The leukemic fusion gene AML1-MDS1-EVI1 suppresses CEBPA in acute myeloid leukemia by activation of Calreticulin.
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C/EBPα Dysregulation in AML and ALLTribbles homolog 2 inactivates C/EBPalpha and causes acute myelogenous leukemiaReintroduction of CEBPA in MN1-overexpressing hematopoietic cells prevents their hyperproliferation and restores myeloid differentiationEvolved Cellular Mechanisms to Respond to Genotoxic Insults: Implications for Radiation-Induced Hematologic MalignanciesHzf regulates adipogenesis through translational control of C/EBPalphaRetrotranslocation of the chaperone calreticulin from the endoplasmic reticulum lumen to the cytosol.Proteomics of acute myeloid leukaemia: Cytogenetic risk groups differ specifically in their proteome, interactome and post-translational protein modifications.Chronic myeloid leukemia: mechanisms of blastic transformationThe tumour-suppressive miR-29a/b1 cluster is regulated by CEBPA and blocked in human AML.The biological effects of C/EBPalpha in K562 cells depend on the potency of the N-terminal regulatory region, not on specificity of the DNA binding domain.The multifaceted functions of C/EBPα in normal and malignant haematopoiesis.Unfolded protein response suppresses CEBPA by induction of calreticulin in acute myeloid leukaemia.Calreticulin promotes cell motility and enhances resistance to anoikis through STAT3-CTTN-Akt pathway in esophageal squamous cell carcinoma.Gene expression profiles associated with pediatric relapsed AML.Calreticulin is a negative regulator of bronchial smooth muscle cell proliferationPhosphorylation of serine 21 modulates the proliferation inhibitory more than the differentiation inducing effects of C/EBPα in K562 cells.Asthma and COPD - The C/EBP ConnectionCDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alphaMonocyte-macrophage differentiation of acute myeloid leukemia cell lines by small molecules identified through interrogation of the Connectivity Map database.Acetylation of C/EBPα inhibits its granulopoietic function.mRNA stability control: a clandestine force in normal and malignant hematopoiesis.Transcriptional dysregulation during myeloid transformation in AML.EVI1 Interferes with Myeloid Maturation via Transcriptional Repression of Cebpa, via Binding to Two Far Downstream Regulatory Elements.Dysregulation of the C/EBPalpha differentiation pathway in human cancer.Heterogeneity within AML with CEBPA mutations; only CEBPA double mutations, but not single CEBPA mutations are associated with favourable prognosisThe role of aberrant transcription factor in the progression of chronic myeloid leukemia.The significance of c.690G>T polymorphism (rs34529039) and expression of the CEBPA gene in ovarian cancer outcome.Programmed cell removal: a new obstacle in the road to developing cancer.Bone marrow neoplastic niche in leukemia.Computational identification of the normal and perturbed genetic networks involved in myeloid differentiation and acute promyelocytic leukemia.Expressional profiles of transcription factors in the progression of Helicobacter pylori-associated gastric carcinoma based on protein/DNA array analysis.The tumor suppressor gene DAPK2 is induced by the myeloid transcription factors PU.1 and C/EBPα during granulocytic differentiation but repressed by PML-RARα in APL.C/EBPα deregulation as a paradigm for leukemogenesis.Acute myeloid leukemia with t(3;21)(q26.2;q22) developing following low-dose methotrexate therapy for rheumatoid arthritis and expressing two AML1/MDS1/EVI1 fusion proteins: A case report.Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemia.The Evi1 proto-oncoprotein blocks endomitosis in megakaryocytes by inhibiting sustained cyclin-dependent kinase 2 catalytic activity.Leukemogenesis induced by wild-type and STI571-resistant BCR/ABL is potently suppressed by C/EBPalpha.Ectopic expression of C/EBPalpha and ID1 is sufficient to restore defective neutrophil development in low-risk myelodysplasiaCEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia.RNA CUG-binding protein 1 increases translation of 20-kDa isoform of CCAAT/enhancer-binding protein beta by interacting with the alpha and beta subunits of eukaryotic initiation translation factor 2.
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P2860
The leukemic fusion gene AML1-MDS1-EVI1 suppresses CEBPA in acute myeloid leukemia by activation of Calreticulin.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
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artigo científico
@pt
bilimsel makale
@tr
scientific article published on 23 August 2004
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@en
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@nl
type
label
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@en
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@nl
prefLabel
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@en
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@nl
P2093
P2860
P356
P1476
The leukemic fusion gene AML1- ...... by activation of Calreticulin.
@en
P2093
Andrew Lister
Anne Hagemeijer
Barbara Huegli
Beatrice U Mueller
Daniel Helbling
Janet D Rowley
Martin F Fey
Martine Jotterand
Nikolai A Timchenko
Sandrine Meyer-Monard
P2860
P304
13312-13317
P356
10.1073/PNAS.0404731101
P407
P577
2004-08-23T00:00:00Z