ライフサイエンスコーパス: mitogen

1 mbers, and normal proliferative responses to mitogens.

2 miR-184 secreted lower amounts of angiogenic mitogens.

3 several TLR agonists acting as known B cell mitogens.

4 e exchange factor, and the activation of the mitogen activated protein kinase (MAPK) cascade.

5 We apply the method to the mitogen activated protein kinase (MAPK) p38gamma.

6 ORC and late endosomal/lysosomal adaptor and mitogen activated protein kinase and mechanistic target

7 Messenger RNA expression levels of p38 mitogen activated protein kinase and nuclear factor kapp

8 The phosphorylation state of p38 mitogen activated protein kinase and nuclear factor kapp

9 of heparin and potent anti-neointimal drug (Mitogen Activated Protein Kinase II inhibitory peptide;

10 ted and ddPCR confirmed somatic mutations in mitogen activated protein kinase kinase 1 (MAP2K1), the

11 uclear cells of sepsis patients, whereas p38 mitogen activated protein kinase messenger RNA was up-re

12 In neutrophils of sepsis patients, mitogen activated protein kinase phosphatase-1 messenger

13 sis factor-alpha-induced protein 3 (A20) and mitogen activated protein kinase phosphatase-1 were dete

14 rhabditis elegans, we implicate the atypical mitogen activated protein kinase, SWIP-13, in DAT regula

15 2, 4, 12 and 24 h, to analyse activation of mitogen activated protein kinases (MAPKs) and phosphatid

16 show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary f

17 nate response was dependent on activation of mitogen activated protein kinases (MAPKs) via stimulatin

18 ivates nuclear factor-kappaB (NF-kappaB) and mitogen activated protein kinases, thus upregulating dow

19 ays, we show that only combined treatment of mitogen-activated extracellular signal-regulated kinase

20 rwent a redifferentiation treatment with the mitogen-activated extracellular signal-related kinase ki

21 mmalian sPLA2s, as well as inhibitors of the mitogen-activated kinase cascade (MAPK) and cPLA2alpha,

22 d peptides, receptor kinases, and downstream mitogen-activated kinase cascades enforces proper stomat

23 , in a PKA- and cADPR-dependent fashion, the mitogen-activated kinase ERK 1/2, resulting in the modul

24 1 (FGFR1) or pretreatment with inhibitors of mitogen-activated kinase kinase 1 or FGFR ablated these

25 ethal toxin (LT), whose proximal targets are mitogen-activated kinase kinases (MKKs).

26 , we demonstrated that lymphostatin inhibits mitogen-activated proliferation of bovine T cells and, t

27 growth rate through their activation of the mitogen-activated protein (MAP) kinase (extracellular si

28 c sterol precursors target a single ERK-like mitogen-activated protein (MAP) kinase (MAK-1)-signaling

29 analyses revealed a drought stress-activated mitogen-activated protein (MAP) kinase cascade consistin

30 ivate their common downstream effectors, the mitogen-activated protein (MAP) kinase Erk and protein k

31 T/phosphatydylinositol-3'-kinase (PI3-K) and mitogen-activated protein (MAP) kinase pathways via TpoR

32 duction of reactive oxygen species (ROS) and mitogen-activated protein (MAP) kinase phosphorylation,

33 Stress-associated p38 and JNK mitogen-activated protein (MAP) kinase signaling cascade

34 Mitogen-activated protein (MAP) kinase substrates are be

35 of TAK1 as well as downstream NF-kappaB and mitogen-activated protein (MAP) kinases.

36 Chemical inhibition of IkappaB kinase (IKK), mitogen-activated protein extracellular signal-regulated

37 ial damage, epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) signalling

38 Pathogen-responsive mitogen-activated protein kinase (MAPK or MPK) cascades

39 ls converging at the MOR promoter, involving mitogen-activated protein kinase (MAPK) activation and m

40 ly led to decrease in negative regulators of mitogen-activated protein kinase (MAPK) activation, incl

41 ed phosphorylation of BRAF-S729 and retained mitogen-activated protein kinase (MAPK) activation.

