ライフサイエンスコーパス: MEK

1 MEK inhibition during DOX treatment simultaneously enhan

2 MEK inhibition during treatment enhanced the late ERK ac

3 MEK inhibition was sufficient to promote lamellipodia fo

4 MEK inhibitor and digitoxin do not induce cell death in

5 MEK inhibitor and digitoxin together cause intracellular

6 MEK is activated by HSR and contributes to the regulatio

7 MEK signaling downstream of RAS leads to phosphorylation

8 inhibitor with other targeted agents (eg, a MEK inhibitor and/or an anti-CD20 monoclonal antibody).

9 and induced steroid resistance of ILC2s in a MEK- and STAT5-dependent manner.

10 eted therapeutically by the combination of a MEK inhibitor with PI3K or cyclin-dependent kinase 4/6 i

11 le in this regulation, and the addition of a MEK/Erk pathway inhibitor significantly enhanced the PD-

12 a(2+)-sensitive PYK2 inhibitor, and U0126, a MEK/ERK inhibitor.

13 perproliferative skin changes improve when a MEK inhibitor is co-administered, as it blocks paradoxic

14 Accordingly, MEK-ERK depletion decreased EZH2 expression in cells har

15 d M1R, beta-arrestin scaffolds and activates MEK-dependent ERK.

16 BRAF(V600E) melanoma cell lines, activating MEK mutations drive resistance and contribute to subopti

17 gly, we discovered that intrinsically active MEK variants can both increase and reduce the levels of

18 We found that active MEK significantly alters TDP-43-regulated splicing and t

19 esis in concert with mortalin, which affects MEK/ERK activity in tumor cells.

20 orylates ERK in the absence of FSH, allowing MEK-phosphorylated ERK to accumulate in the presence of

21 ity to subsequent treatment with alternative MEK inhibitor-based combination therapies.

22 f oncogenic transcription factor FOXM1 in an MEK/ERK-dependent manner.

23 Lastly, combination of AURKA and MEK inhibitors induces a deleterious effect on mutant KR

24 n factors also require extracellular BMP and MEK signalling to cooperatively effectuate reprogramming

25 Inhibition of BRAF and MEK in combination with the A2A adenosine receptor provi

26 RAF inhibition (BRAFi) and combined BRAF and MEK inhibition (BRAFi and MEKi) therapies have markedly

27 llowing simultaneous treatment with BRAF and MEK inhibitors aligned to standard-of-care combination t

28 s on purified HCL cells proved that BRAF and MEK inhibitors can induce marked dephosphorylation of ME

29 ical for resistance of melanomas to BRAF and MEK inhibitors due to emergence of heterogeneous subpopu

30 to and confer drug tolerance toward BRAF and MEK inhibitors early during treatment.

31 Specific BRAF and MEK inhibitors have shown clinical efficacy in patients

32 Dual MAPK pathway inhibition with BRAF and MEK inhibitors in BRAF(V600E)-mutant NSCLC might improve

33 B1) oncogene with a combination of BRAF and MEK inhibitors is plagued by the development of drug res

34 Combinatorial treatment using BRAF and MEK inhibitors reversed the developmental effects induce

35 gy when evaluating a combination of BRAF and MEK inhibitors versus a combination of BRAF and PI3K inh

36 elapse from combined treatment with BRAF and MEK inhibitors.

37 APK pathway and sensitized cells to BRAF and MEK inhibitors.

38 resistant cells, PAKs phosphorylate CRAF and MEK to reactivate ERK.

39 o received BRAF inhibitor dabrafenib (D) and MEK inhibitor trametinib (T) combination therapy versus

40 cancer and modulate competitive fitness and MEK dependency.

41 ere treated with inhibitors of both FLT3 and MEK in combination, ERK reactivation was abrogated and a

42 AF inhibition, exhibiting reduced growth and MEK/ERK activity during inhibitor treatment.

43 e blocked by combined inhibition of Her2 and MEK.

44 adhesion molecules through the NF-kappaB and MEK/Erk pathways, in particular by preventing the protea

45 esponses to combinations of AKT (MK2206) and MEK (GSK1120212; trametinib) inhibitors, in the presence

46 se studies demonstrate that combined MNK and MEK suppression represents a promising therapeutic strat

47 fering RNAs targeting BDNF or TrkB mRNA, and MEK/ERK (U0126) or PI3 kinase/Akt (PI828) inhibitors.

