Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias.
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The evi-1 oncoprotein inhibits c-Jun N-terminal kinase and prevents stress-induced cell deathEvi-1 transforming and repressor activities are mediated by CtBP co-repressor proteinsActivation of AML1-mediated transcription by MOZ and inhibition by the MOZ-CBP fusion proteinA novel transcript encoding an N-terminally truncated AML1/PEBP2 alphaB protein interferes with transactivation and blocks granulocytic differentiation of 32Dcl3 myeloid cellsCloning and characterization of mCtBP2, a co-repressor that associates with basic Krüppel-like factor and other mammalian transcriptional regulatorsAML1 interconnected pathways of leukemogenesisCooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemiaMutational analyses of the AML1 gene in patients with myelodysplastic syndromeThe RUNX genes: gain or loss of function in cancerRUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.Molecular basis of tissue-specific gene expression mediated by the runt domain transcription factor PEBP2/CBF.An engineered PAX3-KRAB transcriptional repressor inhibits the malignant phenotype of alveolar rhabdomyosarcoma cells harboring the endogenous PAX3-FKHR oncogeneRole of regulatory elements and the MAPK/ERK or p38 MAPK pathways for activation of human cytomegalovirus gene expression.Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice.The molecular mechanism of chronic myelogenous leukemia and its therapeutic implications: studies in a murine model.Role of AML1/Runx1 in the pathogenesis of hematological malignancies.The AML1/ETO fusion protein activates transcription of BCL-2Leukemia fusion proteins and co-repressor complexes: changing paradigms.Expression of the zinc finger gene EVI-1 in ovarian and other cancers.Proviral insertions induce the expression of bone-specific isoforms of PEBP2alphaA (CBFA1): evidence for a new myc collaborating oncogeneThe 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.Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AMLRole of the RUNX1-EVI1 fusion gene in leukemogenesis.The leukemic fusion gene AML1-MDS1-EVI1 suppresses CEBPA in acute myeloid leukemia by activation of Calreticulin.Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.MicroRNA-27 enhances differentiation of myeloblasts into granulocytes by post-transcriptionally downregulating Runx1.AML1 is functionally regulated through p300-mediated acetylation on specific lysine residues.The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP.Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.Identification of the chimeric protein product of the CBFB-MYH11 fusion gene in inv(16) leukemia cells.Three distinct domains in TEL-AML1 are required for transcriptional repression of the IL-3 promoter.AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1.The t(8;21) fusion protein, AML1/ETO, transforms NIH3T3 cells and activates AP-1.Tumourigenicity of MTG8, a leukaemia-related gene, in concert with v-Ha-ras gene in BALB/3T3 cells.Mutations of the Smad4 gene in acute myelogeneous leukemia and their functional implications in leukemogenesis.Fadd and Skp2 are possible downstream targets of RUNX1-EVI1.The fusion protein AML1-ETO in acute myeloid leukemia with translocation t(8;21) induces c-jun protein expression via the proximal AP-1 site of the c-jun promoter in an indirect, JNK-dependent manner.RUNX1/EVI1, which blocks myeloid differentiation, inhibits CCAAT-enhancer binding protein alpha function.
P2860
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P2860
Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
1995年论文
@zh
1995年论文
@zh-cn
name
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@ast
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@en
type
label
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@ast
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@en
prefLabel
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@ast
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@en
P2093
P2860
P356
P1476
Dual functions of the AML1/Evi ...... ogenesis in t(3;21) leukemias.
@en
P2093
Kurokawa M
P2860
P304
P356
10.1128/MCB.15.5.2383
P407
P577
1995-05-01T00:00:00Z