42 ene required p38 and c-Jun N-terminal kinase mitogen-activated protein kinase (MAPK) activity, which

43 A. actinomycetemcomitans activates the p38 mitogen-activated protein kinase (MAPK) and MAPK-activat

44 innate immune response, we observed that the mitogen-activated protein kinase (MAPK) and nuclear tran

45 gnal through multiple effectors, such as the mitogen-activated protein kinase (MAPK) and PI3K pathway

46 The roles of EGFR ligands, p38 mitogen-activated protein kinase (MAPK) and tumour necro

47 e to mating pheromone activates a prototypic mitogen-activated protein kinase (MAPK) cascade and trig

48 Activating mutations in the mitogen-activated protein kinase (MAPK) cascade, also kn

49 phosphorylation, including the activation of mitogen-activated protein kinase (MAPK) cascades.

50 ERK3 is an atypical mitogen-activated protein kinase (MAPK) containing an S-

51 f nuclear factor-kappa B (NF-kappaB) and p38 mitogen-activated protein kinase (MAPK) correlated with

52 The protein p38 mitogen-activated protein kinase (MAPK) delta isoform (p

53 (ERK1), a member of the extensively studied mitogen-activated protein kinase (MAPK) family, serves a

54 KO mice with enhanced phosphorylation of p38 mitogen-activated protein kinase (MAPK) in podocytes.

55 Smk1 is a meiosis-specific mitogen-activated protein kinase (MAPK) in Saccharomyces

56 sed sensitivity to nuclear factor-kappaB and mitogen-activated protein kinase (MAPK) inhibition, a re

57 The anti-inflammatory potential of p38 mitogen-activated protein kinase (MAPK) inhibitors was c

58 Targeted inhibition of mitogen-activated protein kinase (MAPK) kinase (MEK) can

59 MLK3 is a mitogen-activated protein kinase (MAPK) kinase kinase (M

60 In VSMC, p42/p44 mitogen-activated protein kinase (MAPK) pathway activati

61 Mitogen-activated protein kinase (MAPK) pathway antagoni

62 In melanoma, activation of the mitogen-activated protein kinase (MAPK) pathway driven b

63 chymal transition and by reactivation of the mitogen-activated protein kinase (MAPK) pathway followin

64 arget the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway have led

65 ditions due to paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in BRAF

66 "paradoxical" upregulation of the downstream mitogen-activated protein kinase (MAPK) pathway in cance

67 Signaling analysis indicated decreased mitogen-activated protein kinase (MAPK) pathway signalin

68 ic cells (DCs) with constitutively activated mitogen-activated protein kinase (MAPK) pathway signalin

69 regulate host protein synthesis through the mitogen-activated protein kinase (MAPK) pathway.

70 t encode components or regulators of the Ras/mitogen-activated protein kinase (MAPK) pathway.

71 Mitogen-activated protein kinase (MAPK) pathways are con

72 through mechanistic target of rapamycin and mitogen-activated protein kinase (MAPK) pathways blocks

73 daily rhythms in the activation of conserved mitogen-activated protein kinase (MAPK) pathways when ce

74 Mitogen-activated protein kinase (MAPK) scaffold protein

75 Mitogen-activated protein kinase (MAPK) signal transduct

76 t phosphoinositide 3-kinase (PI3K)-dependent mitogen-activated protein kinase (MAPK) signaling and in

77 ng in NRAS(G12V) mutant cells and pronounced mitogen-activated protein kinase (MAPK) signaling in NRA

78 We show that mitogen-activated protein kinase (MAPK) signaling is lin

79 tions promote constitutive activation of the mitogen-activated protein kinase (MAPK) signaling pathwa

80 and cell migration, associated with the p38 mitogen-activated protein kinase (MAPK) signaling pathwa

81 AF gene fusions that aberrantly activate the mitogen-activated protein kinase (MAPK) signaling pathwa

82 ming growth factor beta1 (TGF-beta1) and p38 mitogen-activated protein kinase (MAPK) signaling, which

83 lin D1 expression and profound inhibition of mitogen-activated protein kinase (MAPK) signaling.

84 downstream of its receptor via activation of mitogen-activated protein kinase (MAPK) signaling.

85 mas, which are characterized by elevated RAS-mitogen-activated protein kinase (MAPK) signaling.

