ライフサイエンスコーパス: MAP

1 MAP is based on the observation that preventing crosslin

2 MAP kinase (MPK) cascades in Arabidopsis thaliana and ot

3 MAP kinase inducing activity was dependent on CRAF dimer

4 MAP kinase phosphatases (MKPs), such as Arabidopsis (Ara

5 MAP kinases of the ERK family are conserved from yeast t

6 MAP phosphatases (MKP)-1 acts as an important regulator

7 MAP was reduced by -11 +/- 7% during SNP, and increased

8 MAP-SIM can potentially reduce reconstruction artifacts,

9 that the microtubule-bundling protein SPD-1/MAP-65 and BMK-1/kinesin-5 act as a brake opposing the f

10 /2-extracellular-signal regulated kinase 1/2 MAP kinase signaling pathway following Toll-like recepto

11 d 2 suggested that activation of ERK 1 and 2 MAP kinases is required for BAFF-R to promote B cell sur

12 activation of other pathways, such as Erk1/2 MAP kinase and Akt, were not affected.

13 ress-induced cell death by regulating ERK1/2 MAP kinase in intestinal epithelial cells.

14 ionate-mediated regulation of phospho-ERK1/2 MAP kinase signaling in FFA2-expressing 293 cells, the G

15 n of KRAS, resulting in activation of ERK1/2 MAP kinase signaling, leading to enhanced cell prolifera

16 e kinase that then activates MKK7 and ERK1/2 MAP kinases.

17 ng proteogenomics, we have identified 25,270 MAPs isolated from the B lymphocytes of 18 individuals w

18 lpha phosphorylation and activation of all 3 MAP kinases (ERK1/2, c-Jun kinase, and p38 MAP kinase).

19 ontinuation within the Mammary Prevention.3 (MAP.3) breast cancer prevention trial.

20 onsented to random assignment (MAP, n = 359; MAP plus IFN-alpha-2b, n = 357), with baseline character

21 MAPs, while 59% of genes generated up to 64 MAPs, often derived from adjacent regions and presented

22 rrents and that this effect is mediated by a MAP kinase cascade, including ASK1 and c-Jun N-terminal

23 ctivates dual leucine-zipper kinase (DLK), a MAP-kinase kinase kinase that then activates MKK7 and ER

24 ent of the root growth defects observed in a MAP kinase 4 (MPK4) single-mutant line.

25 gene cluster and CrMYC2 act downstream of a MAP kinase cascade that includes a previously uncharacte

26 roviding the first such insight into which a MAP can modulate motor motility.

27 ated molecular patterns (PAMPs) and activate MAP kinase cascades, which regulate changes in gene expr

28 Stress-activated MAP kinase signaling cascades that mediate cytokine synt

29 ry scaffolding in mammalian stress-activated MAP kinase signaling.

30 We used AD-MAP to discover DNA aptamer pairs that bind distinct sit

31 9 miRNAs were differentially expressed after MAP infection.

32 nd basic FGF induced phosphorylation of Akt, MAP kinases, and S6 kinase and Fos expression in the abs

33 ucose excretion (P < 0.001) without altering MAP, HR, RBF, or CrCl.

34 Also, systemic administration of an MAP kinase kinase inhibitor increased breakpoint ratios,

35 rebrovascular resistance (CVR = MAP/CBF) and MAP relative to baseline values.

36 The combination of freezing and MAP treatments as preservative treatment method shows hi

37 ion of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kinase signaling.

38 P production, beta-arrestin interaction, and MAP kinase activity.

39 nd one or more MAP kinase kinase kinases and MAP kinase kinases.

40 in healthy controls were disrupted in MA and MAP groups; these involved areas of the brain critical f

41 oastal and inland wetlands combined, MAT and MAP explained 71%, 54%, and 57% of the variations in GPP

42 Leaf area index, MAT and MAP, predicted 74% of variation in ES at global scales.

43 /-)mice WAT, including smad, NFAT, NFkB, and MAP kinases.

