ArticleThe Journal of biological chemistry2012
Ubiquitination of retinoblastoma family protein 1 potentiates gene-specific repression function.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Retinoblastoma protein activity revealed by CRISPRi study of divergent Rbf1 and Rbf2 paralogs.G3 (Bethesda, Md.) · 2024Article
- Complex cis-regulatory landscape of the insulin receptor gene underlies the broad expression of a central signaling regulator.Development (Cambridge, England) · 2016Article
- Regulation of cell polarity determinants by the Retinoblastoma tumor suppressor protein.Scientific reports · 2016Article
- The Evolutionarily Conserved C-terminal Domains in the Mammalian Retinoblastoma Tumor Suppressor Family Serve as Dual Regulators of Protein Stability and Transcriptional Potency.The Journal of biological chemistry · 2015Article
- Genome-Wide Analysis of Drosophila RBf2 Protein Highlights the Diversity of RB Family Targets and Possible Role in Regulation of Ribosome Biosynthesis.G3 (Bethesda, Md.) · 2015Article
- Role of Drosophila retinoblastoma protein instability element in cell growth and proliferation.Cell cycle (Georgetown, Tex.) · 2015Article
- Integrated stability and activity control of the Drosophila Rbf1 retinoblastoma protein.The Journal of biological chemistry · 2014Article
- Rbf1 degron dysfunction enhances cellular DNA replication.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The retinoblastoma (RB) tumor suppressor family functions as a regulatory node governing cell cycle progression, differentiation, and apoptosis. Post-translational modifications play a critical role in modulating RB activity, but additional levels of control, including protein turnover, are also essential for proper function. The Drosophila RB homolog Rbf1 is subjected to developmentally cued proteolysis mediated by an instability element (IE) present in the C terminus of this protein. Paradoxically, instability mediated by the IE is also linked to Rbf1 repression potency, suggesting that proteolytic machinery may also be directly involved in transcriptional repression. We show that the Rbf1 IE is an autonomous degron that stimulates both Rbf1 ubiquitination and repression potency. Importantly, Rbf1 IE function is promoter-specific, contributing to repression of cell cycle responsive genes but not to repression of cell signaling genes. The multifunctional IE domain thus provides Rbf1 flexibility for discrimination between target genes embedded in divergent cellular processes.
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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.