Oncogene-induced senescence: an essential role for Runx.
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Oncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer CellsEvaluating the mechanistic evidence and key data gaps in assessing the potential carcinogenicity of carbon nanotubes and nanofibers in humansNew biomarkers probing depth of cell senescence assessed by laser scanning cytometry.The RUNX2 cistrome in osteoblasts: characterization, down-regulation following differentiation, and relationship to gene expression.Runt-related transcription factor RUNX3 is a target of MDM2-mediated ubiquitinationCancer-related ectopic expression of the bone-related transcription factor RUNX2 in non-osseous metastatic tumor cells is linked to cell proliferation and motilityPAI-1 Expression Is Required for HDACi-Induced Proliferative Arrest in ras-Transformed Renal Epithelial Cells.Genomic promoter occupancy of runt-related transcription factor RUNX2 in Osteosarcoma cells identifies genes involved in cell adhesion and motility.Lipidomic approach for stratification of acute myeloid leukemia patients.The RUNX Genes as Conditional Oncogenes: Insights from Retroviral Targeting and Mouse Models.Is Runx a linchpin for developmental signaling in metazoans?Co-activator activator (CoAA) prevents the transcriptional activity of Runt domain transcription factorsRUNX3 is multifunctional in carcinogenesis of multiple solid tumors.The RUNX family: developmental regulators in cancer.Proteomic analysis reveals a role for Bcl2-associated athanogene 3 and major vault protein in resistance to apoptosis in senescent cells by regulating ERK1/2 activation.Knockdown of core binding factorβ alters sphingolipid metabolism.Differential BMI1, TWIST1, SNAI2 mRNA expression pattern correlation with malignancy type in a spectrum of common cutaneous malignancies: basal cell carcinoma, squamous cell carcinoma, and melanoma.RUNX1 and its fusion oncoprotein derivative, RUNX1-ETO, induce senescence-like growth arrest independently of replicative stress.Runx regulation of sphingolipid metabolism and survival signaling.Mitochondrial defects trigger proliferation of neighbouring cells via a senescence-associated secretory phenotype in Drosophila.
P2860
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P2860
Oncogene-induced senescence: an essential role for Runx.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 29 May 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Oncogene-induced senescence: an essential role for Runx.
@en
Oncogene-induced senescence: an essential role for Runx.
@nl
type
label
Oncogene-induced senescence: an essential role for Runx.
@en
Oncogene-induced senescence: an essential role for Runx.
@nl
prefLabel
Oncogene-induced senescence: an essential role for Runx.
@en
Oncogene-induced senescence: an essential role for Runx.
@nl
P2093
P2860
P356
P1433
P1476
Oncogene-induced senescence: an essential role for Runx.
@en
P2093
Anna Kilbey
Anne Terry
Ewan R Cameron
James C Neil
P2860
P304
P356
10.4161/CC.6368
P577
2008-05-29T00:00:00Z