ライフサイエンスコーパス: mixed lineage

1 nto 2 categories, those that are composed of mixed lineage cells and those that are predominantly T c

2 roliferation in Lin(-) cells and led to more mixed lineage colonies from transduced KI BM cells.

3 ated colonies showed improved maintenance of mixed lineage colonies with both erythroid and megakaryo

4 mixed population, as a minority give rise to mixed-lineage colonies while the majority of cells are t

5 tor-interacting protein kinase 3 (RIPK3) and mixed lineage domain-like protein (MLKL), targeting necr

6 Here we show that the mixed-lineage dual leucine zipper kinase (DLK) is an ess

7 MLK4 is a member of the mixed-lineage family of kinases that regulate the JNK, p

8 ferentiated prematurely, and often adopted a mixed lineage fate.

9 e show that this analysis captured prevalent mixed-lineage intermediates that manifested concurrent e

10 these events, the effect of Tat and gp120 on mixed lineage kinase (MLK) 3 activation was examined.

11 This analysis identified mixed lineage kinase 3 (MLK3) as a putative NS5A interac

12 Mixed lineage kinase 3 (MLK3) deficiency reduces macroph

13 Mixed lineage kinase 3 (MLK3) functions in migration and

14 on in the kinase activity of a pro-apoptotic mixed lineage kinase 3 (MLK3) in HER2-positive (HER2+) b

15 Mixed lineage kinase 3 (MLK3) is a MAP3K that activates

16 Mixed lineage kinase 3 (MLK3) is a mitogen-activated pro

17 Inhibition of mixed lineage kinase 3 (MLK3) is a potential strategy fo

18 noted that the activity of the proapoptotic mixed lineage kinase 3 (MLK3) kinase was relatively high

19 possible cross-talk between beta-catenin and mixed lineage kinase 3 (MLK3), a MAPK kinase kinase memb

20 protein (merlin/schwannomin) associates with mixed lineage kinase 3 (MLK3), a mitogen-activated prote

21 MLK3 (mixed lineage kinase 3) is a widely expressed, mammalian

22 Here, we report that mixed lineage kinase 4 (MLK4) is overexpressed in MES bu

23 e mutational analyses have revealed that the mixed lineage kinase 4 (MLK4) protein kinase is frequent

24 ptor-interacting protein kinase 3 (RIPK3) or mixed lineage kinase domain like (MLKL), two core protei

25 acting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and generally ma

26 The pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) is an essential

27 with subsequent RIP3-dependent activation of mixed lineage kinase domain-like (MLKL) leading to necro

28 grammed form of necrosis, is executed by the mixed lineage kinase domain-like (MLKL) protein, which i

29 Total levels of RIP1, RIP3, and mixed lineage kinase domain-like (MLKL) proteins were in

30 tor-interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL) proteins.

31 interacting protein kinase 3 (RIPK3) and the mixed lineage kinase domain-like (MLKL) pseudokinase.

32 r RIP3 activation and phosphorylation of the mixed lineage kinase domain-like (MLKL) pseudokinase.

33 ylates and activates the downstream effector mixed lineage kinase domain-like (MLKL) to induce necrop

34 nd its downstream effector, the pseudokinase mixed lineage kinase domain-like (MLKL).

35 protein kinase 3 (RIPK3) and its substrate, mixed lineage kinase domain-like (MLKL).

36 e-3, eventually leading to the activation of mixed lineage kinase domain-like and plasma membrane per

37 HFD did not increase phosphorylated mixed lineage kinase domain-like in RIP3(-/-) mice.

38 kinase activity, but it remains dependent on mixed lineage kinase domain-like protein (MLKL) downstre

39 events in two forms of programmed necrosis [mixed lineage kinase domain-like protein (MLKL) in necro

40 is is not involved in APAP toxicity by using mixed lineage kinase domain-like protein (MLKL) knockout

41 her et al. demonstrate that the pseudokinase mixed lineage kinase domain-like protein (MLKL) particip

42 The expression level of mixed lineage kinase domain-like protein (MLKL), a key d

43 , we have demonstrated that the pseudokinase mixed lineage kinase domain-like protein (MLKL), which p

44 g virus infections, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which t

45 nery in the CNS, including RIPK1, RIPK3, and mixed lineage kinase domain-like protein (MLKL).