86 s of congenital myopathies and implicate the mitogen-activated protein kinase (MAPK) signalling as a

87 acellular Ca(2+) levels via calcineurin, p38 mitogen-activated protein kinase (MAPK), and nitric oxid

88 -related transcription factor (MRTF) and p38 mitogen-activated protein kinase (MAPK), down-regulating

89 its rapid basal turnover in neurons and that mitogen-activated protein kinase (MAPK)-dependent phosph

90 l GTPases, p21-activated kinase, and the p38 mitogen-activated protein kinase (MAPK)-MAPK-activated p

91 Notably, mitogen-activated protein kinase (MAPK)-targeted therapy

92 he cornea by blocking phosphorylation of p38 mitogen-activated protein kinase (MAPK).

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

94 Recently, an interaction between mitogen-activated protein kinase (MAPK1) and vinculin wa

95 Mitogen-activated protein kinase (MAPK; 37%), cell cycle

96 am effector is RAF, leading to activation of mitogen-activated protein kinase (MEK)-extracellular sig

97 Mitogen-activated protein kinase (MPK) cascades are cons

98 ene editing in the family of closely related mitogen-activated protein kinase (MPK) genes in Oryza sa

99 s upregulated with aging, which enhances p38 mitogen-activated protein kinase (p38 MAPK) activation a

100 s, hyperglycemia stimulated proliferation by mitogen-activated protein kinase 1 (MAPK1)- and MAPK3-de

101 We previously demonstrated that the mitogen-activated protein kinase 1/2 inhibitor trametini

102 udy, we show that TGF-beta induces p38alpha (mitogen-activated protein kinase 14 [MAPK14]), which in

103 Here, we report that mitogen-activated protein kinase 3 (MPK3) and MPK6 inter

104 d 8 [CXCL8]), and response to stress (CXCL8, mitogen-activated protein kinase 3, BCL2-associated X pr

105 n-activated Protein Kinase Kinase 4 (GhMKK4)-Mitogen-activated Protein Kinase 6 (GhMPK6) that directl

106 Previously, we demonstrated that Arabidopsis mitogen-activated protein kinase 6 (MPK6) and MPK3 play

107 G sites that was annotated to 9 genes [e.g., mitogen-activated protein kinase 7 (MAPK7), melanin conc

108 g22, PLC2-silenced plants maintain wild-type mitogen-activated protein kinase activation and PHI1, WR

109 mation mainly by inhibition of NF-kappaB and mitogen-activated protein kinase activation but does not

110 IKE KINASE1, reduced callose deposition, and mitogen-activated protein kinase activation upon MAMP tr

111 GF-beta1 was dependent on both SMAD3 and p38 mitogen-activated protein kinase activation.

112 modules associated with lipid metabolism and mitogen-activated protein kinase activity upregulated in

113 2 phosphorylation, suggesting an increase in mitogen-activated protein kinase activity.

114 ntracellular domain-dependent CD133-mediated mitogen-activated protein kinase and activator protein-1

115 an increase in downstream signaling via the mitogen-activated protein kinase and AKT pathway.

116 nterstitial fibrosis, and phosphorylated p38 mitogen-activated protein kinase and decreases in left v

117 overexpression decreases phosphorylated p38 mitogen-activated protein kinase and elevates tetrahydro

118 ts transforming growth factor beta-activated mitogen-activated protein kinase and hedgehog signaling.

119 3 and PLD1, genes downstream of CDC42 in the mitogen-activated protein kinase and mammalian target of

120 scovery of recurrent mutations affecting the mitogen-activated protein kinase and mTOR-AKT pathways i

121 CXCL2/MIF-stimulated activation of the mitogen-activated protein kinase and nuclear factor kapp

122 h levels of reactive oxygen species in a p38 mitogen-activated protein kinase and phosphatidylinosito

123 ionable mutations, most in components of the mitogen-activated protein kinase and phosphoinositol kin

124 extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase and protein kinase B (P

125 TNFAIP3/A20 promotes kinase activity of p38 mitogen-activated protein kinase and protein kinase C, w

126 via the gp130 signaling receptor, activating mitogen-activated protein kinase and signal transducer a

