An Mll-AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes.
about
MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25)Cloning and characterization of the EAP30 subunit of the ELL complex that confers derepression of transcription by RNA polymerase IIAF5q31, a newly identified AF4-related gene, is fused to MLL in infant acute lymphoblastic leukemia with ins(5;11)(q31;q13q23)The cloning, mapping and expression of a novel gene, BRL, related to the AF10 leukaemia geneGAS41, a highly conserved protein in eukaryotic nuclei, binds to NuMAAF15q14, a novel partner gene fused to the MLL gene in an acute myeloid leukaemia with a t(11;15)(q23;q14)New insight into the molecular mechanisms of MLL-associated leukemiaMLL-AFX requires the transcriptional effector domains of AFX to transform myeloid progenitors and transdominantly interfere with forkhead protein functionThe leucine zipper motif of the Drosophila AF10 homologue can inhibit PRE-mediated repression: implications for leukemogenic activity of human MLL-AF10 fusionsProteolytic cleavage of MLL generates a complex of N- and C-terminal fragments that confers protein stability and subnuclear localizationThe elongation domain of ELL is dispensable but its ELL-associated factor 1 interaction domain is essential for MLL-ELL-induced leukemogenesisMLL and CREB bind cooperatively to the nuclear coactivator CREB-binding proteinLeukemic HRX fusion proteins inhibit GADD34-induced apoptosis and associate with the GADD34 and hSNF5/INI1 proteinsEEN encodes for a member of a new family of proteins containing an Src homology 3 domain and is the third gene located on chromosome 19p13 that fuses to MLL in human leukemiaTargeted transgenesisRetrovirus-mediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in miceThe Ews-ERG fusion protein can initiate neoplasia from lineage-committed haematopoietic cells.Systematic Classification of Mixed-Lineage Leukemia Fusion Partners Predicts Additional Cancer PathwaysHijacked in cancer: the KMT2 (MLL) family of methyltransferasesAnimal models of leukemia: any closer to the real thing?Targeted Cancer Therapy: Vital Oncogenes and a New Molecular Genetic Paradigm for Cancer Initiation Progression and TreatmentPhysical interaction and functional antagonism between the RNA polymerase II elongation factor ELL and p53Human LPP gene is fused to MLL in a secondary acute leukemia with a t(3;11) (q28;q23)The polycomb protein MPc3 interacts with AF9, an MLL fusion partner in t(9;11)(p22;q23) acute leukemiasThe ENL moiety of the childhood leukemia-associated MLL-ENL oncoprotein recruits human Polycomb 3Structure and function of RNA polymerase II elongation factor ELL. Identification of two overlapping ELL functional domains that govern its interaction with polymerase and the ternary elongation complexHRX leukemic fusion proteins form a heterocomplex with the leukemia-associated protein SET and protein phosphatase 2AMitochondrial pro-apoptotic ARTS protein is lost in the majority of acute lymphoblastic leukemia patientsCo-regulation of histone-modifying enzymes in cancerDisruption of Sept6, a fusion partner gene of MLL, does not affect ontogeny, leukemogenesis induced by MLL-SEPT6, or phenotype induced by the loss of Sept4.Mouse Af9 is a controller of embryo patterning, like Mll, whose human homologue fuses with Af9 after chromosomal translocation in leukemiaThe rate of spontaneous mutations in human myeloid cellsGenomic and epigenomic landscapes of adult de novo acute myeloid leukemia.Structure of AF3p21, a new member of mixed lineage leukemia (MLL) fusion partner proteins-implication for MLL-induced leukemogenesis.ENL, the MLL fusion partner in t(11;19), binds to the c-Abl interactor protein 1 (ABI1) that is fused to MLL in t(10;11)+.Yaf9, a novel NuA4 histone acetyltransferase subunit, is required for the cellular response to spindle stress in yeastdELL, a drosophila homologue of transcription elongation factor ELL (Eleven-nineteen Lysine rich Leukemia), is required for early development.Translocations, cancer and the puzzle of specificity.Niche-based screening identifies small-molecule inhibitors of leukemia stem cellsMurine models of acute leukemia: important tools in current pediatric leukemia research.
P2860
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P2860
An Mll-AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes.
description
1996 nî lūn-bûn
@nan
1996 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
1996 թվականի հունիսին հրատարակված գիտական հոդված
@hy
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
name
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@ast
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@en
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@nl
type
label
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@ast
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@en
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@nl
prefLabel
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@ast
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@en
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@nl
P2093
P1433
P1476
An Mll-AF9 fusion gene made by ...... od to create fusion oncogenes.
@en
P2093
A J Warren
A N McKenzie
T A Larson
T H Rabbitts
P304
P356
10.1016/S0092-8674(00)81269-6
P407
P577
1996-06-01T00:00:00Z