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1 sociated with infant acute lymphoblastic and mixed lineage leukemia.
2 s cytogenetics in acute myeloid leukemia and mixed lineage leukemia.
3 an inv(8)(p11q13) from a patient with acute mixed lineage leukemia.
4 ole and is a potential therapeutic target in mixed lineage leukemia.
5 ing response to therapy, of 35 patients with mixed-lineage leukemia.
6 methyltranferases (H3K4MTs) MLL3 and MLL4 in mixed-lineage leukemia.
7 F23, and NUP98-TOP1 physically interact with mixed lineage leukemia 1 (MLL1) and the non-specific let
11 Menin is an essential oncogenic cofactor for mixed lineage leukemia 1 (MLL1)-mediated leukemogenesis
14 of acute leukemias arise from fusion of the mixed lineage leukemia 1 protein (MLL) N terminus to a v
15 oregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding prot
17 gnificant overlap in genes regulated by MOZ, mixed lineage leukemia 1, and mixed lineage leukemia 1 c
18 down (KD) of a writer, the methyltransferase mixed-lineage leukemia 1 (Mll1) (n = 26), and an eraser,
20 ity for a truncated, lacZ knock-in allele of mixed-lineage leukemia 1 (Mll1), a histone methyltransfe
22 f the H3K4-specific methyltransferase, Kmt2a/Mixed-lineage leukemia 1 (Mll1), in mouse postnatal fore
24 he histone methyltransferases Set1 and MLL1 (mixed-lineage leukemia 1), leading to histone H3K4 trime
27 Translocations and amplifications of the mixed lineage leukemia-1 (MLL1) gene are associated with
29 Lpt) is the N-terminal homolog of mammalian Mixed Lineage Leukemia 2 (MLL2/ALR), a core component of
30 transferases such as enhancer of zeste 2 and mixed lineage leukemia 2, histone demethylases including
31 istone-methyltransferase myeloid/lymphoid or mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult fore
32 ximately 50% reduction in gene dosage of the mixed lineage leukemia 3 (MLL3) gene, located on 7q36.1,
34 s identified were all of the subunits of the mixed-lineage leukemia 3 (Mll3) and 4 (Mll4) complexes,
35 The histone H3-lysine-4 methyltransferase mixed-lineage leukemia 3 (MLL3) and its closest homolog,
36 Although PTIP is a unique component of the mixed-lineage leukemia 3 (MLL3)/MLL4 chromatin-modifying
37 deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3)-MLL4 complex display impaired
43 eptor NKp44 (NKp44L), a novel isoform of the mixed-lineage leukemia-5 protein, as a cellular ligand f
44 lso suppresses proliferation of leukemogenic mixed lineage leukemia-AF9 fusion-protein-transformed my
46 mia (ALL), acute myelogenous leukemia (AML), mixed lineage leukemia, and also in therapy AML (t-AML)
47 ragile sites, and breakpoints, including the mixed-lineage leukemia breakpoint cluster region (MLL BC
48 y, although PTIP and PA1 associate with MLL (mixed lineage leukemia) complexes and participate in tra
49 effectively treats aggressive AML, including mixed-lineage leukemia-driven AML, and outperforms stand
50 f conditional transformation by an inducible mixed lineage leukemia-eleven-nineteen leukemia (MLL-ENL
51 A murine retroviral transduction model of mixed lineage leukemia fused to CREB binding protein suc
52 rmined that minimally, the amino terminus of mixed lineage leukemia fused to the bromodomain and hist
53 upport of this idea, we showed recently that mixed lineage leukemia fusion oncoproteins can convert c
56 ort that hDOT1L interacts with AF10, an MLL (mixed lineage leukemia) fusion partner involved in acute
57 ves as a critical oncogenic cofactor of MLL (mixed lineage leukemia) fusion proteins in acute leukemi
58 in leukemogenesis driven by a subset of MLL (mixed-lineage leukemia) fusion proteins raises the possi
59 ias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologi
66 adults as a result of rearrangements to the mixed-lineage leukemia gene (MLL) located on chromosome
67 atient-derived xenografts (PDX) of pediatric mixed-lineage leukemia gene (MLL)-rearranged ALL were es
69 ng a chromosomal translocation involving the mixed-lineage leukemia gene (MLL, ALL1, HRX) have a part
74 ene involved in translocations with the MLL (mixed-lineage leukemia) gene, was 631 bp away in a head-
75 to as MLL to denote the gene associated with mixed-lineage leukemia) generate MLL fusion proteins tha
77 iginally identified as a fusion partner with mixed-lineage leukemia in a patient with acute myeloid l
