ライフサイエンスコーパス: myeloid differentiation

1 Myc function or sterol biosynthesis impaired myeloid differentiation.

2 upstream regulator of KDR activation during myeloid differentiation.

3 s and the diabetes-induced propensity toward myeloid differentiation.

4 CDK6 depletion is mediated through enhanced myeloid differentiation.

5 phosphorylation, increased p53 activity, and myeloid differentiation.

6 n and leads to a reduced CD11b expression in myeloid differentiation.

7 nscription factor PU.1 controls lymphoid and myeloid differentiation.

8 y 5, member a (Clec5a), which is involved in myeloid differentiation.

9 tes myeloid progenitor expansion and impedes myeloid differentiation.

10 used to shed new light on the mechanisms for myeloid differentiation.

11 ge colony-stimulating factor (M-CSF)-induced myeloid differentiation.

12 oes not induce caspase 8 activity to promote myeloid differentiation.

13 pamycin complex 1 as a critical regulator of myeloid differentiation.

14 ed to the study of the mechanisms underlying myeloid differentiation.

15 elf-renewal, causes lineage bias, and blocks myeloid differentiation.

16 s mainly involved in cell fate decisions for myeloid differentiation.

17 pattern of JAK2, which markedly increases on myeloid differentiation.

18 rate that E47 is not required for short-term myeloid differentiation.

19 r that regulates genes that are required for myeloid differentiation.

20 ich occurs in both early and later stages of myeloid differentiation.

21 cued defects in myeloid colony formation and myeloid differentiation.

22 roid differentiation, but severely perturbed myeloid differentiation.

23 igated its transcriptional activation during myeloid differentiation.

24 lements of identity and function in terminal myeloid differentiation.

25 e in the transcriptional program that drives myeloid differentiation.

26 HoxA9, a gene normally downregulated during myeloid differentiation.

27 the importance of C/EBPalpha acetylation in myeloid differentiation.

28 ;17), or t(8;21) and is downregulated during myeloid differentiation.

29 Myeloid differentiation-2 (MD-2) acts as an essential co

30 Myeloid differentiation 88 (MyD88) is the key signaling

31 acteria-derived LPS, activates NFkappaB in a myeloid differentiation 88 (MyD88)-dependent manner.

32 ate the caspase 3 activity needed to promote myeloid differentiation, a key process in the viral diss

33 iduals resulted in markedly reduced in vitro myeloid differentiation accompanied by cell-cycle arrest

34 and high levels of Ly6G, a component of the myeloid differentiation Ag Gr-1, are also highly expande

35 ch suggests the effect of FLT3 inhibition on myeloid differentiation and a manifestation of a broader

36 We also apply the algorithm to mouse myeloid differentiation and demonstrate its generalizati

37 n vitro and in vivo, accompanied by terminal myeloid differentiation and elimination of leukaemia ste

38 shown that Notch2, and not Notch1, inhibits myeloid differentiation and enhances generation of primi

39 ription factor PU.1 is a master regulator of myeloid differentiation and function.

40 L-6 is a particularly important regulator of myeloid differentiation and HSPC proliferation in a para

41 mber A signaling to SRF, results in aberrant myeloid differentiation and hyperactivity of the immune

42 t DNA methylation is markedly altered during myeloid differentiation and identifies critical regions

43 stemic reduction of EPO in the host enhanced myeloid differentiation and improved BM homing of UCB CD

44 cating Asxl1 mutations (ASXL1-MTs) inhibited myeloid differentiation and induced MDS-like disease in

45 s, confirm that KLF4 overexpression promotes myeloid differentiation and inhibits cell proliferation

46 hat reintroducing miR-150 expression induces myeloid differentiation and inhibits proliferation of AM

47 scription factor C/EBPalpha is essential for myeloid differentiation and is frequently dysregulated i

48 factor C/EBPalpha is a critical mediator of myeloid differentiation and is often functionally impair

49 8), an integral transcriptional component of myeloid differentiation and lineage commitment.

50 our understanding of the sheer diversity of myeloid differentiation and phenotypic regulation.