127 Mitogen-activated protein kinase cascades are conserved

128 Mitogen-activated protein kinase cascades are important

129 in the calcium-dependent protein kinase and mitogen-activated protein kinase cascades, as well as pr

130 es the role of the protein kinase MK2, a p38 mitogen-activated protein kinase downstream target, in t

131 ditionally, pretreatments with inhibitors of mitogen-activated protein kinase enzymes or endocytosis

132 turn, amplifies TRPV3 via activation of the mitogen-activated protein kinase ERK in a positive feedb

133 otch1 intracellular domain, CD133, and p-p38 mitogen-activated protein kinase expression and malignan

134 n N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and controls var

135 of CDKN2C and TP53, and mutations affecting mitogen-activated protein kinase genes.

136 ssociated proteins: PKCdelta, ERK1/2 and p38 mitogen-activated protein kinase in HEK 293T.

137 p38 mitogen-activated protein kinase inhibition via SB203580

138 pretreatment with an oral small-molecule p38 mitogen-activated protein kinase inhibitor (Losmapimod;

139 Finally, it reveals that mitogen-activated protein kinase interacting kinase-1 ha

140 The maintenance of new spines driven by mitogen-activated protein kinase interacting kinase-1 wa

141 tion-independent protein synthesis driven by mitogen-activated protein kinase interacting kinase-1, d

142 Mitogen-activated protein kinase interacting protein kin

143 isphosphate 3-kinase, Akt, or p38 downstream mitogen-activated protein kinase interacting serine/thre

144 To compare efficacy of the mitogen-activated protein kinase kinase (MEK) inhibitor

145 h paradoxical MAPK activation; addition of a mitogen-activated protein kinase kinase (MEK) inhibitor

146 rous retinal disturbances in patients taking mitogen-activated protein kinase kinase (MEK) inhibitors

147 Mitogen-activated protein kinase kinase (MEK) mutations

148 TSLP induced mitogen-activated protein kinase kinase (MEK), c-Fos, in

149 by cytokines and suppressed by inhibition of mitogen-activated protein kinase kinase 1/2, whereas STE

150 idated six candidate proteins, including the mitogen-activated protein kinase kinase 2 (MEK2), that i

151 Mitogen-activated protein kinase kinase 3 (MKK3) is a du

152 (MAP) kinase cascade consisting of GhMAP3K15-Mitogen-activated Protein Kinase Kinase 4 (GhMKK4)-Mitog

153 cific transgenic overexpression of activated mitogen-activated protein kinase kinase 6, a direct indu

154 mice with fibroblast-specific activation of mitogen-activated protein kinase kinase 6-p38 developed

155 A specific upstream activator of JNKs is the mitogen-activated protein kinase kinase 7 (MKK7).

156 Focusing on mitogen-activated protein kinase kinase and Bcl-XL targe

157 ASK1, also known as MAP3K5), a member of the mitogen-activated protein kinase kinase kinase (MAP3K) f

158 nd repressing the downstream gene encoding a mitogen-activated protein kinase kinase kinase (MAPKKK)

159 appaB pathway, including the upstream kinase mitogen-activated protein kinase kinase kinase 14 (MAP3K

160 e suggested a role for endothelial cell (EC) mitogen-activated protein kinase kinase kinase kinase 4

161 Previous studies revealed a paradox whereby mitogen-activated protein kinase kinase kinase kinase 4

162 ibers, including, most prominently, MEKK4, a mitogen-activated protein kinase kinase kinase that was

163 Wnt signals, a temporal control pathway, and mitogen-activated protein kinase kinase signaling contro

164 lockade of this rebound activation with MEK (mitogen-activated protein kinase kinase) inhibition enha

165 phorylation and activation of KSR-bound MEK (mitogen-activated protein kinase kinase).

