RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
about
The RUNX genes: gain or loss of function in cancerRunx1 directly promotes proliferation of hair follicle stem cells and epithelial tumor formation in mouse skin.The bone-specific expression of Runx2 oscillates during the cell cycle to support a G1-related antiproliferative function in osteoblasts.MIRTFnet: analysis of miRNA regulated transcription factorsThe hematopoietic transcription factor AML1 (RUNX1) is negatively regulated by the cell cycle protein cyclin D3.Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice.AML1/RUNX1 phosphorylation by cyclin-dependent kinases regulates the degradation of AML1/RUNX1 by the anaphase-promoting complexRunx1 loss minimally impacts long-term hematopoietic stem cellsThe RUNX Genes as Conditional Oncogenes: Insights from Retroviral Targeting and Mouse Models.LRG1 promotes proliferation and inhibits apoptosis in colorectal cancer cells via RUNX1 activationThe RUNX1 transcription factor is expressed in serous epithelial ovarian carcinoma and contributes to cell proliferation, migration and invasion.Oncogene-induced senescence: an essential role for Runx.'Runxs and regulations' of sensory and motor neuron subtype differentiation: implications for hematopoietic development.RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response.Gene array analysis reveals a common Runx transcriptional programme controlling cell adhesion and survival.The RUNX family: developmental regulators in cancer.Runt-related transcription factor 1 (RUNX1) stimulates tumor suppressor p53 protein in response to DNA damage through complex formation and acetylation.RUNX in Invertebrates.Runx1 Orchestrates Sphingolipid Metabolism and Glucocorticoid Resistance in Lymphomagenesis.The core binding factor CBF negatively regulates skeletal muscle terminal differentiationRUNX1 and its fusion oncoprotein derivative, RUNX1-ETO, induce senescence-like growth arrest independently of replicative stress.Addiction to Runx1 is partially attenuated by loss of p53 in the Eµ-Myc lymphoma model.Response: the role of RUNX1 isoforms in hematopoietic commitment of human pluripotent stem cells.Runx regulation of sphingolipid metabolism and survival signaling.Runx2 disruption promotes immortalization and confers resistance to oncogene-induced senescence in primary murine fibroblasts.RUNX-mediated growth arrest and senescence are attenuated by diverse mechanisms in cells expressing RUNX1 fusion oncoproteins.Roles of AML1/RUNX1 in T-cell malignancy induced by loss of p53.
P2860
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P2860
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
@en
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
@nl
type
label
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
@en
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
@nl
prefLabel
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
@en
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
@nl
P2093
P2860
P356
P1433
P1476
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53
@en
P2093
Alan D Friedman
Alma Jenkins
Anna Kilbey
Anne Terry
Ewan R Cameron
Florence Bernardin-Fried
James C Neil
Sandy F Wotton
P2860
P2888
P304
P356
10.1038/SJ.ONC.1207729
P407
P577
2004-07-01T00:00:00Z
P6179
1037822233