48 15 robustly stimulated the PI3K/Akt/mTOR and MEK/ERK pathways in CD56bright compared with CD56dim NK

49 mechanistic target of rapamycin (mTOR), and MEK/ERK pathways in the regulation of RPE phagocytosis,

50 5.1 and pharmacologic inhibition of PI3K and MEK also produced significant but smaller effects.

51 Inhibition of PI3K and MEK in combination or of CDK2 by their respective small-

52 Moreover, combining PI3K and MEK inhibition was effective against imatinib-resistant

53 In UN-KC-6141 cells, PI3K and MEK signaling increased expression of KLF5; a high level

54 d that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effe

55 DNA binding 3, and pSTAT3 but not pSTAT5 and MEK.

56 While targeting upstream nodes with RAF and MEK inhibitors has proven effective clinically, resistan

57 ion has limited the effectiveness of Raf and MEK inhibitors in RAS-mutant cancers.

58 To determine if RAF and MEK inhibitors together can overcome single-agent resist

59 blastoma cells, inhibition of JAK2/STAT3 and MEK/ERK/1/2 by ruxolitinib and trametinib potentiated tu

60 endent on the coactivation of JAK2/STAT3 and MEK/ERK1/2 in neuroblastoma cells.

61 receptor activation, new BDNF synthesis, and MEK/ERK signaling (the Q pathway).

62 ing a partial divergence between TGFbeta and MEK/ERK in early carcinogenesis.

63 t, everolimus, lapatinib or trastuzumab, and MEK inhibitor in patients with advanced sarcoma.

64 p9x and therapeutic combination of Usp9x and MEK inhibitor fully suppressed melanoma growth.

65 aive mouse embryonic stem cell (ESC) WNT and MEK/ERK signal inhibition (2i) culture.

66 Our study also introduces the FDA-approved MEK antagonist trametinib as an effective inhibitor for

67 particular, we found that recently approved MEK inhibitors displayed potent suppressive effects on T

68 ng of multiple nodes in the pathway, such as MEK and ERK, offers the prospect of enhanced efficacy as

69 marked synergy in tumor cell killing between MEK inhibitors (trametinib) and retinoids (isotretinoin)

70 anoparticles (PBNPs) as PTT agents, to block MEK activity and simultaneously ablate MPNSTs.

71 ially the regulatory effects of BCL6 on both MEK-ERK (mitogen-activated protein/extracellular signal-

72 ive migration of which acutely requires both MEK and Rac1 signaling.

73 phosphorylation and activation of KSR-bound MEK (mitogen-activated protein kinase kinase).

74 ts the longest follow-up to date with BRAF + MEK inhibitor combination therapy in BRAF V600-mutant MM

75 l growth factor receptor activation of BRAF, MEK, and AKT; HUH7 cells with MAN2A1-FER knockout had si

76 ene deletion screens in the setting of BRAF, MEK, EGFR, and ALK inhibition.

77 NFE2L2/NRF2, modulated the response to BRAF, MEK, EGFR, and ALK inhibition in BRAF-, NRAS-, KRAS-, EG

78 m cellular changes induced by Hsp90 and BRAF-MEK-targeted therapies in melanoma cells with potential

79 ommon synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction cascade.

80 Targeted therapies specific to the BRAF-MEK-ERK signaling pathway have shown great promise in th

81 BRAF/MEK inhibitors only show a temporary benefit due to rapi

82 BRAF/MEK was associated with higher ORR (OR, 2.00; 95% CrI, 1

83 no significant difference in OS between BRAF/MEK and PD-1 (HR, 1.02; 95% credible interval [CrI], 0.7

84 Both BRAF/MEK and PD-1 were associated with improved OS benefit co

85 nflammatory niches counteracts combined BRAF/MEK (MAPK/extracellular signal-regulated kinase kinase)

86 However, even BRAF/MEK inhibitor combination therapy has failed to offer a

87 lysis showed a significant advantage of BRAF/MEK compared with all other treatment strategies for PFS

88 to the ongoing efforts of simultaneous BRAF/MEK inhibition as a promising strategy in ECD.