44 arget of HopAI when it is overexpressed, and MAP kinase signalling is important for cell-to-cell move

45 progression of parkinsonian signs in ROS and MAP (odds ratio [OR] for TBI with LOC </=1 hour, 1.65; 9

46 All ROS and MAP participants and a subset of ACT participants consen

47 Studies performed annual (ROS and MAP) or biennial (ACT) cognitive and clinical testing to

48 progression of parkinsonian signs in ROS and MAP.

49 OC >1 hour, 1.18; 95% CI, 0.77-1.78; ROS and MAP: HR for TBI with LOC </=1 hour, 0.87; 95% CI, 0.58-1

50 farcts (any cortical microinfarct in ROS and MAP: RR for TBI with LOC >1 hour, 2.12; 95% CI, 1.12-4.0

51 OC >1 hour, 5.73; 95% CI, 2.18-15.0; ROS and MAP: RR for TBI with LOC </=1 hour, 1.64; 95% CI, 1.00-2

52 Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enz

53 cell transcripts is consistent with the anti-MAP antibody responses in paratuberculosis sheep.

54 icity phosphatase 10 (DUSP10), also known as MAP kinase phosphatase 5 (MKP5), negatively regulates th

55 kinase (HvCERK1) and protein kinases such as MAP kinase 3 (HvMPK3) and MAPK substrate 1 (HvMKS1), and

56 atients; 716 consented to random assignment (MAP, n = 359; MAP plus IFN-alpha-2b, n = 357), with base

57 The packaging under modified atmosphere MAP was carried out by using a gas mixture of 66% O2, 25

58 tored in air or passive modified atmosphere (MAP) during 12 days of cold storage, was monitored by so

59 hly conserved ortholog of the human atypical MAP kinase ERK8.

60 The atypical MAP kinases ERK3 and ERK4 are activated by phosphorylati

61 athways and to the activation of PKC-betaII, MAP kinase, and NF-kappaB signaling to induce the produc

62 ere was also no adjusted association between MAP hypotension time and SSI, with estimated odds ratio

63 KP-1 was a pivotal feedback control for both MAP kinases and NF-kappaB pathway in response to S. aure

64 , we examined the biological properties both MAP (CsMAP34) and MASP (CsMASP1) molecules from tongue s

65 ase 2 upon phosphorylation, thereby bridging MAP kinase and G-Protein-Coupled Receptor signaling.

66 non-essential enzymes which are activated by MAP kinases.

67 d upregulated energy sensor AMPKs, CDC25B/C, MAP/Tau and Wee1 protein expression.

68 e phosphorylation (OXPHOS), BRSKs, CDC25B/C, MAP/Tau, Wee1 and epigenetics remodeling complex SWI/SNF

69 urons whereby ApoE activates a non-canonical MAP kinase cascade that enhances APP transcription and a

70 In one case (MAP-1) where stapling enhanced alpha-helicity in aqueous

71 useogliflozin (0.9 mg kg(-1)) did not change MAP, HR, RBF, or creatinine clearance (CrCl) in SD rats

72 icago-area adults in retirement communities (MAP).

73 Our study identified a complete MAP kinase cascade that phosphorylates and activates a k

74 th modified atmosphere packaging conditions (MAP), in our case, aerobic, vacuum or high O2, to extend

75 We propose that the conserved MAP kinase pathway coordinates CO designation with the d

76 changes in cerebrovascular resistance (CVR = MAP/CBF) and MAP relative to baseline values.

77 fferentially regulated by employing distinct MAP subunits.

78 ansport function, via the Wallenda (Wnd)/DLK MAP kinase axonal damage signaling pathway.

79 ripts and proteins associated with efficient MAP production.

80 ase kinase 1 (MAP2K1), the gene that encodes MAP-extracellular signal-regulated kinase 1 (MEK1).

81 na there are approximately 80 genes encoding MAP kinase kinase kinases (MAP3K), 10 genes encoding MAP

82 se kinase kinases (MAP3K), 10 genes encoding MAP kinase kinases (MAP2K), and 20 genes encoding MAP ki

83 inase kinases (MAP2K), and 20 genes encoding MAP kinases (MAPK).