46 The mixed lineage kinase domain-like protein MLKL is a funct

47 RIP1 and RIP3 and their interaction with the mixed lineage kinase domain-like protein MLKL.

48 es receptor-interacting proteins 1 and 3 and mixed lineage kinase domain-like protein necroptotic sig

49 RIPK1 or RIPK3, but not the RIPK3 substrate mixed lineage kinase domain-like protein, attenuated TNF

50 lving receptor-interacting protein 1 and the mixed lineage kinase domain-like protein.

51 ptosis, assessed by levels of phosphorylated mixed lineage kinase domain-like protein.

52 rylation and plasma membrane localization of mixed lineage kinase domain-like pseudokinase (MLKL).

53 ivated, RIP3 kinase targets the pseudokinase mixed lineage kinase domain-like to drive cell lysis.

54 nase 1) and RIPK3, and a pseudo-kinase MLKL (Mixed Lineage Kinase domain-Like) associated in a multi-

55 or of necroptosis, as well as phosphorylated mixed lineage kinase domain-like, an effector of necropt

56 Here we report the identification of mixed lineage kinase domain-like, MLKL, as a key RIP3 do

57 eficiency, cells develop sensitivity to RIP3-mixed lineage kinase domain-like-mediated necroptosis as

58 , which eventually lead to the activation of mixed lineage kinase domain-like.

59 In this paper, we show that the mixed lineage kinase dual leucine zipper kinase (DLK) se

60 ring Kinase (LZK/MAP3K13) is a member of the mixed lineage kinase family with high sequence identity

61 The mixed lineage kinase MLK3 plays a crucial role in compro

62 I receptor (TGF-beta RI), TGF-beta RII, and mixed lineage kinase-7 (MLK-7).

63 The activation of mixed lineage kinase-like (MLKL) by receptor-interacting

64 eceptor-interacting protein kinase 3 (RIPK3)-mixed lineage kinase-like (MLKL) signaling pathway in eo

65 eptor-interacting protein kinase-3 (RIPK3)-a mixed lineage kinase-like (MLKL) signaling pathway in ne

66 g aberrant caspase-8-dependent apoptosis and mixed lineage kinase-like (MLKL)-dependent necroptosis.

67 ic cells also expose PS after phosphorylated mixed lineage kinase-like (pMLKL) translocation to the m

68 e the endogenous dp5, its induction requires mixed-lineage kinase (MLK) and c-Jun N-terminal kinase (

69 The mixed-lineage kinase 3 (MLK-3) inhibitor URMC-099 provid

70 Mixed-lineage kinase 3 (MLK3) activates mitogen-activate

71 The MAPK kinase kinase (MAP3K) mixed-lineage kinase 3 (MLK3) is required for mitogen ac

72 goal of this study was to determine whether mixed-lineage kinase 3 (MLK3) mediates the initial, ASK1

73 Here we demonstrate that mixed-lineage kinase 3 (MLK3), a MAP3K family member, ph

74 in-penetrant inhibitor with activity against mixed-lineage kinase 3 (MLK3), named URMC-099.

75 ts initiated by FGD1 that involves the MAP3K mixed-lineage kinase 3 (MLK3).

76 nscript stabilization required activation of mixed-lineage kinase 3 and p38 mitogen-activated protein

77 r-interacting protein kinase (RIPK) 1/3- and mixed-lineage kinase domain-like (MLKL)-dependent necrop

78 ng protein kinase 3 (RIP3) and its substrate mixed-lineage kinase domain-like protein (MLKL) are core

79 The effector of necroptosis, phosphorylated mixed-lineage kinase domain-like protein (MLKL), was det

80 protein kinase-3 (RIPK3) phosphorylation of mixed-lineage kinase domain-like protein (MLKL), which r

81 inhibitor Clostridium difficile toxin B, the mixed-lineage kinase inhibitor CEP11004, and the JNK inh

82 Mixed-lineage kinase-3 (MLK3) is a mammalian mitogen-act

83 dynamics and activation of components of the mixed-lineage kinase-dependent JNK module.