89 A better understanding of the BRAF/MEK/ERK pathway and the B-cell signaling pathway has all

90 even further in cell lines resistant to BRAF/MEK inhibitors.

91 Compared with other treatments, BRAF/MEK and PD-1 inhibition significantly improved OS.

92 on Thr(202)/Tyr(204) was PKA-dependent, but MEK(Ser(217)/Ser(221)) phosphorylation was not regulated

93 Similar effects were elicited by MEK and ERK inhibitors but not AKT or Rac inhibitors.

94 mutations, EZH2 expression was modulated by MEK-ERK and PI3K/AKT signaling, respectively.

95 TDP-43 dual phosphorylation by MEK, at threonine 153 and tyrosine 155 (p-T153/Y155), wa

96 2 and Bcl-xL to Mcl-1, an effect reversed by MEK inhibition.

97 Therapeutic strategies that combine MEK inhibitors with agents that target apoptotic pathway

98 in a panel of cancer cell lines and combined MEK/mTOR inhibition displayed highly synergistic pharmac

99 file modification(s) in response to combined MEK/mTOR inhibition in PTEN-loss contexts and identified

100 While combined MEK and mTORC1 suppression causes regression of NF1-defi

101 Combining MEK inhibition with anti-programmed death-ligand 1 (PD-L

102 Although combining MEK inhibition with T-cell-directed immunotherapy might

103 We investigated combining MEK and MDM2 inhibitors as a potential treatment strateg

104 tential promise and limitations of combining MEK and MDM2 inhibitors for treatment of KRAS mutant NSC

105 s8 (to suppress the Sos1-Abi1-Eps8 complex), MEK inhibition had no effect on RhoGTPase activity and d

106 enic regulation of c-Fos through controlling MEK/ERK.

107 EGFR tyrosine kinase activity or downstream MEK activity attenuated the fibrotic phenotype.

108 s resulting in superior therapeutic efficacy.MEK inhibition in breast cancer is associated with incre

109 Moreover, dual inhibition of the EGFR-MEK-ERK pathway in RAS mutant organoids induced a transi

110 ntrast, pharmacological inhibition of either MEK or Rac1 signaling acutely blocked both cell migratio

111 on in breast cancer cells increased MEK-EMT (MEK-epithelial-to-mesenchymal transition) signaling, tra

112 nges caused by mutations in MAP2K1 (encoding MEK), a core component of the Ras pathway that is mutate

113 23 cells were reported to exhibit robust ERK/MEK activity concomitant with reduced growth sensitivity

114 al examination and OCT were used to evaluate MEK inhibitor-associated subretinal fluid.

115 ion were mediated through activation of FGFR/MEK/Erk1/2 signaling and downregulation of bone morphoge

116 he authors show that TILs activity following MEK inhibition can be enhanced by agonist immunotherapy

117 For MEK and EGFR inhibitors, discriminative power was more t

118 selective inhibitors for TRPV4 and also for MEK, the kinase upstream of ERK, suggesting that calcium

119 high clonal self-renewal, independence from MEK/ERK signaling, dependence on JAK/STAT3 and BMP4 sign

120 pathway in some aspects of T cell function, MEK-targeted agents can be compatible with T-cell-depend

121 Furthermore, MEK inhibition abrogated RCP/alpha5beta1/EGFR1-driven in

122 uritogenic cAMP sensor-Rapgef2 --> B-Raf --> MEK --> ERK pathway mediating neuritogenesis in NS-1 cel

123 , by providing a more incisive view into how MEK inhibitors may act against tumors, our findings expa

124 rexpression in breast cancer cells increased MEK-EMT (MEK-epithelial-to-mesenchymal transition) signa

125 ons from closed to open conformation induced MEK-ERK1/2-dependent Tyr-447 phosphorylation.

126 and demonstrates that a simple intervention (MEK-inhibition) could be of therapeutic benefit in preve

127 f targeted therapy that has been explored is MEK inhibition.

128 cetaldehyde (MeCHO) and methyl ethyl ketone (MEK) among others.

129 slurry-borne odorants ((methyl ethyl ketone (MEK), isobutyl alcohol (i-BuAl), benzene (B), toluene (T

130 f a mitogen-activated protein kinase kinase (MEK) inhibitor reverses the benefit of vemurafenib-accel

131 the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib + docetaxel with docetaxel al

132 the Mitogen-activated protein kinase kinase (MEK) inhibitor, selumetinib, for 14 consecutive days.