51 t Forkhead box class O genes (FoxOs) inhibit myeloid differentiation and prevent differentiation of l

52 factors, particularly CEBPalpha, involved in myeloid differentiation and retinoid responsiveness.

53 kaemic effects, including increased terminal myeloid differentiation and suppression of leukaemia gro

54 g for stem cell development and maintenance, myeloid differentiation, and apoptosis.

55 , including impaired proliferation, enhanced myeloid differentiation, and depletion of LSCs.

56 ewal capacity by myeloid progenitors, biased myeloid differentiation, and the development of a myelop

57 es up-regulated in WG PBMCs were involved in myeloid differentiation, and these included the WG autoa

58 cancer and stromal cells and, subsequently, myeloid differentiation antigen-positive (Gr-1(+)) myelo

59 ever, the consequences of JAK2 mutations for myeloid differentiation are poorly understood.

60 esults indicate that C/EBPgamma mediates the myeloid differentiation arrest induced by C/EBPalpha def

61 it did increase H3K4(me2) and expression of myeloid-differentiation-associated genes.

62 inappropriately expressed, delays or blocks myeloid differentiation at least in part by DNA hypermet

63 ct the expansion, increased self-renewal, or myeloid differentiation bias in Nras(G12D/+) HSCs.

64 CCR2(-)CD150(+)CD48(-) LSK cells, displays a myeloid differentiation bias, and dominates the migrator

65 expansion of hematopoietic progenitors, and myeloid differentiation bias.

66 Moreover, miR-9 expression reverses a myeloid differentiation block that is induced by EVI1.

67 tant WT1 in CD34(+) cord blood cells induced myeloid differentiation block.

68 g cells in recipient mice with an unexpected myeloid differentiation blockade and lymphoid-lineage bi

69 hus, LBR plays a critical role in regulating myeloid differentiation, but how the two functional doma

70 n of the gene encoding Triad1 (ARIH2) during myeloid differentiation, but the contribution of increas

71 /megakaryocyte progenitors but with residual myeloid differentiation capacity; "E-MEP," strongly bias

72 of the mechanisms underlying the diminished myeloid differentiation caused by reduced SLPI levels re

73 tro behavior but generate expansion of later myeloid differentiation compartments, where homozygous e

74 We conclude that Gabp is required for myeloid differentiation due, in part, to its regulation

75 expression by direct promoter binding during myeloid differentiation, enforced expression of miR-182

76 IFNgamma, MCP1, MIP1alpha, and TNFalpha) and myeloid differentiation factor (Endoglin) were increased

77 Although in mammals the TLR4/myeloid differentiation factor (MD)2/CD14 complex is res

78 ecognition by the human Toll-like receptor 4-myeloid differentiation factor 2 (hTLR4-MD2) complex, al

79 ctivation of the Toll-like Receptor 4 (TLR4)-myeloid differentiation factor 2 (MD-2) complex, which r

80 t productively engage the mouse TLR4 (mTLR4)/myeloid differentiation factor 2 (MD-2) complex.

81 immune response against LPS is triggered by myeloid differentiation factor 2 (MD-2) in association w

82 Myeloid differentiation factor 2 (MD-2) is an extracellu

83 The human TLR4.myeloid differentiation factor 2 (MD-2) LPS receptor com

84 nstrate that the extracellular TLR4 adaptor, myeloid differentiation factor 2 (MD-2), binds specifica

85 by endotoxin presented as a monomer bound to myeloid differentiation factor 2 (MD-2).

86 ated through the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 2 (MD2) complex.

87 Dimerization of Toll-like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD2) heterodimers is c

88 phisms on TLR4 expression, interactions with myeloid differentiation factor 2 (MD2), LPS binding, and

89 saccharide binding to a toll-like receptor-4/myeloid differentiation factor 2 fusion protein.

