Exit from G1 and S phase of the cell cycle is regulated by repressor complexes containing HDAC-Rb-hSWI/SNF and Rb-hSWI/SNF

Article Abstract:

Exit from G1 and S phase of the cell cycle is regulated by repressor complexes which contain retinoblastoma protein (Rb)-hSWI/SNF and histone deacetylase (HDAC)-Rb-hSWI/SNF. Evidence that Rb forms a repressor with HDAC and the hSWI/SNF nucleosome remodeling complex exists. The complex works against transcription of genes for cyclins E and A and stops the cell cycle in the G1 phase. Phosphorylation of Rb by cyclin D/cdk4 messes up association with HDAC, cutting back on repression of the cyclin E gene and G1 arrest.

author: Zhang, H.S., Gavin, M., Dahiya, A., Postigo, A.A., Ma, D., Luo, R.X., Harbour, J.W., Dean, D.C.
Histones, Retinoblastoma

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Drosophila p53 is a structural and functional homolog of the tumor suppressor p53

Article Abstract:

Drosophila p53 has been found to be a structural and functional homolog of the tumor suppressor p53. A Drosophila homolog of p53 has been identified. A function contributing to apoptosis has been found for p53. Drosophila is an good model system in which to find out about p53 apoptotic pathways brought on by DNA damage.

author: Ollmann, M., Young, L.M., De Como, C.J., Karim, F., Belvin, M., Robertson, S., Whittaker, K., Demsky, M., Fisher, W.W., Buchman, A., Duyk, G., Friedman, L., Prives, C., Kopczynski, C.
Usage, DNA damage, Cellular signal transduction, Drosophila, Biological models, Tumor suppressor genes

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Parsing Ink4a/Arf: "pure" p16-null mice

Article Abstract:

The INK4a/ARF locus encoded proteins inhibit cell proliferation and the proteins themselves do not bear any amino acid homology. Research findings reveal that melanomas arise from Ink4a loss and arf heterozygosity. Mice lacking Ink4a/Arf develop melanoma spontaneously.

author: Sherr, Charles J.
Analysis, Gene expression, Melanoma

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subjects list: Research, United States, Physiological aspects, Genetic aspects, Genetic regulation, Genetic transcription, Transcription (Genetics), Cytochemistry, Cell cycle, Cell death, Carcinogenesis
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