133 ing mitogen-activated protein kinase kinase (MEK) inhibitors.

134 Mitogen-activated protein kinase kinase (MEK) mutations are found in primary melanomas and freque

135 ced mitogen-activated protein kinase kinase (MEK), c-Fos, inhibitor of DNA binding 3, phosphorylated

136 xtracellular signal-regulated kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) scaffol

137 an oral selective inhibitor of MAPK kinase (MEK) 1 and 2, in children who had neurofibromatosis type

138 wed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and patient samples.

139 ogen-activated protein kinase (MAPK) kinase (MEK) can induce regression of tumors bearing activating

140 ogen-activated protein kinase (MAPK) kinase (MEK) inhibitors has become more common in the treatment

141 ivation of mitogen-activated protein kinase (MEK)-extracellular signal-regulated protein kinase 1/2 s

142 otein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited inductio

143 m flux that led to activation of the kinases MEK-ERK.

144 loop's TEY motif, catalyzed by MAPK kinases (MEKs).

145 gen-activated protein kinase (MAPK) kinases (MEKs).

146 y is a key feature in cancer, high-magnitude MEK/ERK activity can paradoxically induce growth inhibit

147 In melanoma, MEK inhibitor reduces ERK phosphorylation, while digitox

148 additional mechanisms may exist to modulate MEK/ERK activity in favor of tumor cell proliferation.

149 tain KRAS and BRAF tumor cells by modulating MEK/ERK activity.

150 ilizing a genetic approach to control mutant MEK expression in vivo, we were able to induce tumor reg

151 inhibitor ZSTK474 and the ATP-noncompetitive MEK inhibitor PD0325901 is described.

152 ptional activation of beta-catenin and NRF2, MEK-inhibitor sensitivity, and KRAS dependency.

153 sporter 1 by TGF-beta involves activation of MEK and mammalian target of rapamycin complex 2 pathways

154 quires endocytosis, the kinase activities of MEK-ERK and CK2, and the presence of KSR1.

155 decreases AXL expression and the activity of MEK-ERK and S6K-RPS6 cascades but also displays a potent

156 of BRAF(V600E) Accordingly, the addition of MEK-inhibiting trametinib to BRAF-inhibiting dabrafenib

157 Tyr-447) we demonstrated the contribution of MEK/ERK-dependent phosphorylation, which is regulated by

158 itors can induce marked dephosphorylation of MEK/ERK, silencing of RAF-MEK-ERK pathway transcriptiona

159 Although deregulation of MEK/extracellular signal-regulated kinase (ERK) activity

160 kinase signaling and the additive effects of MEK and BRAF mutations are counterproductive.

161 antibodies can rescue the adverse effects of MEK inhibition on T cells in both mouse and human T cell

162 o overcome the T-cell-suppressive effects of MEK inhibitors and illustrates how to reconcile the defi

163 Finally, conditional induction of MEK activity was sufficient to induce collective cell mi

164 Inhibition of MEK (mitogen-activated protein kinase (MAPK)/ERK kinase)

165 versed by clinically available inhibitors of MEK and STAT5.

166 ay promote the migration and invasiveness of MEK-inhibited mutant NRAS melanoma, especially in respon

167 und state of pluripotency in the presence of MEK and GSK3 inhibitors.

168 We report here that TDP-43 is a substrate of MEK, a central kinase in the MAPK/ERK signaling pathway.

169 resulted in a dose-dependent suppression of MEK/ERK activity (Figure 3I).

170 e themselves at least partially dependent on MEK activity.

171 ntly, resistance of melanomas to BRAF and/or MEK inhibitors is associated with increased CD20 and IGF

172 Patients with previous BRAF or MEK inhibitor treatment were ineligible.

173 hese data suggest that resistance to BRAF or MEK inhibitors is probably inevitable, and novel therape

174 Notably, Ets-1 is induced by BRAF or MEK kinase inhibition, resulting in increased NRAS expre

175 least 1 intervention was a targeted (BRAF or MEK) or an immune checkpoint (cytotoxic T-lymphocyte-ass

176 by exploitable dependencies on BCR, mTOR, or MEK signaling and associated with mutations, gene expres

177 that can be blocked by inhibitors of PAK or MEK.