84 l death dependent on RIPK-1, RIPK-3, and the mixed-lineage kinase-like protein (MLKL).

85 CD40L induced activation of mixed-lineage-kinase-3 and JNK, leading to the subsequen

86 Here we demonstrate that the mixed lineage kinases (MLK1-4) are MEK kinases that reac

87 Mixed lineage kinases (MLKs) function as Jun-N-terminal

88 Mixed lineage kinases (MLKs) have been implicated in cyt

89 In turn, the expression of activated mixed lineage kinases (MLKs) induced JNK activation and

90 tivation of the MAPK-kinase-kinases (MAP3Ks) mixed lineage kinases (MLKs)-2 and -3.

91 One is CEP-1347, an inhibitor of mixed lineage kinases that elicits neuroprotective and a

92 way) that includes activation of Rac1/Cdc42, mixed lineage kinases, MAP kinase kinases 4 and 7, and J

93 e PAMPs, in a GCK-dependent manner, activate mixed lineage kinases-2 and -3, MAPK kinase kinases upst

94 rotein that binds and promotes activation of mixed lineage kinases.

95 Similar to the closely related mixed-lineage kinases, LRRK2 can undergo autophosphoryla

96 kinase domain based on sequence homology to mixed-lineage kinases.

97 The conserved Mixed Lineage Leukaemia (MLL) complex deposits activatin

98 The mixed lineage leukaemia (MLL) family of proteins (includ

99 ent chromosomal translocations involving the mixed lineage leukaemia (MLL) gene initiate aggressive f

100 ions found in leukaemia patients involve the mixed lineage leukaemia (MLL) gene.

101 and MEIS1 have essential oncogenic roles in mixed lineage leukaemia (MLL)-rearranged leukaemia.

102 Menin also interacts with mixed lineage leukaemia protein 1 (MLL1), a histone H3 l

103 The mixed-lineage leukaemia (MLL) CXXC domain selectively bi

104 Chromosomal translocations involving the Mixed-Lineage Leukaemia (MLL) gene underlie many human l

105 ted or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight ce

106 Here we show that the trxG member Mll1 (mixed-lineage leukaemia 1) is required for neurogenesis

107 216 patients with AML, excluding those with mixed-lineage leukaemia.

108 Mixed lineage leukemia (MLL) and its metazoan Trithorax

109 c-Myb, GATA-3, Menin, and mixed lineage leukemia (MLL) bound to CGRE in human prim

110 nic fusions of the Trithorax-related protein mixed lineage leukemia (MLL) can initiate aggressive leu

111 allosteric changes that transcription factor mixed lineage leukemia (MLL) causes to the interactions

112 WDR5 is a component of the mixed lineage leukemia (MLL) complex, which methylates l

113 The oncoprotein Ash2L is a component of the mixed lineage leukemia (MLL) family members 1-4, Setd1A,

114 Although misregulation of mixed lineage leukemia (MLL) family proteins has been as

115 Mixed lineage leukemia (MLL) fusion genes arise from chr

116 unctions and in leukemogenesis driven by the mixed lineage leukemia (MLL) fusion oncogene MLL-AF9.

117 ough menin acts as an oncogenic cofactor for mixed lineage leukemia (MLL) fusion protein-mediated his

118 polymerase-associated factor complex (PAFc), mixed lineage leukemia (MLL) fusion proteins activate ge

119 unctions as a critical oncogenic cofactor of mixed lineage leukemia (MLL) fusion proteins in the deve

120 The interaction between menin and oncogenic mixed lineage leukemia (MLL) fusion proteins is required

121 Mixed lineage leukemia (MLL) fusion-driven acute leukemi

122 Chromosomal translocations of the mixed lineage leukemia (MLL) gene are a common cause of

123 Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are associated with ag

124 ith chromosomal translocations involving the mixed lineage leukemia (MLL) gene are usually associated

125 Chromosome translocations involving the mixed lineage leukemia (MLL) gene fuse it in frame with

126 first identified as a fusion partner of the mixed lineage leukemia (MLL) gene in acute myeloid leuke

127 The mixed lineage leukemia (MLL) gene is also frequently inv

128 Translocations of the mixed lineage leukemia (MLL) gene occur in 60% to 80% of

129 The mixed lineage leukemia (MLL) gene plays a critical role

130 Chromosomal translocations involving the Mixed Lineage Leukemia (MLL) gene produce chimeric prote

131 of infants with ALL, particularly those with mixed lineage leukemia (MLL) gene rearrangements, is onl

132 Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion p

133 to be a drug target for acute leukemia with mixed lineage leukemia (MLL) gene translocations.