84 y) induced rapid cell death despite enhanced MAP kinase and AKT activation.

85 The entire MAP repertoire presented by these 27 allotypes covered o

86 f a broad set of GPCRs without affecting ERK MAP kinase activation.

87 nteraction of betaarrs with clathrin and ERK MAP kinase.

88 Activation of ERK MAP kinases occurred in these cells by 30 min postchalle

89 it mainly facilitates the activation of ERK MAP kinases.

90 T-2, functions through the conserved RAS/ERK MAP kinase signaling pathway in the C. elegans germline

91 Inhibiting BDNF's receptor, TrkB, ERK/MAP kinase activation, or NMDA receptors blocks this att

92 nalysis identified MAPK3, which encodes ERK1 MAP kinase, as the most topologically important hub in p

93 m a posteriori probability image estimation (MAP-SIM), an alternative method for reconstruction of st

94 ay is a potential good diagnostic marker for MAP persistent infections and predictor of disease speci

95 shedding experimental sensitivity scores for MAP infection detection and disease progression.

96 ii) prevents activation of the Kss1 and Fus3 MAP kinases of the mating pheromone pathway, which in tu

97 so called FMRP) acts independently of futsch/MAP-1B to abolish activity-dependent, but not constituti

98 e set of protein-coding genes could generate MAPs and whether specific features influence the ability

99 ce the ability of discrete genes to generate MAPs.

100 with good accuracy whether a gene generates MAPs.

101 ockout mutants of the ortholog of yeast HOG1 MAP kinase gene in U. virens.

102 Here we identify MAP kinase-interacting serine/threonine protein kinase 1

103 a without documented infection (149 [50%] in MAP vs 217 [73%] in MAPIE).

104 0%] in MAPIE), thrombocytopenia (231 [78% in MAP vs 248 [83%] in MAPIE), and febrile neutropenia with

105 for detecting pathophysiological changes in MAP and describe a potential diagnostic fingerprint of t

106 d body weight by 6% but caused no changes in MAP or HR.

107 e matter integrity and axon demyelination in MAP.

108 0.97 (0.81, 1.17) for a 5-minute increase in MAP hypotension < 55 mm Hg time (P = 0.71).

109 ents were neutropenia (268 [89%] patients in MAP vs 268 [90%] in MAPIE), thrombocytopenia (231 [78% i

110 C2 and APOH, which differed significantly in MAP compared to MA and controls.

111 of downstream signaling pathways, including MAP kinase and Akt.

112 sion did not alter food intake but increased MAP and HR (8 +/- 1 mmHg and 33 +/- 7 bpm), while Vo2 in

113 E2 exposure increased MAP after pellet implantation.

114 increased kinase activity in vitro, induced MAP kinase signaling and conferred vemurafenib resistanc

115 sin stimulates AQP2 exocytosis by inhibiting MAP kinase signaling.

116 We then integrated MAP infection dynamics into the model.

117 Failure of large groups of interconnecting MAP tau proteins leads to detachment of MT filaments fro

118 eractions that may provide new insights into MAP kinase signaling.

119 ides not only a valuable tool to investigate MAP transmission dynamics but also offers adaptability t

120 ral different cellular stresses that involve MAP kinase signaling.

121 totic function of augmin is dependent on its MAP subunit EDE1, which cannot be replaced by AUG8, and

122 SK1-3) are apical kinases of the p38 and JNK MAP kinase pathways.

123 inase previously shown to inhibit NF-kappaB, MAP kinase and Wnt signalling.

124 dermal extracellular-signal-regulated kinase-MAP-kinase signalling results in epidermal inflammation,

125 kinase-interacting serine-threonine kinases MAP kinase-interacting kinase 1 (Mnk1/2), the eIF4E upst

126 fluence the mechanical response, with larger MAP tau spacing resulting in a higher rate of turns.

