Loss of protooncogene c-Myc function impedes G1 phase progression both before and after the restriction point
about
Proteomic profiling of Myc-associated proteinsA genome-wide screen for beta-catenin binding sites identifies a downstream enhancer element that controls c-Myc gene expressionStress response gene ATF3 is a target of c-myc in serum-induced cell proliferationThe oncogene c-Myc coordinates regulation of metabolic networks to enable rapid cell cycle entryThe cell cycle time of CD8+ T cells responding in vivo is controlled by the type of antigenic stimulus.RNA interference-mediated c-MYC inhibition prevents cell growth and decreases sensitivity to radio- and chemotherapy in childhood medulloblastoma cells.cMyc increases cell number through uncoupling of cell division from cell size in CHO cells.MYC and the control of DNA replication.You Don't Muck with MYCDeregulation of common genes by c-Myc and its direct target, MT-MC1.The RAS-dependent ERF control of cell proliferation and differentiation is mediated by c-Myc repression.The role of Myc-induced protein synthesis in cancer.Phosphoinositide 3-kinase activation in late G1 is required for c-Myc stabilization and S phase entryKinetic profiling of the c-Myc transcriptome and bioinformatic analysis of repressed gene promoters.The c-MYC oncoprotein as a treatment target in cancer and other disorders of cell growth.Suppression of Myc oncogenic activity by nucleostemin haploinsufficiencyMnt-Max to Myc-Max complex switching regulates cell cycle entry.Analysis of cell cycle phases and progression in cultured mammalian cells.c-Myc is a novel target of cell cycle arrest by honokiol in prostate cancer cells.c-Myc activates multiple metabolic networks to generate substrates for cell-cycle entry.Disruption of Stat3 reveals a critical role in both the initiation and the promotion stages of epithelial carcinogenesis.Role for BRG1 in cell cycle control and tumor suppression.A constitutively active arylhydrocarbon receptor induces growth inhibition of jurkat T cells through changes in the expression of genes related to apoptosis and cell cycle arrest.Activating transcription factor 3, a stress-inducible gene, suppresses Ras-stimulated tumorigenesis.c-Myc regulates the CDK1/cyclin B1 dependent‑G2/M cell cycle progression by histone H4 acetylation in Raji cells.
P2860
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P2860
Loss of protooncogene c-Myc function impedes G1 phase progression both before and after the restriction point
description
2003 nî lūn-bûn
@nan
2003 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի մարտին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@ast
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@en
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@nl
type
label
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@ast
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@en
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@nl
prefLabel
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@ast
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@en
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@nl
P2860
P356
P1476
Loss of protooncogene c-Myc fu ...... nd after the restriction point
@en
P2093
Christoph Schorl
John M Sedivy
P2860
P304
P356
10.1091/MBC.E02-10-0649
P577
2003-03-01T00:00:00Z