166 particular, we report synergistic effects of mitogen-activated protein kinase kinase, ribosomal S6 ki

167 NF-kappaB-inducing kinase (NIK) and mitogen-activated protein kinase kinase-1 (MEKK-1) were

168 Mitogen-activated protein kinase kinase/extracellular re

169 ghly specific protease, exclusively cleaving mitogen-activated protein kinase kinases (MKKs) and rode

170 y PIP5K6 as a target of the pollen-expressed mitogen-activated protein kinase MPK6 and characterize t

171 icity phosphatase 1, impairs the activity of mitogen-activated protein kinase p38, increases the acti

172 The mitogen-activated protein kinase p38alpha (Mapk14 gene)

173 to 50-fold higher potency in activating the mitogen-activated protein kinase pathway compared with S

174 idence that these mutations activate the RAS/mitogen-activated protein kinase pathway in melanoma and

175 breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-mutant c

176 We also found out that p38 mitogen-activated protein kinase pathway may be implicat

177 ted the overexpression of a regulator of the mitogen-activated protein kinase pathway, mitogen-activa

178 Strained cells activated the mitogen-activated protein kinase pathway, whereas specif

179 es have shown the frequent alteration of the mitogen-activated protein kinase pathway.

180 ination of mutations of the beta-catenin and mitogen-activated protein kinase pathways as characteris

181 , inactivation and subsequent degradation of mitogen-activated protein kinase phosphatase 1 (MKP-1) i

182 lular signal-regulated kinase 1/2, increased mitogen-activated protein kinase phosphatase 1 expressio

183 ious studies identified a potential role for mitogen-activated protein kinase phosphatase-1 (MKP-1) i

184 he mitogen-activated protein kinase pathway, mitogen-activated protein kinase phosphatase-1 (MKP-1).

185 roteins that contribute to this process, the mitogen-activated protein kinase phosphatases (MKPs), di

186 is regulated independently of DNA binding by mitogen-activated protein kinase phosphorylation of the

187 on into early endosomes, and reduces delayed mitogen-activated protein kinase phosphorylation require

188 elanoma cells evolve a 'just right' level of mitogen-activated protein kinase signaling and the addit

189 Whereas suppressing or enhancing Ras/mitogen-activated protein kinase signaling changed how s

190 e renin-angiotensin system in the kidney and mitogen-activated protein kinase signaling in the heart.

191 es, harbor germline mutations in various RAS/mitogen-activated protein kinase signaling pathway genes

192 us system activates a microbicidal PMK-1/p38 mitogen-activated protein kinase signaling pathway that

193 found that ERK1, a downstream kinase in the mitogen-activated protein kinase signaling pathway, phos

194 ed with wild-type mice, along with decreased mitogen-activated protein kinase signaling, tumor angiog

195 crease in NE expression, and upregulation of mitogen-activated protein kinase signaling.

196 GF-induced phosphatidylinositol-3-kinase and mitogen-activated protein kinase signaling.

197 nsducer and activator of transcription 3 and mitogen-activated protein kinase signalling in an inocul

198 observed upon treatment with an inhibitor to mitogen-activated protein kinase that prevents phosphory

199 diverse modes of injury converge on p38alpha mitogen-activated protein kinase within the fibroblast t

200 RES activity was dependent on upstream MAPK (mitogen-activated protein kinase) and MNK1 (MAPK-interac

201 phosphoinositide 3-kinase)/AKT and RAS/MAPK (mitogen-activated protein kinase) pathway coactivation i

202 The RAS/MAPK (mitogen-activated protein kinase) signalling pathway is

203 efective in activating PAK3 as well as MAPK (mitogen-activated protein kinase).

204 ) and K(+) gradients, phosphorylation of p38 mitogen-activated protein kinase, and cell death, withou

205 of phosphorylated heat shock protein 27, p38 mitogen-activated protein kinase, and glycogen synthase

206 pathways, phosphatidylinositol-3-kinase and mitogen-activated protein kinase, but express higher lev

207 n in keratinocytes evokes phosphorylation of mitogen-activated protein kinase, ERK, for histaminergic

208 receptor 4 (TLR4) promotes activation of p38 mitogen-activated protein kinase, extracellular signal-r

209 athways, including Toll-like receptor (TLR), mitogen-activated protein kinase, Jak-STAT, and the nucl

210 s lost by suppressing the activity of Ras or mitogen-activated protein kinase, whereas the overexpres

211 ease passive loading of an anti-inflammatory mitogen-activated protein kinase-activated protein kinas

212 of the extracellular signal-regulated kinase mitogen-activated protein kinase-dependent pathway and 2

213 by treatment with CGP57380 (an inhibitor of mitogen-activated protein kinase-interacting serine-thre

214 the skin in the same subjects related to p38 mitogen-activated protein kinase-related proinflammatory

215 minal kinase, but not by an inhibitor of p38 mitogen-activated protein kinase.