90 tent ligand of the Toll-like receptor (TLR)4/myeloid differentiation factor 2 receptor of the innate

91 which signals through the adapter molecules myeloid differentiation factor 88 (MyD88) and toll/inter

92 ice lacking both Lyn and the adaptor protein myeloid differentiation factor 88 (MyD88) in DCs, specif

93 ial Toll-like receptor (TLR) adaptor protein myeloid differentiation factor 88 (MyD88) in systemic an

94 Myeloid differentiation factor 88 (MyD88) is an adaptor

95 Signaling through myeloid differentiation factor 88 (MyD88) is critical fo

96 Myeloid differentiation factor 88 (MYD88) L265P somatic

97 Furthermore, B cell-intrinsic expression of myeloid differentiation factor 88 (MyD88) was required t

98 of which signal through the adaptor protein myeloid differentiation factor 88 (MyD88), have been sug

99 Mice deficient in TLR-2, myeloid differentiation factor 88 (MyD88), or NOD-2 and

100 pe I IFN expression proceeded independent of myeloid differentiation factor 88 (MyD88), which is the

101 umbers in a Toll-like receptor 4 (TLR4)- and myeloid differentiation factor 88 (MyD88)-dependent mann

102 deletion of the inflammatory adaptor protein myeloid differentiation factor 88 (MyD88).

103 or 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD88).

104 toll-like receptor 4 (TLR4) and its adaptor myeloid differentiation factor 88 (MyD88).

105 Using myeloid differentiation factor 88 (MyD88)/TIR-domain-con

106 r p65 translocation, and colocalization with myeloid differentiation factor 88 and calcium-modulating

107 as a scaffold to promote the interaction of myeloid differentiation factor 88 and IL-1R-associated k

108 is is dependent on TLR2 and TLR4, as well as myeloid differentiation factor 88 and Toll/IL-1R domain-

109 ectly targeted Th17 cells by down-regulating myeloid differentiation factor 88 expression to suppress

110 ucing IFN-beta, P. gingivalis utilizes TLR2/ myeloid differentiation factor 88 in modulating osteocla

111 Toll-like receptor signaling through myeloid differentiation factor 88 maintains segregation

112 ts from mice with genetic deletion of MyD88 (myeloid differentiation factor 88) or TLRs (Toll-like re

113 Myeloid differentiation factor 88-deficient (MyD88(-/-))

114 on are uncertain, although a role for a TLR4/myeloid differentiation factor 88-dependent pathway lead

115 by the microbiota via Toll-like receptor and myeloid differentiation factor 88-mediated signalling pa

116 hese outcomes by using the signaling adaptor myeloid differentiation factor 88.

117 nterleukin; TIR, Toll/IL-1R homology; MyD88, myeloid differentiation factor 88; IFN, interferon; TRIF

118 onstrate that NQO1 controls the stability of myeloid differentiation factor C/EBPalpha against 20S pr

119 20 S proteasome and NQO2 both interact with myeloid differentiation factor CCAAT-enhancer-binding pr

120 signaling through the IL-33 receptor ST2 and myeloid differentiation factor MyD88 is essential for de

121 schlafen 4 (Slfn4) as a GLI1 target gene and myeloid differentiation factor that correlates with spas

122 racted with the LPS receptors, CD14 and TLR4/myeloid differentiation factor-2 (MD-2) complex, indicat

123 In this study, we demonstrated that myeloid differentiation factor-2 (MD-2) is also tyrosine

124 ctions in complex with its accessory protein myeloid differentiation factor-2 (MD-2), is a therapeuti

125 receptor 4 (TLR4), along with its coreceptor myeloid differentiation factor-2 (MD-2), mediates these

126 In this article, we identify myeloid differentiation factor-2 (MD-2), the coreceptor

127 Here, we show that Myeloid differentiation factor-2-related lipid-recogniti

128 r protein inducing interferon beta (TRIF) or myeloid differentiation factor-88 (MyD88) and CX3CR1 kno

129 s for targeted disruption of TLR9, TLR3, and myeloid differentiation factor-88 (MyD88), and most of t

130 a), which in turn activate a well-described, myeloid-differentiation factor 88 (MYD88)-mediated, nucl

131 pression of chromatin-remodeling enzymes and myeloid differentiation factors.