127 g, systolic (SBP), diastolic (DBP) and mean (MAP) BP progressively increased from KOP, to KOM, and pe

128 ve cisplatin, doxorubicin, and methotrexate (MAP) or MAP plus ifosfamide and etoposide (MAPIE) using

129 n requires a chitin receptor and one or more MAP kinase kinase kinases and MAP kinase kinases.

130 ointing to increased activity of one or more MAP kinases in PKA knockout cells.

131 t PERK signaling is a component of the mouse MAP kinase neuronal stress response controlled by the Du

132 The Pmk1 and Mps1 MAP kinases are essential for appressorium formation and

133 K3) MoGSK1 in M. oryzae is regulated by Mps1 MAP kinase, particularly under the stressed conditions.

134 The neuronal MAP tau is also not sensitive to tubulin acetylation, bu

135 expressed protein-coding genes generated no MAPs, while 59% of genes generated up to 64 MAPs, often

136 First messenger-dependent activation of MAP kinases in neuronal and endocrine cells is critical

137 KP5), negatively regulates the activation of MAP kinases.

138 The MAPIE regimen consisted of MAP as a base regimen, with the addition of high-dose if

139 the use of a based assay in the diagnosis of MAP infections.

140 It was the active form of MAP kinase that was enriched with microtubules and follo

141 Inactivation of MAP kinase at late pachytene is critical for timely disa

142 Inhibition of MAP kinase signaling, suppressing c-Myc expression, or i

143 paper presents an individual-based model of MAP infection dynamics and assesses the relative perform

144 lt task due to the long incubation period of MAP, inefficient diagnostic tests, and delayed clinical

145 We detected the expected phosphorylation of MAP kinases, translational regulatory proteins, and subu

146 e protein is implicated in the regulation of MAP kinase-controlled processes involved in mating, fila

147 At the root of MAP kinase signaling complexity is the differential use

148 ide an improved mechanistic understanding of MAP, that could in turn drive the development of better

149 Our results show preferential selection of MAPs from a limited repertoire of proteins with distinct

150 lation, we hypothesized that E2's effects on MAP are mediated through central ET-1.

151 atin, doxorubicin, and methotrexate (MAP) or MAP plus ifosfamide and etoposide (MAPIE) using conceale

152 ranscription factor Msn2 with Dot6, Sfp1, or MAP kinase Hog1, revealed both coordinated and decoupled

153 p38 without simultaneously activating other MAP kinases in neuronal and endocrine cells.

154 In contrast to other MAP kinase substrates, the transcription factor Ets-1 ha

155 on extending the inhibition profile of a p38 MAP kinase inhibitor toward mutant EGFR inhibition.

156 Blockade of CCR7, or treatment with a p38 MAP kinase inhibitor, reduced lymphatic dissemination of

157 pathways interact to converge on Hog1, a p38 MAP kinase.

158 3 MAP kinases (ERK1/2, c-Jun kinase, and p38 MAP kinase).

159 le pockets on the proteins Factor Xa and p38 MAP kinase.

160 mily function through phosphorylation by p38 MAP kinase and Akt/protein kinase B signaling pathways h

161 An enzyme called p38 MAP kinase helps nematodes to adapt to low-oxygen enviro

162 tein kinase Sty1, a homolog of mammalian p38 MAP kinase, regulates localization of the Cdc42 polarity

163 t, FSH stimulated the phosphorylation of p38 MAP kinase but PKA-CQR did not.

164 s requires Epac2-dependent activation of p38 MAP kinase, which posed the important question of how Ep

165 r alpha from microglia via activation of p38 MAP kinase.

166 of the pharmacologically relevant target p38 MAP kinase.