216 thelial growth factor receptor 2, and p42/44 mitogen-activated protein kinase.

217 levels of the IL-1 receptor and phospho-p38 mitogen-activated protein kinase.

218 llagen associated with the activation of p38 mitogen-activated protein kinase.

219 ic phosphorylation and activation of the p38 mitogen-activated protein kinase.

220 it also inhibited the phosphorylation of p38 mitogen-activated protein kinase.

221 receptor also known as TrkA that upregulates mitogen-activated protein kinase.

222 with the BRAF inhibitor vemurafenib and the mitogen-activated protein kinase/extracellular signal-re

223 mained intact following CD63 knockout, while mitogen-activated protein kinase/extracellular signal-re

224 n metastatic melanoma with combined BRAF and mitogen-activated protein kinase/extracellular signal-re

225 ed changes in learning-related expression of mitogen-activated protein kinase/extracellular signal-re

226 The mitogen-activated protein kinase/extracellular signal-re

227 For example, Toll-like receptors activate mitogen-activated protein kinase/transcription factor pa

228 Mitogen-activated protein kinases (MAPK) promote MAPK-ac

229 d kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)] were assessed

230 KIM-PTPs bind and dephosphorylate mitogen-activated protein kinases (MAPKs) and thereby cr

231 Mitogen-activated protein kinases (MAPKs) are important

232 The molecular actions of mitogen-activated protein kinases (MAPKs) are ultimately

233 Mitogen-activated protein kinases (MAPKs) form important

234 Cellular mitogen-activated protein kinases (MAPKs) have been show

235 It also modulated the phosphorylation of mitogen-activated protein kinases (MAPKs) in a time- dep

236 Mitogen-activated protein kinases (MAPKs) including Erk,

237 Mitogen-activated protein kinases (MAPKs) regulate brain

238 HopAI1 targets and suppresses mitogen-activated protein kinases (MAPKs).

239 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated protein kinases (MAPKs).

240 Moreover, GOS stimulates mitogen-activated protein kinases (MAPKs); notably, c-Ju

241 , oxidative stress, early phosphorylation of mitogen-activated protein kinases and Akt, and upregulat

242 sin II-induced redox-sensitive activation of mitogen-activated protein kinases and phosphoinositide 3

243 tracellular signal-regulated kinases and p38 mitogen-activated protein kinases in primary human kerat

244 Surprisingly, S382 can be phosphorylated by mitogen-activated protein kinases in vitro.

245 sponses were influenced by the MpkC and SakA mitogen-activated protein kinases of the high-osmolarity

246 eceptor antagonist, and inhibitors of either mitogen-activated protein kinases or phosphoinositide 3-

247 , which dephosphorylates and inactivates the mitogen-activated protein kinases p38 and Jun N-terminal

248 st transdifferentiation by activation of p38 mitogen-activated protein kinases resulting in upregulat

249 tivity and hyperactivation of its downstream mitogen-activated protein kinases that are centrally imp

250 phospholipase A2(cPLA2alpha) by calcium- and mitogen-activated protein kinases triggers the rapid pro

251 ied out to characterize the effect of P3G on mitogen-activated protein kinases, and on nuclear transc

252 cantly disrupted 7 signaling pathways (i.e., mitogen-activated protein kinases, tight junctions, foca

253 unomodulatory activity of cNK-2 involves the mitogen-activated protein kinases-mediated signalling pa

254 lmodulin-dependent protein kinase II, Akt or mitogen-activated protein kinases.

255 ns and a homozygous nonsense mutation in the mitogen-activated protein triple kinase ZAK.

256 regulatory effects of BCL6 on both MEK-ERK (mitogen-activated protein/extracellular signal-regulated

257 ision by converting the memories of variable mitogen and stress signals into a competition between cy

258 sion based on competing memories of variable mitogen and stress signals.

