The amino terminal and E2F interaction domains are critical for C/EBP alpha-mediated induction of granulopoietic development of hematopoietic cells.
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Repression of transcriptional activity of C/EBPalpha by E2F-dimerization partner complexesUpstream open reading frames: molecular switches in (patho)physiologyCell-cycle regulator E2F1 and microRNA-223 comprise an autoregulatory negative feedback loop in acute myeloid leukemiaPharmacological targeting of the Wdr5-MLL interaction in C/EBPα N-terminal leukemia.C/EBP and DEK coordinately regulate myeloid differentiationEVI2B is a C/EBPα target gene required for granulocytic differentiation and functionality of hematopoietic progenitors.Proteomic identification of C/EBP-DBD multiprotein complex: JNK1 activates stem cell regulator C/EBPalpha by inhibiting its ubiquitination.Loss of C/EBP alpha cell cycle control increases myeloid progenitor proliferation and transforms the neutrophil granulocyte lineageDisruption of the C/EBPα-miR-182 balance impairs granulocytic differentiation.Elevated PIN1 expression by C/EBPalpha-p30 blocks C/EBPalpha-induced granulocytic differentiation through c-Jun in AMLLong intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.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.Expression of the transcriptional repressor Gfi-1 is regulated by C/EBP{alpha} and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cellsC/EBPdelta expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation.CEBPA point mutations in hematological malignancies.CEBPA-dependent HK3 and KLF5 expression in primary AML and during AML differentiationmiR-511 and miR-1297 inhibit human lung adenocarcinoma cell proliferation by targeting oncogene TRIB2.C/EBPα regulated microRNA-34a targets E2F3 during granulopoiesis and is down-regulated in AML with CEBPA mutationsProteomic discovery of Max as a novel interacting partner of C/EBPalpha: a Myc/Max/Mad link.Absence of the transcription factor CCAAT enhancer binding protein alpha results in loss of myeloid identity in bcr/abl-induced malignancy.The gene signature in CCAAT-enhancer-binding protein α dysfunctional acute myeloid leukemia predicts responsiveness to histone deacetylase inhibitors.Regulation of apoptotic and growth inhibitory activities of C/EBPalpha in different cell lines.CCAAT/enhancer binding proteins alpha and epsilon cooperate with all-trans retinoic acid in therapy but differ in their antileukemic activitiesPhosphorylation of serine 21 modulates the proliferation inhibitory more than the differentiation inducing effects of C/EBPα in K562 cells.CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alphaPhosphorylation of C/EBPalpha inhibits granulopoiesis.Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.C/EBPγ deregulation results in differentiation arrest in acute myeloid leukemia.Acetylation of C/EBPα inhibits its granulopoietic function.Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells.Transcription factor C/EBPα-induced microRNA-30c inactivates Notch1 during granulopoiesis and is downregulated in acute myeloid leukemiaDistinct microRNA expression profile and targeted biological pathways in functional myeloid-derived suppressor cells induced by Δ9-tetrahydrocannabinol in vivo: regulation of CCAAT/enhancer-binding protein α by microRNA-690.The role of transcription factors in the guidance of granulopoiesis.Tamoxifen induction of CCAAT enhancer-binding protein alpha is required for tamoxifen-induced apoptosis.Gfi-1 inhibits proliferation and colony formation of p210BCR/ABL-expressing cells via transcriptional repression of STAT 5 and Mcl-1.Shwachman-Bodian-Diamond syndrome (SBDS) protein deficiency impairs translation re-initiation from C/EBPα and C/EBPβ mRNAsLineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration.A tumor suppressor role for C/EBPα in solid tumors: more than fat and blood.C/EBPα deregulation as a paradigm for leukemogenesis.The proline-histidine-rich CDK2/CDK4 interaction region of C/EBPalpha is dispensable for C/EBPalpha-mediated growth regulation in vivo
P2860
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P2860
The amino terminal and E2F interaction domains are critical for C/EBP alpha-mediated induction of granulopoietic development of hematopoietic cells.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
The amino terminal and E2F int ...... opment of hematopoietic cells.
@en
The amino terminal and E2F int ...... opment of hematopoietic cells.
@nl
type
label
The amino terminal and E2F int ...... opment of hematopoietic cells.
@en
The amino terminal and E2F int ...... opment of hematopoietic cells.
@nl
prefLabel
The amino terminal and E2F int ...... opment of hematopoietic cells.
@en
The amino terminal and E2F int ...... opment of hematopoietic cells.
@nl
P2093
P1433
P1476
The amino terminal and E2F int ...... opment of hematopoietic cells.
@en
P2093
Claus Nerlov
Erica K Evans
Erik A Nelson
Francesco D'Alo'
Hanna S Radomska
Lisa M Johansen
P304
P356
10.1182/BLOOD-2003-02-0479
P407
P577
2003-07-17T00:00:00Z