167 Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pathwa

168 In this study, we showed that p38 MAP kinase (p38) is expressed in doublecortin-positive a

169 Furthermore, it suggests that p38 MAP kinase inhibition may be a useful strategy to inhibi

170 ay, either with direct inhibitors of the p38 MAP kinase or a small-molecule therapeutic that also inh

171 ted CCR7 expression in EMT cells through p38 MAP kinase-mediated activation of the JunB transcription

172 protease TNF-alpha-converting enzyme via p38 MAP kinase activation and its concurrent export to the c

173 imulating ROS production that signal via p38 MAP kinase to the transcription factor SKN-1/NRF1,2,3 to

174 ported 1a (skepinone-L) as a type I p38alpha MAP kinase inhibitor with high potency and excellent sel

175 Pa-MAP 1.9 was active against Gram-negative planktonic bact

176 Here we focused on the study of Pa-MAP 1.9, a rationally designed AMP derived from the pola

177 eatures that favor antibiotic-resistance, Pa-MAP 1.9 could be a promising candidate in the developmen

178 oscopy and in silico tools, we found that Pa-MAP 1.9 may be acting both on intracellular targets and

179 freezing and modified atmosphere packaging (MAP) (100% N2 and 50% N2+50% CO2) on some quality charac

180 fect of three modified atmosphere packaging (MAP) conditions, all with high CO2 and residual or low O

181 Mycobacterium avium subsp. paratuberculosis (MAP) have poor sensitivities and cannot detect early sta

182 Mycobacterium avium subsp. paratuberculosis (MAP) infection during the early subclinical stage are st

183 Mycobacterium avian subsp. paratuberculosis (MAP).

184 imulation of the cell wall integrity pathway MAP kinase Slt2 initially phosphorylates cyclin C to tri

185 MHC class I-associated peptides (MAPs) define the immune self for CD8+ T lymphocytes and

186 in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiatin

187 TRIF pathways and to the activation of PKC, MAP kinase, and NF-kappaB signaling to induce the produc

188 Our results place MAP kinase Sty1 as an important physiological regulator

189 gae effector HopAI known to inactivate plant MAP kinases in M. oryzae.

190 In Magnaporthe oryzae, the Mst11-Mst7-Pmk1 MAP kinase pathway is essential for appressorium formati

191 annual temperature (MAT) and precipitation (MAP)?

192 erature (MAT) and mean annual precipitation (MAP) will be sufficient to predict annual ES across fore

193 erature (MAT) and mean annual precipitation (MAP).

194 Search increased the mean average precision (MAP) for a set of queries.

195 ctive Management of Asthma during Pregnancy (MAP) program.

196 7beta (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (SD) rats, however,

197 ady-state changes in mean arterial pressure (MAP) induced by intravenous infusion of sodium nitroprus

198 al blood flow (RBF), mean arterial pressure (MAP), and heart rate (HR) were continuously measured and

199 Mean arterial pressure (MAP), heart rate (HR), BT, motor activity (MA), and oxyg

200 ressure (SBP) and/or mean arterial pressure (MAP).

201 testing through the MinION Access Programme (MAP), promises long reads in real-time from an inexpensi

202 rders Study (ROS), Memory and Aging Project (MAP), and Adult Changes in Thought study (ACT).

203 activation of the mitogen-activated protein (MAP) kinase (extracellular signal-regulated kinase [ERK]

204 a single ERK-like mitogen-activated protein (MAP) kinase (MAK-1)-signaling cascade, whereas a second

205 d substitution in MITOGEN-ACTIVATED PROTEIN (MAP) KINASE 12 (MPK12).

206 stress-activated mitogen-activated protein (MAP) kinase cascade consisting of GhMAP3K15-Mitogen-acti

207 am effectors, the mitogen-activated protein (MAP) kinase Erk and protein kinase B (Akt).

208 s-activated plant mitogen-activated protein (MAP) kinase pathways play roles in growth adaptation to

209 inase (PI3-K) and mitogen-activated protein (MAP) kinase pathways via TpoR, and autonomous growth in

210 species (ROS) and mitogen-activated protein (MAP) kinase phosphorylation, but exhibited normal respon

211 ucer and the Hog1 mitogen-activated protein (MAP) kinase seem to determine the different dose-respons

212 iated p38 and JNK mitogen-activated protein (MAP) kinase signaling cascades trigger specific cellular

213 Mitogen-activated protein (MAP) kinase substrates are believed to require consensus

214 K) 3 and p38alpha mitogen-activated protein (MAP) kinase.

215 taII isoform, the mitogen-activated protein (MAP) kinases p38 and extracellular signal-regulated kina

216 eam NF-kappaB and mitogen-activated protein (MAP) kinases.