132 F), which are required for growth arrest and myeloid differentiation following Hhex deletion.

133 e hematopoietic progenitors increased NK and myeloid differentiation, further supporting a role of TN

134 tor of nuclear receptor signaling, represses myeloid differentiation genes and drives acute promyeloc

135 Transcription of PR3 and related myeloid differentiation genes in PBMCs may represent nov

136 The coordinated regulation of myeloid differentiation genes was confirmed by GSEA.

137 e-specifying TFs (eg, PU.1/SPI1) to activate myeloid differentiation genes, such as macrophage and gr

138 induced rapid proliferation and induction of myeloid-differentiation genes.

139 wn to be involved in choice between lymphoid/myeloid differentiation have been identified, such as Ar

140 age 5-fold increase), cell-cycle arrest, and myeloid differentiation in AML cell lines and patient bl

141 long-term repopulating HSCs, while delaying myeloid differentiation in BM following injury.

142 However, restoring myeloid differentiation in C/EBPa mutants with inflammat

143 program of self-renewal and expansion toward myeloid differentiation in GMPs.

144 dihydroorotate dehydrogenase (DHODH) enables myeloid differentiation in human and mouse AML models.

145 ated factor 60b), as a critical regulator of myeloid differentiation in humans, mice, and zebrafish.

146 ate that S100A8 and S100A9 are regulators of myeloid differentiation in leukemia and have therapeutic

147 aling intermediates by flow cytometry during myeloid differentiation in MPN patients.

148 ompound from this series was found to induce myeloid differentiation in primary human IDH1 R132H AML

149 well understood, the spatial organization of myeloid differentiation in the bone marrow remains unkno

150 in regions as well as its ability to prevent myeloid differentiation in vivo.

151 ir self-renewal and markedly alters lymphoid/myeloid differentiation in vivo.

152 nscriptionally represses genes that regulate myeloid differentiation, including genes involved in cel

153 CR-ABL1 murine leukemia stem cells, arrested myeloid differentiation, inhibited genotoxic stress-indu

154 Together, these findings show that myeloid differentiation is a prerequisite for LSC format

155 oplasmic relocalization that occurred during myeloid differentiation is essential for PCNA antiapopto

156 ed cells to differentiation, suggesting that myeloid differentiation is promoted by loss of genome in

157 In this study, we show that accelerated myeloid differentiation, known as emergency myelopoiesis

158 ed metabolic state, which drives accelerated myeloid differentiation mainly through epigenetic deregu

159 ma balance and upregulated the expression of myeloid differentiation markers.

160 ing late sepsis might involve alterations in myeloid differentiation/maturation that generate circula

161 A transcription and consequent impairment of myeloid differentiation may contribute to leukemic trans

162 hat upregulation of GFI1 expression leads to myeloid differentiation morphologically and immunophenot

163 eated with quizartinib, we observed terminal myeloid differentiation of BM blasts in association with

164 rrest and apoptosis, and relieves a block in myeloid differentiation of FLT3-ITD(+) AML in vitro.

165 G-CSF)-induced proliferation with diminished myeloid differentiation of hematopoietic CD34(+) cells c

166 issues and was recently shown to inhibit the myeloid differentiation of hematopoietic stem/progenitor

167 w that E47 is dispensable for the short-term myeloid differentiation of HSCs but regulates their long

168 Deletion of MLL4 enhances myelopoiesis and myeloid differentiation of leukaemic blasts, which prote

169 Silencing of METTL14 promotes terminal myeloid differentiation of normal HSPCs and AML cells an

170 G2/M cell-cycle progression and induction of myeloid differentiation of the leukemic blasts.

171 Understanding the process of myeloid differentiation offers important insights into b

172 volved in cell growth and proliferation, and myeloid differentiation pathways were among the most sig

173 profiling of pre-GMs, we identified distinct myeloid differentiation pathways: a pathway expressing t

174 Leukemia blasts show a myeloid differentiation phenotype when these lncRNAs wer

175 (2B) receptor antagonist resulted in altered myeloid differentiation potential.