78 ize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the path
82 ing translocation t(11;16) (q23;p13.3), MLL (mixed-lineage leukemia) is fused in frame to CBP (CREB b
83 horax family member MLL (myeloid/lymphoid or mixed-lineage leukemia) is presumed to activate Hox expr
84 tool for understanding the biologic basis of mixed lineage leukemia leukemogenesis and for developing
85 One such gene is MLL (myeloid-lymphoid or mixed lineage leukemia) located at chromosome band 11q23
86 5 (WDR5) is a common component of mammalian mixed lineage leukemia methyltransferase family members
89 e II (TOP2)-mediated DNA cleavage within the mixed lineage leukemia (MLL) breakpoint cluster region (
90 nic fusions of the Trithorax-related protein mixed lineage leukemia (MLL) can initiate aggressive leu
91 allosteric changes that transcription factor mixed lineage leukemia (MLL) causes to the interactions
93 The oncoprotein Ash2L is a component of the mixed lineage leukemia (MLL) family members 1-4, Setd1A,
95 in, the MEN1 protein product, interacts with mixed lineage leukemia (MLL) family proteins in a histon
98 unctions and in leukemogenesis driven by the mixed lineage leukemia (MLL) fusion oncogene MLL-AF9.
99 ough menin acts as an oncogenic cofactor for mixed lineage leukemia (MLL) fusion protein-mediated his
100 polymerase-associated factor complex (PAFc), mixed lineage leukemia (MLL) fusion proteins activate ge
101 unctions as a critical oncogenic cofactor of mixed lineage leukemia (MLL) fusion proteins in the deve
102 The interaction between menin and oncogenic mixed lineage leukemia (MLL) fusion proteins is required
105 Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are associated with ag
106 Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are often observed in
107 ith chromosomal translocations involving the mixed lineage leukemia (MLL) gene are usually associated
110 first identified as a fusion partner of the mixed lineage leukemia (MLL) gene in acute myeloid leuke
113 A partial nontandem duplication (PNTD) of mixed lineage leukemia (MLL) gene is described in B-cell
115 en mutated in ALLs with rearrangement of the mixed lineage leukemia (MLL) gene on chromosome 11q23.
117 Chromosomal translocations involving the Mixed Lineage Leukemia (MLL) gene produce chimeric prote
118 of infants with ALL, particularly those with mixed lineage leukemia (MLL) gene rearrangements, is onl
119 Chromosomal translocations disrupting the Mixed lineage leukemia (Mll) gene result in leukemia, wi
120 Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion p
123 kemia (B-ALL) harboring rearrangement of the mixed lineage leukemia (MLL) gene with CD19 CAR-T cells.
124 Chromosomal translocations that fuse the mixed lineage leukemia (MLL) gene with multiple partners
125 L) is characterized by rearrangements of the mixed lineage leukemia (MLL) gene with one of its >50 pa
126 lso interacts with translocation partners of Mixed Lineage Leukemia (MLL) gene, which is commonly tra
127 receptors (ERs) and ER coregulators such as mixed lineage leukemia (MLL) histone methylases (MLL2 an
128 ights into the role of the Trithorax protein mixed lineage leukemia (MLL) in maintaining cancer stem
134 plex (DotCom), which includes several of the mixed lineage leukemia (MLL) partners in leukemia such a
135 -protein interaction (PPI) between menin and mixed lineage leukemia (MLL) plays a critical role in ac
137 e Men1 gene product menin interacts with the mixed lineage leukemia (MLL) protein, a histone H3 lysin
138 WD repeat domain 5 (WDR5) and block the WDR5-mixed lineage leukemia (MLL) protein-protein interaction
139 ENL, and AF9, is recruited by HIV-1 Tat and mixed lineage leukemia (MLL) proteins to activate the ex
140 Aven stimulates the mRNA translation of the mixed lineage leukemia (MLL) proto-oncogene in an argini
142 third plant homeodomain (PHD3) finger of the mixed lineage leukemia (MLL) proto-oncoprotein and a pol
144 sents the most common leukemogenic fusion of mixed lineage leukemia (MLL) to a cytoplasmic partner pr
145 ing of activation domains from the c-Myb and mixed lineage leukemia (MLL) transcription factors to th
146 regulator in the expression of HOX genes in mixed lineage leukemia (MLL)-based hematological maligna
147 d the miRNAs are aberrantly overexpressed in mixed lineage leukemia (MLL)-rearranged acute leukemias.