217 h antagonizes the mitogen-activated-protein (MAP) kinase pathway downstream of the FGFR3 receptor and

218 ification of microtubule-associated protein (MAP) 1B as the antigen of the previously described Purki

219 nan-binding lectin (MBL) associated protein (MAP) and MBL associated serine protease (MASP) are scarc

220 Doublecortin (DCX), a MT-associated protein (MAP) required for neuronal migration during cortical dev

221 by which the microtubule-associated protein (MAP) tau regulates the formation of microtubules (MTs) i

222 xpression of microtubule-associated protein (MAP)-1A was significantly up-regulated in the P0 Mapt(-/

223 ing AUG8, which is an MT-associated protein (MAP).

224 by numerous microtubule-associated proteins (MAPs) that have the capacity to affect various cellular

225 Microtubules and their associated proteins (MAPs) underpin the polarity of specialised cells.

226 rray is regulated by MT-associated proteins (MAPs), which include a subset of highly specialized plus

227 ves various microtubule-associated proteins (MAPs).

228 , called magnified analysis of the proteome (MAP), linearly expands entire organs fourfold while pres

229 Methamphetamine-associated psychosis (MAP) involves widespread neurocognitive and molecular de

230 n to be hyperactive in PCa including the RAS/MAP kinase pathway, which phosphorylates Runx2 on multip

231 Signaling through RAS/MAP kinase pathway is central to biology.

232 ponse were randomly assigned; 310 to receive MAP and 308 to receive MAPIE.

233 nome-duplication Dig1/Dig2 proteins regulate MAP kinase controlled signalling pathways involved in ma

234 positive feedback loop of GhWRKY59-regulated MAP kinase activation in response to drought stress.

235 ae Slt2 encoding cell wall integrity-related MAP kinase.

236 Surgical pathology of the resected MAP(+) areas contained mainly non-balloon-cell focal cor

237 (MAK-1)-signaling cascade, whereas a second MAP kinase pathway (MAK-2), which is also involved in ce

238 way by inhibiting the activation of the Slt2 MAP kinase, and synergizes with cell wall stressors such

239 Smk1 is a meiosis-specific MAP kinase (MAPK) in budding yeast that is required for

240 that the inducible nuclear dual-specificity MAP kinase phosphatase (MKP) DUSP2, a known regulator of

241 es and delayed induction of dual-specificity MAP kinase phosphatases (MKPs/DUSPs).

242 Recent data indicate that the structural MAP tau modulates EB subcellular localization in neurons

243 at microtubule plus ends, whereas structural MAPs bind along the microtubule lattice.

244 y and, strikingly, we find that loss of Sty1 MAP kinase signaling prevents latrunculin A-induced disp

245 runculin A treatment also activates the Sty1 MAP kinase pathway and, strikingly, we find that loss of

246 One such MAP is She1, a dynein effector that polarizes dynein-med

247 Adenomatous polyposis coli (APC) is one such MAP with a multifunctional agenda that requires precise

248 s indicate for the first time that a teleost MAP acts one hand as a regulator that promotes the lecti

249 ifically contributes to sustaining long-term MAP kinase signaling and cytokine production downstream

250 e MAPK scaffold (CST5), and the two terminal MAP kinases (CEK1/CEK2).

251 role for Arabidopsis (Arabidopsis thaliana) MAP KINASE17 (MPK17) in affecting peroxisome division in

252 ent grade 4 non-haematological toxicity than MAP (35 [12%] of 301 in the MAP group vs 71 [24%] of 298

253 The results indicated that MAP treatment, particularly MAP1 had an obvious preserva

254 ation of endothelial cells", indicating that MAP infection may lead to the over-proliferation of endo

255 The MAP Bayesian estimator of all important chromatographic

256 The MAP kinase TGFbeta-activated kinase (TAK1) plays a cruci

257 The MAP kinase-interacting kinases (MNK1 and MNK2) are non-e

258 The MAP regimen consisted of cisplatin 120 mg/m(2), doxorubi

259 vating mutations in the beta-catenin and the MAP-kinase pathways; this characteristic can help in the

260 memory formation and cognition, such as the MAP kinases, MKPs, CaMKII, CREB, Fyn, and Tau.