176 TLR4 and the key adaptor/signaling proteins myeloid differentiation primary response (MyD88), interl

177 Mutations in Toll-like receptor (TLR) and myeloid differentiation primary response 88 (MYD88) gene

178 9; 55.5%), especially those with concomitant myeloid differentiation primary response 88 (MYD88) muta

179 significantly reduced upon gene knockdown of myeloid differentiation primary response 88 (MyD88), TAN

180 on-beta (TRIF) but less so for signaling via myeloid differentiation primary response 88 (MyD88).

181 iments show that the described phenomenon is myeloid differentiation primary response 88, IFN-gamma,

182 tive effect of gedunin on MyD88-adapter-like/myeloid differentiation primary response 88- and TRIF-re

183 mechanism dependent on the adaptor molecule myeloid differentiation primary response gene (88) (MyD8

184 s that are dependent on the adaptor proteins Myeloid differentiation primary response gene (88) (MyD8

185 A mild and transient up-regulation of myeloid differentiation primary response gene (88), TLR9

186 NA) levels of TLR4 and its adapter molecule, myeloid differentiation primary response gene (MYD) 88,

187 Deletion of the innate immune adaptor myeloid differentiation primary response gene 88 (MyD88)

188 Myeloid differentiation primary response gene 88 (MyD88)

189 LRs except TLR3, recruitment of the adapter, myeloid differentiation primary response gene 88 (MyD88)

190 In human myeloid differentiation primary response gene 88 (MyD88)

191 Using tissue-specific myeloid differentiation primary response gene 88 (Myd88)

192 s dependent upon TLR4 and TLR7 signaling via myeloid differentiation primary response gene 88 (MyD88)

193 ltiple innate signaling adaptor pathways for myeloid differentiation primary response gene 88 (MyD88)

194 IL1RL1, its coreceptor IL1RAcP, its adaptors myeloid differentiation primary response gene 88 (MyD88)

195 to mice deficient in the downstream adaptor, Myeloid differentiation primary response gene 88 (MYD88)

196 response were specifically upregulated in a myeloid differentiation primary response gene 88 (MyD88)

197 sion was induced by the oral microbiota in a myeloid differentiation primary response gene 88 (MyD88)

198 M1-pUb linkages are added subsequently, and myeloid differentiation primary response gene 88 (MyD88)

199 signaling including the key adapter protein myeloid differentiation primary response gene 88 (MyD88)

200 or (TIR) domain-containing adapters, such as myeloid differentiation primary response gene 88 (MyD88)

201 Biologic pathways mediated by myeloid differentiation primary response gene 88 (MyD88)

202 containing adapter-inducing IFN-beta (TRIF), myeloid differentiation primary response gene 88 (MyD88)

203 RV-induced myositis/arthritis, we found that myeloid differentiation primary response gene 88 (Myd88)

204 he intracellular TLR signal adaptor known as myeloid differentiation primary response gene 88 (MyD88)

205 Myeloid differentiation primary response gene 88 (MyD88)

206 phils and monocytes that is dependent on the myeloid differentiation primary response gene 88 (MyD88)

207 Myeloid differentiation primary response gene 88 (MyD88)

208 Abrogating the function of myeloid differentiation primary response gene 88 (MyD88)

209 S activates antigen-presenting cells through myeloid differentiation primary response gene 88 (MyD88)

210 eted inactivation of the TLR adaptor protein myeloid differentiation primary response gene 88 (MyD88)

211 Previous studies suggest the presence of myeloid differentiation primary response gene 88 (MyD88)

212 n is through the toll like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88)

213 and IL-1Rs recruit adaptor proteins, such as myeloid differentiation primary response gene 88 (MyD88)

214 independently of CD14 and triggers canonical myeloid differentiation primary response gene 88 (MyD88)

215 have previously demonstrated that absence of myeloid differentiation primary response gene 88 (MyD88)

216 r the Toll-like receptor signaling component myeloid differentiation primary response gene 88 (MyD88)

217 o carcinogen-induced skin cancer, similar to myeloid differentiation primary response gene 88 (MyD88)

218 polysaccharide (LPS), a process dependent on myeloid differentiation primary response gene 88 (MYD88)

219 (TLR; p < 0.001), IL-1 receptor (p = 0.001), myeloid differentiation primary response gene 88 (p = 0.

