ArticleMolecular and cellular biology1996
Domains A and B in the Rb pocket interact to form a transcriptional repressor motif.
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 34 papers.
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Who cites it
34 citing papers in PubMed, 100 citations in OpenAlex.
- Integrative Genomic Mapping and Visualization From Curated Public Datasets Reveals Germline RB1 Variant Diversity in Retinoblastoma.Investigative ophthalmology & visual science · 2026Article
- Expanding the RB1 variant landscape of heritable retinoblastoma: unlocking precision oncology potential in Southern Africa.BMC cancer · 2026Article
- Five novel RB1 gene mutations and genotype-phenotype correlations in Chinese children with retinoblastoma.International ophthalmology · 2022Article
- Article
- Spectrum ofFrontiers in genetics · 2020Article
- APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway.Bioscience reports · 2016Review
- Cellular mechanosensing: getting to the nucleus of it all.Progress in biophysics and molecular biology · 2014Review
- The nuclear protein ALY binds to and modulates the activity of transcription factor E2F2.Molecular & cellular proteomics : MCP · 2013Article
- Posttranslational modifications of the retinoblastoma tumor suppressor protein as determinants of function.Genes & cancer · 2012Article
- The retinoblastoma family of proteins and their regulatory functions in the mammalian cell division cycle.Cell division · 2012Article
- 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
- Distinct roles for p107 and p130 in Rb-independent cellular senescence.Cell cycle (Georgetown, Tex.) · 2008Article
- Review
- Restriction beyond the restriction point: mitogen requirement for G2 passage.Cell division · 2006Article
- Tissue-specific tumor suppressor activity of retinoblastoma gene homologs p107 and p130.Genes & development · 2004Article
- Distinct mechanisms for repression of RNA polymerase III transcription by the retinoblastoma tumor suppressor protein.Molecular and cellular biology · 2004Article
- Transcriptional repression by the retinoblastoma protein through the recruitment of a histone methyltransferase.Molecular and cellular biology · 2001Article
- Role of LXCXE motif-dependent interactions in the activity of the retinoblastoma protein.Oncogene · 2001Article
- Histone deacetylase-dependent transcriptional repression by pRB in yeast occurs independently of interaction through the LXCXE binding cleft.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Structural basis for the inactivation of retinoblastoma tumor suppressor by SV40 large T antigen.The EMBO journal · 2001Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The retinoblastoma protein (Rb) is a tumor suppressor that regulates progression from the G1 phase to the S phase of the cell cycle. Previously, we found that Rb is a transcriptional repressor that is selectively targeted to promoters through an interaction with the E2F family of cell cycle transcription factors--when Rb is tethered to a promoter through E2F, it not only blocks E2F activity, it also binds surrounding transcription factors, preventing their interaction with the basal transcription complex, thus resulting in a dominant inhibitory effect on transcription of cell cycle genes. Here we examine the repressor motif of Rb. The two domains in the Rb pocket, A and B, which are conserved across species and in the Rb-related proteins p107 and p130, are both required for repressor activity. The nonconserved spacer separating A and B is not required. Although neither A nor B alone had any repressor activity, surprisingly, repressor activity was observed when the domains were coexpressed on separate proteins. Transfection assays suggest that one domain can recruit the other to the promoter to form a repressor motif that can both interact with E2F and have a dominant inhibitory effect on transcription. Using coimmunoprecipitation and in vitro binding assays, we show that A and B interact directly and that mutations which disrupt this interaction inhibit repressor activity. The Rb pocket was originally defined as the binding site for oncoproteins from DNA tumor viruses such as adenovirus E1a. We present evidence that E1a interacts with a site formed by the interaction of A and B and that this interaction with A and B induces or stabilizes the A-B interaction.
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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.