Tumor Necrosis Factor α Inhibits Cyclin A Expression and Retinoblastoma Hyperphosphorylation Triggered by Insulin-like Growth Factor-I Induction of New E2F-1 Synthesis

Cyclin A is required for cell cycle S phase entry, and its overexpression contributes to tumorigenesis. Release of pre-existing E2Fs from inactive complexes of E2F and hypophosphorylated retinoblastoma (RB) is the prevailing dogma for E2F transcriptional activation of target genes such as cyclin A....

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Veröffentlicht in:	The Journal of biological chemistry 2004-02, Vol.279 (9), p.7438-7446
Hauptverfasser:	Shen, Wen Hong, Yin, Yuxin, Broussard, Suzanne R., McCusker, Robert H., Freund, Gregory G., Dantzer, Robert, Kelley, Keith W.
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenocarcinoma Breast Neoplasms CDC2-CDC28 Kinases - metabolism Cell Cycle Cell Cycle Proteins Cyclin A - genetics Cyclin A - metabolism Cyclin A - pharmacology Cyclin-Dependent Kinase 2 DNA-Binding Proteins E2F Transcription Factors E2F-1 protein E2F1 Transcription Factor Gene Expression - drug effects Humans Immunoblotting Immunosorbent Techniques Insulin-Like Growth Factor I - pharmacology Luciferases - genetics Phosphorylation Phosphoserine - metabolism Promoter Regions, Genetic - genetics Retinoblastoma Protein - metabolism siRNA Transcription Factors - biosynthesis Tumor Cells, Cultured Tumor Necrosis Factor-alpha - pharmacology Tumor Necrosis Factor-alpha - physiology
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