259 tably, we find that Inhbaa functions as a CM mitogen and that its overexpression leads to accelerated

260 Here we show that NETs are induced by mitogens and accompanied by induction of cell-cycle mark

261 sulting in poor in vitro T-cell responses to mitogens and antigens caused by reduced secretion of IFN

262 FGF2 is a known mitogen, and both FGF2/MMP-9 are proangiogenic factors.

263 nflammatory, counterregulatory responses via mitogen- and stress-activated kinase (MSK) 1/2 and Smad3

264 Here we show that the mitogen- and stress-activated kinase (MSK1) is up-regula

265 We examined the involvement of mitogen- and stress-activated kinase 1 (MSK1), a downstr

266 kinases 1 and 2, or blocking or deleting the mitogen- and stress-activated kinases 1 and 2 (MSK1/2),

267 ssion of IFN-beta is negatively regulated by mitogen- and stress-activated kinases 1 and 2 (MSK1/2).

268 tivated protein kinase (MAPK) activation and mitogen- and stress-activated protein kinase 1 (MSK1)-ra

269 d H3K27ac levels and also those of activated mitogen- and stress-activated protein kinase 1 (MSK1).

270 Stimulation of the MAPK pathway results in mitogen- and stress-activated protein kinase 1/2 (MSK1/2

271 ages, previous studies have established that mitogen- and stress-activated protein kinases (MSKs) reg

272 emphasizing the importance of the activated mitogen-associated protein kinase pathway in this diseas

273 imulated cells, but they increased following mitogen-dependent activation.

274 ted with P. knowlesi alone failed to develop mitogen-driven tumor necrosis factor alpha and IL-10, in

275 , including synthetic compounds, chemokines, mitogens, fatty acids, and hormones.

276 N-gamma]) and rendered T cells refractory to mitogen for a least 18 h after transient exposure.

277 telet-derived growth factor (PDGF), a potent mitogen for cells of mesenchymal origin, has been implic

278 Sonic hedgehog (Shh) is a mitogen for spinal cord progenitors, but how cells becom

279 ptor (GPCR) agonist angiotensin II, a potent mitogen for these cells, induced rapid translocation of

280 The CD8(+) T cell mitogen IL-15, which was increased in oxazolone-challeng

281 Furthermore, nicotine may act as a mitogen in cholestatic liver disease processes, thereby

282 ranules are formed upon cell activation with mitogens, including stress granules that contain the RNA

283 sis for this phenomenon in the selection for mitogen-independent (MI) stem-like cells with impaired p

284 (embryonic day 19) fetal rat hepatocytes is mitogen-independent and that mechanisms regulating mRNA

285 Thus, mitogen-induced co-recruitment of EGFR/ERK components to

286 transmit DNA damage-induced p53 protein and mitogen-induced cyclin D1 (CCND1) mRNA to newly born dau

287 Similarly, we show that mitogen-induced H3S10 and H3S28 phosphorylation occurs i

288 Furthermore, elevated cAMP inhibited mitogen-induced nuclear-translocation of MKL1 and MKL2 i

289 ctor serum response factor (SRF) to activate mitogen-induced transcription.

290 Mitogen-inducible gene 6 (Mig-6) is a critical mediator

291 Levels of the potent Schwann cell mitogen neuregulin and its receptor ErbB2 decline during

292 mutations that overexpress the Schwann cell mitogen neuregulin-1 or overexpress the epidermal growth

293 It can have a dual role, acting either as a mitogen or as a tumor suppressor.

294 uclear and MKL2 cytoplasmic, irrespective of mitogens or cAMP.

295 ate and grow in CSF, a remarkably acellular, mitogen-poor metastasis microenvironment.

296 le pathways is due to natural variability in mitogen signalling or other underlying causes is unknown

297 ) proliferation was evident, while decreased mitogen-stimulated gamma interferon (IFN-gamma) producti

298 ins is crucial for transmitting signals upon mitogen stimulation.

299 omponents, including amphiregulin, and other mitogens to enter the CSF and promote cancer cell growth

300 nfected cells can proliferate in response to mitogens without producing virus, generating progeny cel