CBFB-MYH11/RUNX1 together with a compendium of hematopoietic regulators, chromatin modifiers and basal transcription factors occupies self-renewal genes in inv(16) acute myeloid leukemia.
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Stem Cell Modeling of Core Binding Factor Acute Myeloid LeukemiaTranscriptional network control of normal and leukaemic haematopoiesisStructure and Biophysics of CBFβ/RUNX and Its Translocation Products.CBFB-MYH11 hypomethylation signature and PBX3 differential methylation revealed by targeted bisulfite sequencing in patients with acute myeloid leukemia.Spectrum of myeloid neoplasms and immune deficiency associated with germline GATA2 mutations.Transcriptome Profiling of Pediatric Core Binding Factor AML.Identification of a dynamic core transcriptional network in t(8;21) AML that regulates differentiation block and self-renewal.Runx1 is required for hematopoietic defects and leukemogenesis in Cbfb-MYH11 knock-in mice.Helicase-like transcription factor is a RUNX1 target whose downregulation promotes genomic instability and correlates with complex cytogenetic features in acute myeloid leukemia.Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia.The RUNX1-PU.1 axis in the control of hematopoiesis.The AS-RBM15 lncRNA enhances RBM15 protein translation during megakaryocyte differentiation.Developmental Control of NRAMP1 (SLC11A1) Expression in Professional PhagocytesmiR-17 deregulates a core RUNX1-miRNA mechanism of CBF acute myeloid leukemia.MLL-AF9 and MLL-AF4 oncofusion proteins bind a distinct enhancer repertoire and target the RUNX1 program in 11q23 acute myeloid leukemia.AML associated oncofusion proteins PML-RARA, AML1-ETO and CBFB-MYH11 target RUNX/ETS-factor binding sites to modulate H3ac levels and drive leukemogenesis.Genome-wide binding of transcription factors in inv(16) acute myeloid leukemia.CHD7 deficiency delays leukemogenesis in mice induced by CBFB-MYH11.MN1 overexpression is driven by loss of DNMT3B methylation activity in inv(16) pediatric AML.The oncogenic fusion protein CBFB-SMMHC downregulates CD48 to evade NK cell recognition.Pharmacological inhibition of aberrant transcription factor complexes in inversion 16 acute myeloid leukemia
P2860
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P2860
CBFB-MYH11/RUNX1 together with a compendium of hematopoietic regulators, chromatin modifiers and basal transcription factors occupies self-renewal genes in inv(16) acute myeloid leukemia.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
CBFB-MYH11/RUNX1 together with ...... nv(16) acute myeloid leukemia.
@en
CBFB-MYH11/RUNX1 together with ...... nv(16) acute myeloid leukemia.
@nl
type
label
CBFB-MYH11/RUNX1 together with ...... nv(16) acute myeloid leukemia.
@en
CBFB-MYH11/RUNX1 together with ...... nv(16) acute myeloid leukemia.
@nl
prefLabel
CBFB-MYH11/RUNX1 together with ...... nv(16) acute myeloid leukemia.
@en
CBFB-MYH11/RUNX1 together with ...... nv(16) acute myeloid leukemia.
@nl
P2093
P2860
P50
P356
P1433
P1476
CBFB-MYH11/RUNX1 together with ...... inv(16) acute myeloid leukemia
@en
P2093
A T J Wierenga
E Vellenga
H G Stunnenberg
J H A Martens
P W T C Jansen
P2860
P2888
P304
P356
10.1038/LEU.2013.257
P577
2013-09-04T00:00:00Z
P5875
P6179
1027039401