178 gest a potential negative impact of B-Raf or MEK inhibition on TRAIL- or DR5-mediated anticancer ther

179 nt of cancer cell lines with either B-Raf or MEK inhibitors attenuated or abolished cellular apoptoti

180 to be effective anticancer agents, B-Raf or MEK inhibitors have also been associated with early tumo

181 ditioned media did not alter CM spreading or MEK-ERK activation.

182 ized therapeutic approaches targeting Src or MEK in ERalpha-36-positive patients.

183 atter further potentiated by concurrent PI3K/MEK inhibition, consistent with a role for RNF157 in the

184 The combination of pimasertib (MEK inhibitor) and SAR405838 (MDM2 inhibitor) was synerg

185 ed c-Fos expression through repressing a PKC/MEK/ERK/ELK-1 signaling pathway.

186 beta-arrestin-dependent mechanism, promotes MEK-dependent beta-arrestin2 phosphorylation at Thr(383)

187 M mediates crosstalk between the prosurvival MEK/ERK and AKT/mTOR pathways.

188 ncrease in the [Ca(2+)]c to trigger the PYK2/MEK/ERK signalling pathway as a positive feedback mechan

189 was largely abolished by inhibition of RAC1/MEK/ERK pathway.

190 lpha, rapidly accelerated fibrosarcoma (RAF)/MEK/ERK, and PI3K/AKT signaling pathways cooperatively r

191 feedback loop that encompasses RAS and RAF, MEK, and ERK that inhibits SOS via phosphorylation.

192 Concurrent targeting of the RAF, MEK and ERK kinases, however, imposed a sufficiently hig

193 CK2alpha-mediated RAF-MEK kinase inhibitor resistance was tightly linked to it

194 phosphorylation of MEK/ERK, silencing of RAF-MEK-ERK pathway transcriptional output, loss of the HCL-

195 AF activation, and inhibition of the RAS-RAF-MEK pathway.

196 own functional annotation (e.g., the RAS-RAF-MEK-ERK cascade).

197 harbored lesions in elements of the RAS-RAF-MEK-ERK pathway.

198 acts as a positive modulator of the RAS-RAF-MEK-ERK signalling cascade by favouring stable RAF1 inte

199 ctive CK2alpha bound equally well to the RAF-MEK-ERK scaffold kinase suppressor of Ras 1 (KSR1) sugge

200 By aberrantly activating the RAF-MEK-ERK signaling pathway, BRAF-V600E shapes key biologi

201 ds to the constitutive activation of the RAF-MEK-extracellular signal-regulated kinase (ERK) signalin

202 activated HSCs, RAS signaling shifts to RAF-MEK-ERK.

203 ting in the hyperactivation of mTOR- and Raf/MEK/MAPK-dependent signaling that stimulates tumor cell

204 current work sought to address whether B-Raf/MEK/ERK inhibition and the consequent suppression of DR5

205 fically affects the cAMP signal to the B-Raf/MEK/ERK pathway and regulates AVP-induced proliferation

206 Inhibition of B-Raf/MEK/ERK signaling is an effective therapeutic strategy a

207 previously demonstrated that activated B-Raf/MEK/ERK signaling positively regulates DR5 expression.

208 ndings clearly show that inhibition of B-Raf/MEK/ERK signaling suppresses DR5 expression and impairs

209 cells; this effect is dependent on Ras/c-Raf/MEK/ERK signaling activation.

210 n could increase the feasibility of dual RAF/MEK inhibition to overcome sorafenib treatment escape in

211 ncogenic Ras-driven proliferation: MAPK (Raf/MEK/ERK) and PI3Kalpha/Akt/mTOR.

212 vely, which we use to tune the levels of Raf/MEK/ERK signaling.

213 ence of cross-activation between the Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways via a RasPIK3IP1PI3K

214 tivity of EGFRvIII and activates the RAS/RAF/MEK/ERK and STAT3 pathways.