220 ation activation gene [Rag] 1(KO), TLR4(KO), myeloid differentiation primary response gene 88 [MyD88]

221 LPS increased adrenal myeloid differentiation primary response gene 88 and TLR

222 iver genes while also confirming the role of myeloid differentiation primary response gene 88 in the

223 Interestingly, myeloid differentiation primary response gene 88 knockou

224 tumour necrosis factor receptor (TNFR)-1/-2, Myeloid Differentiation primary response gene 88 or Toll

225 inly signal through the Toll-like receptor 4/myeloid differentiation primary response gene 88 pathway

226 ewise, targeted deletion of B-cell-intrinsic myeloid differentiation primary response gene 88 signali

227 Furthermore, pretreatment of DCs with MyD88 (myeloid differentiation primary response gene 88) and IL

228 R4) binds adapter proteins, including MyD88 (myeloid differentiation primary response gene 88) and Ma

229 molecule 1) but does not require the MyD88 (myeloid differentiation primary response gene 88) arm of

230 including the classical NF-kappaB and MYD88 (myeloid differentiation primary response gene 88) pathwa

231 CHOP (C/EBP homologous protein), and MyD88 (myeloid differentiation primary response gene 88), but n

232 f it lacks the innate defense protein MyD88 (myeloid differentiation primary response gene 88), or af

233 MyD88 (myeloid differentiation primary response gene 88)-indepe

234 coli LPS provokes strong inflammatory MyD88 (myeloid differentiation primary response gene 88)-mediat

235 A expressions of NOD2, Toll-like receptor 2, myeloid differentiation primary response gene 88, and re

236 nd reduces eNOS expression via activation of myeloid differentiation primary response gene 88.

237 -3, and IRF-7 to the RANTES independently of myeloid differentiation primary response gene-88 (MyD88)

238 mally induce phosphorylation of CD19 through myeloid differentiation primary response gene-88 (MYD88)

239 for advanced glycation end products (RAGE), myeloid differentiation primary response gene-88, and tu

240 tyrosine phosphorylation, and recruitment of myeloid differentiation primary response protein (MyD) 8

241 blation in THP-1 cells impaired induction of myeloid differentiation primary response protein (MyD88)

242 LR2 polymorphism alters the functions of the myeloid differentiation primary response protein 88 (MyD

243 Myeloid differentiation primary response protein 88 (MyD

244 Myeloid differentiation primary response protein 88 (MyD

245 Reanalysis of the array data set identified myeloid differentiation primary response protein 88 (MYD

246 tor superfamily requires the adapter protein myeloid differentiation primary response protein 88 (MyD

247 infection to investigate the contribution of myeloid differentiation primary response protein 88 (MyD

248 r-2, alphavbeta3 integrin, CR3, and adaptors myeloid differentiation primary response protein 88 (MyD

249 Deletion of myeloid differentiation primary response protein 88 (MyD

250 levels of Toll-like receptors (TLRs), CD14, myeloid differentiation primary response protein 88, and

251 (GC) responses, mice selectively deleted for myeloid differentiation primary-response protein 88 (MyD

252 acrophage ABCA1 also dampens proinflammatory myeloid differentiation primary-response protein 88-depe

253 terferon-beta (TRIF) but were independent of myeloid-differentiation primary response-gene 88 (MYD88)

254 expression changes in two divergent terminal myeloid differentiation processes, namely MAC and OC dif

255 of these cells results from activation of a myeloid differentiation program in bone marrow (BM) by a

256 hanges directly activate the common terminal myeloid differentiation programme.

257 am into macrophage-like cells by exposure to myeloid differentiation-promoting cytokines in vitro or

258 the role of the Toll-like receptor 4 (TLR-4)/myeloid differentiation protein (MyD88) pathway and the

259 r of differentiation 14/Toll-like receptor 4/myeloid differentiation protein 2 (MD-2) complex.