134 kemia (B-ALL) harboring rearrangement of the mixed lineage leukemia (MLL) gene with CD19 CAR-T cells.

135 L) is characterized by rearrangements of the mixed lineage leukemia (MLL) gene with one of its >50 pa

136 lso interacts with translocation partners of Mixed Lineage Leukemia (MLL) gene, which is commonly tra

137 receptors (ERs) and ER coregulators such as mixed lineage leukemia (MLL) histone methylases (MLL2 an

138 ights into the role of the Trithorax protein mixed lineage leukemia (MLL) in maintaining cancer stem

139 Mixed lineage leukemia (MLL) is a key epigenetic regulat

140 The histone methyltransferase Mixed Lineage Leukemia (MLL) is essential to maintain he

141 A critical unanswered question about mixed lineage leukemia (MLL) is how specific MLL fusion

142 ome translocations, most often involving the mixed lineage leukemia (MLL) locus at 11q23.

143 plex (DotCom), which includes several of the mixed lineage leukemia (MLL) partners in leukemia such a

144 -protein interaction (PPI) between menin and mixed lineage leukemia (MLL) plays a critical role in ac

145 The mixed lineage leukemia (MLL) protein and its Drosophila

146 e Men1 gene product menin interacts with the mixed lineage leukemia (MLL) protein, a histone H3 lysin

147 WD repeat domain 5 (WDR5) and block the WDR5-mixed lineage leukemia (MLL) protein-protein interaction

148 ENL, and AF9, is recruited by HIV-1 Tat and mixed lineage leukemia (MLL) proteins to activate the ex

149 Aven stimulates the mRNA translation of the mixed lineage leukemia (MLL) proto-oncogene in an argini

150 The mixed lineage leukemia (MLL) proto-oncogene is a recurre

151 third plant homeodomain (PHD3) finger of the mixed lineage leukemia (MLL) proto-oncoprotein and a pol

152 Mixed lineage leukemia (MLL) represents a genetically di

153 sents the most common leukemogenic fusion of mixed lineage leukemia (MLL) to a cytoplasmic partner pr

154 regulator in the expression of HOX genes in mixed lineage leukemia (MLL)-based hematological maligna

155 d the miRNAs are aberrantly overexpressed in mixed lineage leukemia (MLL)-rearranged acute leukemias.

156 regulator CDK6 as a promising new target in mixed lineage leukemia (MLL)-rearranged acute myeloid le

157 hylation (H3K27me3/2) and inhibits growth of mixed lineage leukemia (MLL)-rearranged leukemia cells.

158 ranslocations, that approximately 43% of all mixed lineage leukemia (MLL)-rearranged leukemias are EV

159 the c-Myb/GATA-3 complex contained Menin and mixed lineage leukemia (MLL).

160 , we identify the histone-remodelling enzyme mixed lineage leukemia (MLL)3 as a clock-controlled fact

161 gulated in the pathophysiology of rearranged mixed lineage leukemia (MLL-r).

162 They demonstrate that the mixed lineage leukemia (MLL1) gene acts independently fr

163 Mixed Lineage Leukemia (MLL1) translocations encode fusi

164 F23, and NUP98-TOP1 physically interact with mixed lineage leukemia 1 (MLL1) and the non-specific let

165 Mixed lineage leukemia 1 (MLL1) is a histone H3 lysine 4

166 The epigenetic activator Mixed lineage leukemia 1 (MLL1) is paramount for embryon

167 We show that the mixed lineage leukemia 1 (MLL1) protein, a histone methy

168 Menin is an essential oncogenic cofactor for mixed lineage leukemia 1 (MLL1)-mediated leukemogenesis

169 ulated by MOZ, mixed lineage leukemia 1, and mixed lineage leukemia 1 cofactor menin.