261 yet it is efficiently phosphorylated by the MAP kinase ERK2 at a consensus threonine site (T38).

262 d the best seizure outcomes, followed by the MAP(-) patients, and patients who had no/partial resecti

263 vated protein kinase, but is mediated by the MAP/microtubule affinity-regulating kinases and salt-ind

264 l contains the MAPK3 gene, which encodes the MAP kinase, ERK1.

265 6-76.6); 62.3 months (IQR 46.9-77.1) for the MAP group and 61.1 months (IQR 46.5-75.3) for the MAPIE

266 fulfilled the criteria for inclusion in the MAP cohort.

267 ee survival events were reported (153 in the MAP group vs 154 in the MAPIE group).

268 al toxicity than MAP (35 [12%] of 301 in the MAP group vs 71 [24%] of 298 in the MAPIE group).

269 193 deaths were reported (101 in the MAP group vs 92 in the MAPIE group).

270 serious adverse reaction was reported in the MAP group: bone marrow infarction due to methotrexate.

271 Methods In the MAP.3 randomized, placebo-controlled trial evaluating ex

272 ddition, a direct PKA site that inhibits the MAP kinase kinase kinase Map3k5 (ASK1) is upstream of JN

273 ed a mutation in the catalytic domain of the MAP kinase 7 orthologue sma-5(kc1) In sma-5(kc1) mutants

274 ng Receptor Tyrosine Kinases, members of the MAP Kinase cascade, and WEE1.

275 ting that a GPI-AP functions upstream of the MAP kinase cascade.

276 eover, these data identify activation of the MAP kinase pathway in microglia as a cause of neurodegen

277 Thus, despite the central importance of the MAP kinase pathway in some aspects of T cell function, M

278 to tumor cells through the activation of the MAP kinase pathway.

279 d a metabolic content similar to that of the MAP samples after 5 and 8 days of storage.

280 patients who had no/partial resection of the MAP(+) region had the worst outcome (p < 0.001).

281 o induce the EGFR-mediated activation of the MAP-kinase signaling pathway and consequently the expres

282 We show that the MAP kinases ERK1/2 phosphorylate TC21 and R-Ras on this

283 Overall, patients with the MAP(+) region completely resected had the best seizure o

284 rmal), which was definitely related to their MAP treatment (specifically doxorubicin and cisplatin),

285 , a homologue of Mst11, which corresponds to MAP kinase kinase kinase in Magnaporthe oryzae, and urat

286 Further studies uncovered defects related to MAP kinase I (Slt2) pathways, and we provide evidence th

287 of single-mutants targeting genes related to MAP kinase signaling.

288 AP-1 factors respond to MAP kinase signalling and comprise dimers of FOS, ATF an

289 hese miRNAs might regulate host responses to MAP infection, such as "proliferation of endothelial cel

290 tant allele frequency were more sensitive to MAP kinase inhibition, and CRISPR-Cas9-mediated replacem

291 e that includes a previously uncharacterized MAP kinase kinase, CrMAPKK1.

292 The results demonstrated that storage under MAP can be recommended to improve quality of whiting fil

293 Further, mutants defective in the upstream MAP kinase kinase MKK3 also display hypersensitivity in

294 alves (n = 5) were used to establish in vivo MAP infection adjacent to an uninfected control intestin

295 A splicing sites may be a mechanism by which MAP escapes host immune responses.

296 T pathway was activated in one subtype while MAP kinase pathway was activated in the other.

297 Ethylene removal in combination with MAP led to a higher content in TP and AA in the short-li

298 ic measurements from patients diagnosed with MAP (N = 12), methamphetamine dependence without psychos

299 57 animals that were naturally infected with MAP.

300 Treatment with MAP kinase phosphatase (MKP3, DUSP6) inhibitors increase