ArticleMolecular and cellular biology1996
Transcriptional repression and growth suppression by the p107 pocket protein.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Kaposi's sarcoma-associated herpesvirus lana2 protein interacts with the pocket proteins and inhibits their sumoylation.Oncogene · 2014Article
- Positive regulation of minichromosome maintenance gene expression, DNA replication, and cell transformation by a plant retinoblastoma gene.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Review
- Tissue-specific tumor suppressor activity of retinoblastoma gene homologs p107 and p130.Genes & development · 2004Article
- Autorepression of c-myc requires both initiator and E2F-binding site elements and cooperation with the p107 gene product.Oncogene · 2004Article
- Emerging roles of DNA tumor viruses in cell proliferation: new insights into genomic instability.Oncogene · 2003Review
- Balance between acetylation and methylation of histone H3 lysine 9 on the E2F-responsive dihydrofolate reductase promoter.Molecular and cellular biology · 2003Article
- Transcriptional repression by the retinoblastoma protein through the recruitment of a histone methyltransferase.Molecular and cellular biology · 2001Article
- Differential control of transcription by DNA-bound cyclins.Molecular biology of the cell · 2001Article
- Requirement for p27(KIP1) in retinoblastoma protein-mediated senescence.Molecular and cellular biology · 2001Article
- Protein expression of the RB-related gene family and SV40 large T antigen in mesothelioma and lung cancer.Oncogene · 2000Article
- E2f3 is critical for normal cellular proliferation.Genes & development · 2000Article
- Repression of Epstein-Barr virus EBNA-1 gene transcription by pRb during restricted latency.Journal of virology · 1999Article
- Article
- The three members of the pocket proteins family share the ability to repress E2F activity through recruitment of a histone deacetylase.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Regulation of cellular genes in a chromosomal context by the retinoblastoma tumor suppressor protein.Molecular and cellular biology · 1998Article
- Influence of promoter potency on the transcriptional effects of YY1, SRF and Msx-1 in transient transfection analysis.Nucleic acids research · 1998Article
- E2F-6, a member of the E2F family that can behave as a transcriptional repressor.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- The J domain of simian virus 40 large T antigen is required to functionally inactivate RB family proteins.Molecular and cellular biology · 1998Article
- Regulation of the human proliferating cell nuclear antigen promoter by the adenovirus E1A-associated protein p107.Journal of virology · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
p107 is a member of the pocket family of proteins that includes the retinoblastoma tumor suppressor. Overexpression of p107 arrests cells in G1, suggesting that it is important for cell cycle control. This growth suppression is mediated at least in part through the interaction of p107 with a member of the E2F family of cell cycle transcription factors, and this interaction can be disrupted by oncoproteins from DNA tumor viruses such as adenovirus E1a that bind p107. Not only does the binding of p107 to E2F inactivate E2F, but also we show that when p107 is tethered to the promoter through binding to E2F it functions as a general transcriptional repressor. This general repressor activity was also evident when p107 was fused to the DNA binding domain of Gal4 so that it could be directly targeted to the promoter in an E2F-independent fashion. Using p107 mutants, we compared the regions of the protein required for transcriptional repression and cell growth suppression. We found that the pocket domain is sufficient for inactivation of E2F, general repressor activity, and most of the growth suppressor activity. Binding of conserved region 1 from Ela to p107 blocked interaction with E2F, but it did not affect general repressor activity, demonstrating that binding and inactivation of E2F and general repressor activity are distinguishable properties of p107. Within the pocket, two conserved domains, A and B, were sufficient for growth suppression and transcriptional repressor activity. Surprisingly, we found that these two domains were fully functional when they were coexpressed as separate proteins, and we present results suggesting that the domains may interact at the promoter to form an active pocket.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.