215 activation negatively regulates the Ras/Raf/MEK/ERK pathway and activates GSK3 to modulate Mcl-1 pho

216 route for the phospho-inhibition of Ras/Raf/MEK/ERK pathway signaling that is mediated by the stress

217 present an essential node within the RAS/RAF/MEK/ERK signaling cascade that is commonly activated by

218 t act as downstream effectors of the Ras/Raf/MEK/ERK signaling pathway.

219 ally used multi-kinase inhibitors of RAS/RAF/MEK/ERK signaling, including regorafenib and sorafenib.

220 Aberrant signaling through the Raf/MEK/ERK (ERK/MAPK) pathway causes pathology in a family

221 changes are induced by activation of the Raf/MEK/ERK kinase cascade, culminating in upregulation of C

222 in NRAS/KRAS, upstream regulators of the RAF/MEK/ERK pathway, have been reported in pulmonary, but no

223 th Raf and reduces signaling through the Raf/MEK/ERK pathway.

224 c mutations in the genes involved in the RAF/MEK/extracellular signal-regulated kinase (ERK) signalin

225 an unanticipated feedback loop, whereby Raf/MEK/ERK signalling maintains suppression of Rac1 by inhi

226 t that paradoxical activation of the RAF-RAS-MEK-ERK pathway by BRAF inhibitors when applied to BRAF(

227 associated with somatic mutations in the RAS-MEK-ERK pathway such as BRAF(V600E), suggests a possible

228 kinase (MAPK) cascade, also known as the RAS-MEK-extracellular signal-related kinase (ERK1/2) pathway

229 hoinositide3-kinase/Akt pathway, but not Ras/MEK pathway, controls MUCL1 expression downstream of HER

230 F receptor (VEGFR) signaling through the Ras/MEK/ERK pathway.

231 ) phosphorylation was not regulated; rather, MEK was already active.

232 uid foci in 50 eyes of 25 patients receiving MEK inhibitors for treatment of their metastatic cancer,

233 , we demonstrated that mortalin can regulate MEK/ERK activity via protein phosphatase 1alpha (PP1alph

234 MAP3K8 (COT/TPL2) directly regulated MEK/ERK phosphorylation, as the treatment of RPMI-7951 c

235 In this series, MEK inhibitors did not cause irreversible loss of vision

236 We also demonstrate that MEK inhibitor-loaded nanoparticles have the capacity to

237 We further demonstrate that MEK/ERK and PI3K-C2beta are required for PCa cell invasi

238 We show here that MEK inhibition did profoundly block naive CD8(+) T cell

239 lymphocytes to the tumor, here we show that MEK inhibition adversely affects early onset T-cell effe

240 t oppose invasive migration, suggesting that MEK-ERK signalling suppresses the Rac-activating Sos1-Ab

241 The MEK inhibitor trametinib, the Janus kinase-STAT inhibito

242 Although the MEK inhibitor selumetinib transiently inhibited ERK sign

243 PI3K inhibitor pictilisib (GDC-0941) and the MEK inhibitor cobimetinib (GDC-0973) suppresses cell pro

244 by morphine, while the inactive PP3, and the MEK inhibitor, SL327, had no effect.

245 The aim of this trial was to block the MEK and PI3K/AKT pathways downstream of the KRAS protein

246 logical inhibition of IFI6 expression by the MEK inhibitor trametinib, when combined with DNA replica

247 We combine the MEK inhibitor, PD-0325901 (PD901), with Prussian blue na

248 M survival signaling pathways, including the MEK-extracellular signal-regulated kinase pathway.

249 Dual targeting of the MEK and PI3K/AKT pathways downstream of KRAS by selumeti

250 med to assess the efficacy and safety of the MEK inhibitor binimetinib versus that of dacarbazine in

251 The addition of the MEK inhibitor PD-325901 or binimetinib further decreased

252 activation, but sustained activation of the MEK-ERK pathway in a TSC1/TSC2/TBC1D7 protein complex an

253 Targeting of the MEK-ERK pathway was effective in fusion-positive Schwann

254 ERK1/2, JNK and PI3K pathways, but only the MEK inhibitor UO126 reduced niacin-mediated inhibition o

255 yr phosphatase inhibitor (NSC 87877), or the MEK inhibitor PD98059 blocked FSH-dependent ERK(Thr(202)

256 ats with PDGF-B neutralizing aptamers or the MEK/ERK inhibitor U0126.