148 regulator CDK6 as a promising new target in mixed lineage leukemia (MLL)-rearranged acute myeloid le
149 hylation (H3K27me3/2) and inhibits growth of mixed lineage leukemia (MLL)-rearranged leukemia cells.
150 ranslocations, that approximately 43% of all mixed lineage leukemia (MLL)-rearranged leukemias are EV
152 , we identify the histone-remodelling enzyme mixed lineage leukemia (MLL)3 as a clock-controlled fact
155 impaired reconstitution of stem cell-derived mixed-lineage leukemia (MLL) AML, which represents an ag
156 isordered transcription factors, such as the mixed-lineage leukemia (MLL) and c-Myb peptides, at isol
157 more, we observed that SALL4 interacted with mixed-lineage leukemia (MLL) and co-occupied the HOXA9 p
158 t multiple MLL-fusion proteins implicated in mixed-lineage leukemia (MLL) associate with AFF4, ELLs,
160 ate maintenance of target gene expression by mixed-lineage leukemia (MLL) chimeras may result from th
161 his targeting strategy does not affect other mixed-lineage leukemia (MLL) family histone methyltransf
162 as the threonine endopeptidase that cleaves mixed-lineage leukemia (MLL) for proper Hox gene express
167 ary acute myelogenous leukemia involving the mixed-lineage leukemia (MLL) gene (11q23) translocations
168 We previously identified a rearrangement of mixed-lineage leukemia (MLL) gene (also known as ALL-1,
170 hromosomal translocation that juxtaposes the mixed-lineage leukemia (MLL) gene and the AF4 gene.
172 OF REVIEW: Leukemia carrying mutation of the mixed-lineage leukemia (MLL) gene is particularly refrac
173 Chromosomal rearrangements involving the mixed-lineage leukemia (MLL) gene occur in primary and t
178 ost cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase c
183 t mutations such as FLT3 internal-tandem and mixed-lineage leukemia (MLL) partial-tandem duplications
184 ax binds KIX at the previously characterized mixed-lineage leukemia (MLL) protein interaction surface
186 Histone lysine methylation, mediated by mixed-lineage leukemia (MLL) proteins, is now known to b
187 determined that MSI2 directly maintains the mixed-lineage leukemia (MLL) self-renewal program by int
189 gements involving the H3K4 methyltransferase mixed-lineage leukemia (MLL) trigger aberrant gene expre
191 omal aberrations and abnormalities involving mixed-lineage leukemia (MLL), an upstream regulator of H
194 t to chromatin as an effective treatment for mixed-lineage leukemia (MLL)-fusion leukemia' by Dawson
196 alignancies, including Hodgkin, myeloma, and mixed-lineage leukemia (MLL)-translocated cell lines.
199 llite markers located at the ATM (D11S2179), mixed-lineage leukemia (MLL; D11S1356), and BCL1 (D11S98
203 ation domain associates with TRRAP/TIP60 and mixed-lineage-leukemia (MLL1/MLL2) SET1-type chromatin-m
206 h an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-P
207 vation domain of the trithorax group protein mixed lineage leukemia protein (MLL), together with eith
209 Several lines of evidence suggest that the mixed lineage leukemia protein (MLL, ALL-1, HRX) plays a
215 DPY-30), a complex that is part of the MLL1 (mixed lineage leukemia protein-1) core complex but that
217 ith the transcriptional activation domain of mixed-lineage leukemia protein leads to an enhancement o
219 lysine 4 (H3K4) methyltransferases including mixed lineage leukemia proteins to regulate homeobox (Ho
221 3 (IGF2BP3) is specifically overexpressed in mixed lineage leukemia-rearranged (MLL-rearranged) B-acu
223 t extremely high levels in ALL patients with mixed lineage leukemia rearrangements or hyperdiploidy a
226 sented with acute myeloid leukemia, one with mixed-lineage leukemia, two with acute lymphoblastic leu
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