170 leukemia cell lines harboring the rearranged mixed lineage leukemia 1 gene.

171 of acute leukemias arise from fusion of the mixed lineage leukemia 1 protein (MLL) N terminus to a v

172 oregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding prot

173 The MLL1 (mixed lineage leukemia 1) protein, which is often disrup

174 gnificant overlap in genes regulated by MOZ, mixed lineage leukemia 1, and mixed lineage leukemia 1 c

175 Lpt) is the N-terminal homolog of mammalian Mixed Lineage Leukemia 2 (MLL2/ALR), a core component of

176 transferases such as enhancer of zeste 2 and mixed lineage leukemia 2, histone demethylases including

177 ximately 50% reduction in gene dosage of the mixed lineage leukemia 3 (MLL3) gene, located on 7q36.1,

178 The MLL3 (mixed lineage leukemia 3) protein is a member of the hum

179 H3.3 is repressed by mixed lineage leukemia 5 (MLL5) in self-renewing GBM cel

180 Taspase1, the mixed lineage leukemia and TFIIAalpha-beta cleaving prot

181 upport of this idea, we showed recently that mixed lineage leukemia fusion oncoproteins can convert c

182 ias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologi

183 Chromosomal translocations affecting mixed lineage leukemia gene (MLL) result in acute leukem

184 Rearrangements of the mixed lineage leukemia gene MLL are associated with aggr

185 5 (WDR5) is a common component of mammalian mixed lineage leukemia methyltransferase family members

186 h an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-P

187 The mixed lineage leukemia protein MLL1 contains four highly

188 The mixed lineage leukemia protein-1 (MLL1) belongs to the S

189 The mixed lineage leukemia protein-1 (MLL1) catalyzes histon

190 The mixed lineage leukemia protein-1 (MLL1) is a member of t

191 Mixed lineage leukemia protein-1 (MLL1) is a member of t

192 DPY-30), a complex that is part of the MLL1 (mixed lineage leukemia protein-1) core complex but that

193 lysine 4 (H3K4) methyltransferases including mixed lineage leukemia proteins to regulate homeobox (Ho

194 t extremely high levels in ALL patients with mixed lineage leukemia rearrangements or hyperdiploidy a

195 y, although PTIP and PA1 associate with MLL (mixed lineage leukemia) complexes and participate in tra

196 ves as a critical oncogenic cofactor of MLL (mixed lineage leukemia) fusion proteins in acute leukemi

197 e a drug target for acute leukemia with MLL (mixed lineage leukemia) gene translocations.

198 AMLs bearing MLL (mixed lineage leukemia) rearrangements are associated wi

199 The mixed lineage leukemia-1 (MLL1) core complex predominant

200 The mixed lineage leukemia-1 (MLL1) enzyme is a histone H3 l

201 Translocations and amplifications of the mixed lineage leukemia-1 (MLL1) gene are associated with

202 lso suppresses proliferation of leukemogenic mixed lineage leukemia-AF9 fusion-protein-transformed my

203 f conditional transformation by an inducible mixed lineage leukemia-eleven-nineteen leukemia (MLL-ENL

204 3 (IGF2BP3) is specifically overexpressed in mixed lineage leukemia-rearranged (MLL-rearranged) B-acu

205 A notable exception is mixed lineage leukemia-rearranged infant ALL, where vene

206 ole and is a potential therapeutic target in mixed lineage leukemia.

207 sociated with infant acute lymphoblastic and mixed lineage leukemia.

208 s cytogenetics in acute myeloid leukemia and mixed lineage leukemia.

209 Moreover, UTX associates with mixed-lineage leukemia (MLL) 2/3 complexes, and during r

210 impaired reconstitution of stem cell-derived mixed-lineage leukemia (MLL) AML, which represents an ag

211 isordered transcription factors, such as the mixed-lineage leukemia (MLL) and c-Myb peptides, at isol

212 more, we observed that SALL4 interacted with mixed-lineage leukemia (MLL) and co-occupied the HOXA9 p

213 t multiple MLL-fusion proteins implicated in mixed-lineage leukemia (MLL) associate with AFF4, ELLs,

214 g to a single surface of the KIX domain, the mixed-lineage leukemia (MLL) binding surface.