257 selective inhibitor PKA inhibitor (PKI), the MEK inhibitor PD98059, or the ribosomal S6 kinase-2 (RSK

258 with the BRAF inhibitor dabrafenib plus the MEK inhibitor trametinib improved survival in patients w

259 signaling, which subsequently rebounded, the MEK inhibitor CKI suppressed ERK signaling in a sustaine

260 Targeting MUC1-C suppresses the MEK --> ERK and PI3K --> AKT pathways, and in turn desta

261 Here, we show that the MEK inhibitor trametinib abrogates cytokine-driven expan

262 Meanwhile, we discovered that the MEK/Erk signaling pathway played a significant role in t

263 noparticles to co-deliver sorafenib with the MEK inhibitor AZD6244 in HCC.

264 astatic cancer undergoing treatment with the MEK inhibitor binimetinib in 1 of 4 clinical trials.

265 y participants undergoing treatment with the MEK inhibitor binimetinib.

266 enesis in Kras(G12D) "knockin" mice with the MEK inhibitor PD0325901 (PD901).

267 sunitinib alone and in combination with the MEK inhibitor trametinib to retard MPNST progression in

268 elanoma to demonstrate that several of these MEK mutants promote the development, growth and maintena

269 e a main regulator of FOXM1 activity through MEK-dependent physical regulation during the cell cycle.

270 of KRAS- or BRAF-mutant lung cancer cells to MEK inhibition.

271 xiliary negative feedback loops, from ERK to MEK and RAF, placed downstream of the positive feedback,

272 nd Akt activation, and are hypersensitive to MEK inhibition.

273 growth of PCa cells that were insensitive to MEK inhibition.

274 ic inactivation renders T-ALL insensitive to MEK inhibitors in both mouse and human cell lines.

275 ept and overcome the intrinsic resistance to MEK inhibition based on ERBB3 upregulation.

276 bination predicted to overcome resistance to MEK inhibitors by coblockade of GSK3, which was not foun

277 Lung cancer cells resistant to MEK inhibition become highly sensitive upon loss of ATM

278 dominant clone and rendered it sensitive to MEK inhibition.

279 hibited marked variability in sensitivity to MEK inhibition, which significantly impacted sensitivity

280 modulates clonal fitness and sensitivity to MEK inhibitors in a model of Kras(G12D) mutant acute mye

281 dabrafenib (BRAF inhibitor), and trametinib (MEK inhibitor) by a mechanism distinct from that of muta

282 In clinical trials, MEK inhibitors have shown disappointing efficacy in muta

283 Thus, combinatorial therapies using MEK or BRD4 inhibitors together with NSD2 inhibition are

284 and Western blot analysis to be mediated via MEK-ERK signaling.

285 o2 protein expression can be upregulated via MEK/ERK signaling and after sciatic nerve crush and Neto

286 in triple-negative breast cancers and while MEK inhibition can promote recruitment of tumor-infiltra

287 However, while MEK and BRD4 inhibitors converge in the downregulation o

288 hat blockade of this rebound activation with MEK (mitogen-activated protein kinase kinase) inhibition

289 g A375 cells treated with PLX4720 along with MEK inhibitors significantly inhibited both cell viabili

290 udies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhibited the xenogr

291 The subretinal fluid foci associated with MEK inhibitors have unique clinical and morphologic char

292 translocation of ERK1/2, in combination with MEK inhibitors can be used for the treatment of differen

293 NSD2 knock down combined with MEK or BRD4 inhibitors causes co-operative inhibitory re

294 nd human cell lines potently cooperated with MEK inhibitors to kill these cancers through effects on

295 include: (1) combining BRAF inhibitors with MEK inhibitors or immunotherapy (anti-CD20 monoclonal an

296 electively in T lymphocytes, synergized with MEK inhibitors in vivo to elicit potent and durable anti

297 tenuated by FPR2 silencing or treatment with MEK inhibitor, PD98059.

298 Cessation of life-extending treatment with MEK inhibitors is not indicated when SRF is present.

299 f skin of patients undergoing treatment with MEK, EGFR, or BRAF inhibitors, which are known to induce

300 mass (ICM)-like naive states with only WNT, MEK/ERK, and tankyrase inhibition (LIF-3i).