Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia
about
P1343
Functional and physical interactions between AML1 proteins and an ETS protein, MEF: implications for the pathogenesis of t(8;21)-positive leukemiasThe evi-1 oncoprotein inhibits c-Jun N-terminal kinase and prevents stress-induced cell deathSubcellular localization of the alpha and beta subunits of the acute myeloid leukemia-linked transcription factor PEBP2/CBFIntergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain familyThe PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasiaFusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemiaThe AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1Oncogenic transcription factor Evi1 regulates hematopoietic stem cell proliferation through GATA-2 expressionThe BCR-ABL oncoprotein potentially interacts with the xeroderma pigmentosum group B proteinAlternative splicing and genomic structure of the AML1 gene involved in acute myeloid leukemiaEngineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?Expression of the Runt domain-encoding PEBP2 alpha genes in T cells during thymic developmentHematopoiesis in the fetal liver is impaired by targeted mutagenesis of a gene encoding a non-DNA binding subunit of the transcription factor, polyomavirus enhancer binding protein 2/core binding factorAbsence of fetal liver hematopoiesis in mice deficient in transcriptional coactivator core binding factor beta.The tumor suppressor PRDM5 regulates Wnt signaling at early stages of zebrafish development.RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.Haploinsufficient tumor suppressor genes.Acetylation of lysine 564 adjacent to the C-terminal binding protein-binding motif in EVI1 is crucial for transcriptional activation of GATA2.Interaction and functional cooperation of the leukemia-associated factors AML1 and p300 in myeloid cell differentiation.AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutationsBiological characteristics of the leukemia-associated transcriptional factor AML1 disclosed by hematopoietic rescue of AML1-deficient embryonic stem cells by using a knock-in strategy.Chronic myeloid leukemia: mechanisms of blastic transformationDichotomy of AML1-ETO functions: growth arrest versus block of differentiationA murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9The leukemic core binding factor beta-smooth muscle myosin heavy chain (CBF beta-SMMHC) chimeric protein requires both CBF beta and myosin heavy chain domains for transformation of NIH 3T3 cells.Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice.Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and unrelated genes at 3q26 in (3;21)(q26;q22) translocationsThe corepressor mSin3A regulates phosphorylation-induced activation, intranuclear location, and stability of AML1.Epstein-Barr virus nuclear protein 2 transactivation of the latent membrane protein 1 promoter is mediated by J kappa and PU.1.EVI1 acts as an inducible negative-feedback regulator of NF-κB by inhibiting p65 acetylation.Human thrombopoietin: gene structure, cDNA sequence, expression, and chromosomal localization.Identification of a nuclear matrix targeting signal in the leukemia and bone-related AML/CBF-alpha transcription factors.Leukemia treatment in severe combined immunodeficiency mice by antisense oligodeoxynucleotides targeting cooperating oncogenesDual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias.c-Myb and core-binding factor/PEBP2 display functional synergy but bind independently to adjacent sites in the T-cell receptor delta enhancer.CCAAT enhancer-binding protein (C/EBP) and AML1 (CBF alpha2) synergistically activate the macrophage colony-stimulating factor receptor promoter.The t(12;21) translocation converts AML-1B from an activator to a repressor of transcription.The extracellular signal-regulated kinase pathway phosphorylates AML1, an acute myeloid leukemia gene product, and potentially regulates its transactivation ability.Applying the discovery of the Philadelphia chromosome.An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms.
P2860
Q22009417-AB8558AA-2719-497B-A271-0E75D0850F16Q22254262-01FFE784-5FDF-42DA-A58C-C3668F742E49Q24314024-F3BF6561-3031-4915-AF9F-0DE5C2EE1061Q24314719-6E34E00D-47A6-4A17-B46C-E1E3DEAA4D37Q24317100-D63CC3A6-C9CF-4C46-A2A8-953AFABFBDD6Q24319864-AAB018F6-13B1-4F84-AB25-37875001CF70Q24324229-24BC6C28-3FBF-4F3C-B5CC-DA2CC1AC71CFQ24529138-03CF08F7-7D01-4975-9532-BF2320C28A60Q24553320-14B98E19-5237-412B-A838-0F4B44FDAB3EQ24626212-FEB49EE2-D579-4922-9554-3A8B89873FA5Q26828777-9AFA08B2-171C-494D-AAFC-804182DE2DFBQ28507097-02C28748-8270-4C59-8845-5CADE99837C6Q28594445-AEEE0B84-F234-4679-9258-855789E16B06Q30530806-6C8D7A35-1C24-4797-A500-4F8FC27544CFQ33402914-787C25ED-EE98-4EF4-BE95-826A24E68C8EQ33759034-189FF576-974E-4067-BEB7-A07001F5A7A2Q33864922-29E096F2-69E8-425A-A600-A4E98166150CQ33883148-6239A128-D776-4672-AD87-7625514A1D65Q33888879-DC1387EA-C7A8-4579-B405-5817A6F91F5BQ33943238-EDE078DB-19CC-4864-A044-CC0CD34A4C08Q33961306-C3341495-633A-4043-9373-23917CC3EF31Q33968037-8A0BE531-2D3B-4770-BFCA-26D564D60DC9Q33969245-976AE85C-881B-4843-A01D-39BC1BB8CED8Q34064832-2D900302-BC97-452B-A9E1-2A3C18653F12Q34552061-CBCF10B2-42BD-4354-882E-62F6FDFE5BA1Q35009923-259723A7-5C83-40DB-9B6C-1A95E71D66D8Q35210567-BC6F0001-2335-4933-91C4-2621075E4792Q35544219-00E04E80-4FE9-43F4-B1CA-BA2B920D36E8Q35829475-9C0EF005-8A53-4915-8074-C4CD0D2558C2Q36016473-E2644123-DDA4-4A86-A2F2-DFA55F42B168Q36018621-4732CC34-1A4D-4032-BAF0-E2EA92C676C2Q36239602-9684885C-D2B5-4FDE-9C89-36968CCAC9E5Q36365540-6070EE26-8F8C-4806-96AF-89CCBB1F1419Q36550719-64819556-72D7-4608-9EB6-D7B9B2EB54ECQ36551352-D440DFF8-BBC7-45E4-B645-A206E386D567Q36557608-6C082EAF-B16B-44D7-AFD7-74D30F9B858AQ36557716-877004EC-444E-406B-A3FB-E370FF915A1BQ36561099-B34895C1-7757-4C3B-97F7-5D7B20CBD6A4Q36900109-277C9667-0CAC-45B2-A600-98CB7896F7BCQ37693756-379BE3E3-DD83-424E-90C6-7660139F8CA6
P2860
Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia
description
1994 nî lūn-bûn
@nan
1994 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
1994 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
1994年の論文
@ja
1994年論文
@yue
1994年論文
@zh-hant
1994年論文
@zh-hk
1994年論文
@zh-mo
1994年論文
@zh-tw
1994年论文
@wuu
name
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@ast
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@en
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@nl
type
label
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@ast
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@en
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@nl
prefLabel
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@ast
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@en
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@nl
P2093
P2860
P1433
P1476
Generation of the AML1-EVI-1 f ...... in chronic myelocytic leukemia
@en
P2093
M Kurokawa
P2860
P304
P407
P4510
P577
1994-02-01T00:00:00Z