260 n this study, we demonstrate that PTX3 binds myeloid differentiation protein 2 (MD-2) in vitro and ex

261 Herein, we show that rifampin binds to myeloid differentiation protein 2 (MD-2), the key corece

262 sory protein of Toll-like receptor 4 (TLR4), myeloid differentiation protein 2 (MD-2), thereby induci

263 Myeloid differentiation protein 2 (MD2) is a TLR4 corece

264 Increased expression of TLR4 and myeloid differentiation protein 2 (MD2) results in Akt p

265 tem following binding with the complex CD14, myeloid differentiation protein 2, and Toll-like recepto

266 The myeloid differentiation protein 88 (MyD88) adapter prote

267 two important TLR adaptor molecules, such as myeloid differentiation protein 88 (MyD88) and TRIF-rela

268 Myeloid differentiation protein 88 (MyD88) is a key sign

269 ls delivered through the TLR adapter protein myeloid differentiation protein 88 (MyD88) play a critic

270 ey role for a cognate TLR4 effector protein, myeloid differentiation protein 88 (MyD88), in this proc

271 , including Toll-like receptor (TLR) 2/4 and myeloid differentiation protein 88 deficiency and neutro

272 orthotopic lung recipients in a TLR2/4- and myeloid differentiation protein 88-dependent fashion and

273 alein bound to the hydrophobic region of the myeloid differentiation protein-2 (MD-2) pocket and inhi

274 novel alternatively spliced isoform of human myeloid differentiation protein-2 (MD-2s) that competiti

275 lyses showed that GKY25 interferes with TLR4/myeloid differentiation protein-2 dimerization.

276 does not show DNA methylation changes during myeloid differentiation, provide evidence that 14q32 hyp

277 ontinuum of progenitors execute lymphoid and myeloid differentiation, rather than only uni-lineage pr

278 promotes CKMT1 expression by repressing the myeloid differentiation regulator RUNX1.

279 Here, we report that the myeloid differentiation-related transcription factor nuc

280 he role of Toll-like receptor (TLR) 2, TLR4, myeloid differentiation response gene 88, and Toll-IL-1

281 In the absence of TLR2, TLR4, myeloid differentiation response gene 88, or TRIF, the c

282 f zeste homolog 2 (EZH2) inhibitors promoted myeloid differentiation, suggesting EZH2 inhibitors may

283 ukaemia (AML) is characterized by a block in myeloid differentiation the stage of which is dependent

284 pendent activation of caspase 3 in promoting myeloid differentiation, the inhibition of caspase 3 blo

285 e to mutant HSC over normal HSC and promotes myeloid differentiation to engender a myeloproliferative

286 LL-AF9 and MOZ-TIF2 AML models, we show that myeloid differentiation to granulocyte macrophage progen

287 However, where IRF8 acts in the pathway of myeloid differentiation to influence PMN-MDSC production

288 Panobinostat triggered terminal myeloid differentiation via proteasomal degradation of A

289 Impaired myeloid differentiation was observed in LIG4-, but not A

290 vere, selective defect in erythroid, but not myeloid, differentiation was observed.

291 To examine the role of GABP in myeloid differentiation, we generated mice in which Gabp

292 gulator of B-lymphoid development and blocks myeloid differentiation when ectopically expressed.

293 rowth of normal cord blood cells by inducing myeloid differentiation, whereas a certain level of RUNX

294 e vitamin A derivative retinoic acid (RA) in myeloid differentiation, whereas fewer studies explore t

295 zed wild-type IDH1 AML cells to ATRA-induced myeloid differentiation, whereas inhibition of 2-HG prod

296 MDL-1, a PU.1 transcriptional target during myeloid differentiation, which orchestrates osteoclast d

297 Instead, it stimulates myeloid differentiation, which progresses into a myelopr

298 reactivates imprinted genes (without causing myeloid differentiation, which would confound downstream

299 y inducing cell-cycle arrest, apoptosis, and myeloid differentiation without general toxicity to norm

300 Finally, in addition to supporting myeloid differentiation, zebrafish Gcsf is required for