215 his targeting strategy does not affect other mixed-lineage leukemia (MLL) family histone methyltransf

216 as the threonine endopeptidase that cleaves mixed-lineage leukemia (MLL) for proper Hox gene express

217 A subgroup of leukemogenic mixed-lineage leukemia (MLL) fusion proteins (MFPs) incl

218 LEDGF associates with mixed-lineage leukemia (MLL) fusion proteins and menin a

219 Mixed-lineage leukemia (MLL) fusion proteins are potent

220 Mixed-lineage leukemia (MLL) fusions are potent oncogene

221 ary acute myelogenous leukemia involving the mixed-lineage leukemia (MLL) gene (11q23) translocations

222 We previously identified a rearrangement of mixed-lineage leukemia (MLL) gene (also known as ALL-1,

223 hromosomal translocation that juxtaposes the mixed-lineage leukemia (MLL) gene and the AF4 gene.

224 OF REVIEW: Leukemia carrying mutation of the mixed-lineage leukemia (MLL) gene is particularly refrac

225 Chromosomal rearrangements involving the mixed-lineage leukemia (MLL) gene occur in primary and t

226 The mixed-lineage leukemia (MLL) gene often fuses with ENL a

227 Chromosomal translocations of the mixed-lineage leukemia (MLL) gene with various partner g

228 t B-ALL is chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene.

229 The mixed-lineage leukemia (MLL) H3K4 methyltransferase prot

230 ost cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase c

231 AF4 gene, frequently translocated with mixed-lineage leukemia (MLL) in childhood acute leukemia

232 It is fused to mixed-lineage leukemia (MLL) in leukemia, and missense m

233 Mixed-lineage leukemia (MLL) is a proto-oncogene frequen

234 t mutations such as FLT3 internal-tandem and mixed-lineage leukemia (MLL) partial-tandem duplications

235 ax binds KIX at the previously characterized mixed-lineage leukemia (MLL) protein interaction surface

236 Histone lysine methylation, mediated by mixed-lineage leukemia (MLL) proteins, is now known to b

237 determined that MSI2 directly maintains the mixed-lineage leukemia (MLL) self-renewal program by int

238 The t(4;11)(q21;q23) fuses mixed-lineage leukemia (MLL) to AF4, the most common MLL

239 gements involving the H3K4 methyltransferase mixed-lineage leukemia (MLL) trigger aberrant gene expre

240 Mixed-lineage leukemia (MLL), an epigenetic regulator, p

241 omal aberrations and abnormalities involving mixed-lineage leukemia (MLL), an upstream regulator of H

242 Mixed-lineage leukemia (MLL)-AF4 fusion arises prenatall

243 Myeloid/lymphoid or mixed-lineage leukemia (MLL)-family genes encode histone

244 t to chromatin as an effective treatment for mixed-lineage leukemia (MLL)-fusion leukemia' by Dawson

245 k the progression of certain cancers such as mixed-lineage leukemia (MLL)-rearranged leukemias.

246 In contrast, leukemia driven by mixed-lineage leukemia (MLL, encoded by KMT2A) fusions w

247 Mixed-lineage leukemia (MLL; also known as myeloid/lymph

248 down (KD) of a writer, the methyltransferase mixed-lineage leukemia 1 (Mll1) (n = 26), and an eraser,

249 Here, we show that mixed-lineage leukemia 1 (MLL1) protein is a key determi

250 ity for a truncated, lacZ knock-in allele of mixed-lineage leukemia 1 (Mll1), a histone methyltransfe

251 Ash1l cooperated functionally with mixed-lineage leukemia 1 (Mll1), as combined loss of Ash

252 f the H3K4-specific methyltransferase, Kmt2a/Mixed-lineage leukemia 1 (Mll1), in mouse postnatal fore

253 ultiprotein complex essential for activating mixed-lineage leukemia 1 (MLL1).

