signalling, mitogen-activated protein kinase signalling and pathways
211 of BRD4 is controlled, in part, by p38 MAPK (mitogen-activated protein kinase) and provide evidence o
212 K (RAS-extracellular signal-regulated kinase/mitogen-activated protein kinase) pathway integrates gro
213 ion of 101 gene transcripts, including MAPK (mitogen-activated protein kinase) signaling targets, HOP
214 s extracellular signal-regulated kinase 1/2, mitogen-activated protein kinase, and Src, shown by immu
217 eltaPMN) neutrophils displayed increased p38 mitogen-activated protein kinase-dependent Ripk1-indepen
218 al-related kinase 1/2 (pERK1/2), a marker of mitogen-activated protein kinase-ERK signal transduction
222 ed that the rapidly accelerated fibrosarcoma/mitogen-activated protein kinase/extracellular signal-re
223 al stem-like (MSL) lineage downregulates the mitogen-activated protein kinase/extracellular signal-re
224 otein expression that was attenuated by MEK (mitogen-activated protein kinase/extracellular signal-re
225 al growth factor receptor (EGFR), as EGFR or mitogen-activated protein kinase/extracellular signal-re
227 ciated protein kinase 70 (ZAP-70), and three mitogen-activated protein kinases (extracellular signal-
228 cular chondrocytes via the inhibition of p38 mitogen-activated protein kinases (MAPK) and increasing
229 transcription factors are phosphorylated by mitogen-activated protein kinases (MAPK) in their transa
232 ar signal-regulated kinase 1 and 2 (ERK1/2), mitogen-activated protein kinases (MAPK), leading to unc
233 relatively rare member of the JNK family of mitogen-activated protein kinases (MAPK), phosphorylates
234 ral detail on docking interactions involving mitogen-activated protein kinases (MAPKs) and their subs
235 s diverse kinase pathways, which include the mitogen-activated protein kinases (MAPKs) ERK and p38, t
237 t/MKP-1 pathway results in the inhibition of mitogen-activated protein kinases (MAPKs) JNK and p38.
239 we show that the rapid activation of clade-A mitogen-activated protein kinases (MAPKs) MPK3 and MPK6
243 (DUSP1), an endogenous negative regulator of mitogen-activated protein kinases (MAPKs), resulting in
245 nd ROS signals compromised the activation of mitogen-activated protein kinases (MPKs) 1/2 in leaves.
246 sion of sequestosome 1 (p62) and phospho-p38 mitogen-activated protein kinases (p-p38) showed a signi
247 were not affected in PAMP/DAMP activation of mitogen-activated protein kinases and expression of the
250 lular signal-regulated kinase), JNK, and p38 mitogen-activated protein kinases as well as NFkappaB (n
252 ptation and stress tolerance, and in several mitogen-activated protein kinases signaling pathways inc
253 of reactive oxygen species and activation of mitogen-activated protein kinases upon exposure to flg22
254 ing a dual-specificity phosphatase targeting mitogen-activated protein kinases, as a type 2 diabetes
256 HAI1 or by HAI1-regulated kinases including mitogen-activated protein kinases, sucrose non-fermentin
258 vers of healthy ducks and was upregulated in mitogen-activated splenic lymphocytes as well as in sple
262 oliferative response to glucose, a beta-cell mitogen and key regulator of beta-cell mass in response
263 ons of patients with idiopathic PAH and is a mitogen and migratory stimulus for pulmonary artery smoo
264 the hexosamine D-mannosamine (ManN) as an EC mitogen and survival factor for bovine and human microva
265 tection circuit linking responses to the Shh mitogen and the extracellular matrix to control cerebell
267 e mice harboring an inactivating mutation of mitogen- and stress-activated protein kinase 1 (MSK1), a
268 cts of experience depend on an enzyme called mitogen- and stress-activated protein kinase 1 (MSK1).
269 Stimulation of the MAPK pathway results in mitogen- and stress-activated protein kinase 1/2 (MSK1/2
271 the RAF-MEK-ERK pathway, the first described mitogen-associated protein kinase (MAPK) cascade, mediat
273 trary to the textbook model that cells sense mitogen availability only in the G(1) cell cycle phase,
274 ork of a minimal theoretical model based on "mitogen competition." We propose that this model provide
275 The level of ubiquitinated ELK-1 rises in mitogen-deprived cells and falls upon mitogen stimulatio
277 the integrator that proportionally converts mitogen history into corresponding levels of cyclin D in
279 is overexpressed in > 60% of TNBCs, drives a mitogen-independent G1/S cell cycle transition through c
281 d hepatocytes responded similarly to hepatic mitogens, indicating that proliferation kinetics are unr
282 creased immune responsiveness with decreased mitogen-induced upregulation of IFN-gamma, TNF, IL-6, CX
283 rexpression potently increased the levels of mitogen-inducible gene 6 (MIG6), which inhibits EGFR and
284 through C-terminal cross-linking of the tear mitogen lacritin, leading to significant loss of lacriti
285 ive of a change resulting from exposure to a mitogen, ligand, or antigen for which it is specific, as
286 cal enterotoxin B and Mycoplasma arthritidis mitogen, on influenza virus- and/or cytomegalovirus-spec
289 ent hysteresis, in CDK4/6 activity following mitogen removal that sustains Rb hyperphosphorylation, d
292 r cell cycle and that even a 1-hour lapse in mitogen signaling can influence cell proliferation more
293 his study uncovers a mechanism whereby serum mitogen signaling regulates Rabin8 preciliary traffickin
294 t baseline and following mycobacterial Ag or mitogen stimulation in individuals with LTB with (Strong
298 15/19 functions as a profibrotic mediator or mitogen to HSCs and increased BAs in Fgf15(-/-) mice lea
299 not act as a direct profibrotic mediator or mitogen to HSCs in our models, and the protection agains