254 he histone methyltransferases Set1 and MLL1 (mixed-lineage leukemia 1), leading to histone H3K4 trime

255 istone-methyltransferase myeloid/lymphoid or mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult fore

256 s identified were all of the subunits of the mixed-lineage leukemia 3 (Mll3) and 4 (Mll4) complexes,

257 The histone H3-lysine-4 methyltransferase mixed-lineage leukemia 3 (MLL3) and its closest homolog,

258 Although PTIP is a unique component of the mixed-lineage leukemia 3 (MLL3)/MLL4 chromatin-modifying

259 deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3)-MLL4 complex display impaired

260 umonji C family of proteins, associates with mixed-lineage leukemia 3/4 complexes.

261 Mixed-lineage leukemia 4 (MLL4/KMT2D) is a major enhance

262 Mixed-lineage leukemia 4 (MLL4; also called MLL2 and ALR

263 The human mixed-lineage leukemia 5 (MLL5) protein mediates hematop

264 ragile sites, and breakpoints, including the mixed-lineage leukemia breakpoint cluster region (MLL BC

265 ses the transcriptional activity of a common mixed-lineage leukemia fusion partner, AF9.

266 Chromosome rearrangements involving the mixed-lineage leukemia gene (MLL) create MLL-fusion prot

267 adults as a result of rearrangements to the mixed-lineage leukemia gene (MLL) located on chromosome

268 atient-derived xenografts (PDX) of pediatric mixed-lineage leukemia gene (MLL)-rearranged ALL were es

269 MEN1 and its coactivator, the mixed-lineage leukemia histone methyltransferase, are re

270 ize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the path

271 Here we demonstrate that the mixed-lineage leukemia protein (MLL) complex, a well-kno

272 ith the transcriptional activation domain of mixed-lineage leukemia protein leads to an enhancement o

273 The mixed-lineage leukemia protein MLL1 is a transcriptional

274 in leukemogenesis driven by a subset of MLL (mixed-lineage leukemia) fusion proteins raises the possi

275 to as MLL to denote the gene associated with mixed-lineage leukemia) generate MLL fusion proteins tha

276 horax family member MLL (myeloid/lymphoid or mixed-lineage leukemia) is presumed to activate Hox expr

277 The MLL (mixed-lineage leukemia) proto-oncogene encodes a histone

278 Mixed-lineage leukemia-1 (MLL1) has been shown to direct

279 eptor NKp44 (NKp44L), a novel isoform of the mixed-lineage leukemia-5 protein, as a cellular ligand f

280 effectively treats aggressive AML, including mixed-lineage leukemia-driven AML, and outperforms stand

281 ing response to therapy, of 35 patients with mixed-lineage leukemia.

282 ation domain associates with TRRAP/TIP60 and mixed-lineage-leukemia (MLL1/MLL2) SET1-type chromatin-m

283 Mixed lineage leukemias (MLLs) are human histone H3 lysi

284 key roles of ERs in the recruitment of these mixed lineage leukemias into the HOXC6 promoter.

285 DM2 activates chk1 phosphorylation, elevates mixed lineage lymphoma histone methyl transferase levels

286 volved in T-cell signaling, and give rise to mixed-lineage lymphoma in vivo.

287 secreted signalling molecule Wnt1 generates mixed-lineage mammary tumours composed of basal and lumi

288 ts exhibited varied morphology, suggesting a mixed-lineage origin of tumor-initiating cells.

289 and accounts for the onset and resolution of mixed lineage patterns during cell fate determination.

290 well as bipotential intermediates, manifest mixed-lineage patterns of gene expression at a single-ce

291 ete differentiation but often also display a mixed lineage phenotype.

292 -) myeloid cells contributes to the observed mixed lineage phenotype.

293 tification of transcriptomes from individual mixed lineage progenitor cells in the chick as these cel

294 We report that disruption of the mixed-lineage protein kinase (MLK) - cJun NH2-terminal k

295 es in mice to demonstrate a central role for mixed-lineage protein kinases (MLK) in this signaling pa

296 e Rac/Cdc42 interaction site (CRIB motif) on mixed-lineage protein kinases (MLKs).

297 We propose that mixed-lineage states are obligatory during cell-fate spe

298 Such mixed-lineage states may reflect the molecular priming o

299 The proposed method is a novel mixed lineage tree/sequence based method to detect withi

300 ting cells (TICs), which proliferate to form mixed-lineage tumors.