ArticleMolecular and cellular biology2004
Distinct mechanisms for repression of RNA polymerase III transcription by the retinoblastoma tumor suppressor protein.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1-bound enhancers through interactions with the EP400 chromatin remodeler.Nucleic acids research · 2024Article
- Article
- Targeting BRF2 in Cancer Using Repurposed Drugs.Cancers · 2021Article
- RNF12 catalyzes BRF1 ubiquitination and regulates RNA polymerase III-dependent transcription.The Journal of biological chemistry · 2019Article
- Abnormal expression of TFIIIB subunits and RNA Pol III genes is associated with hepatocellular carcinoma.Liver research (Beijing, China) · 2017Article
- Gender Specific Differences in RNA Polymerase III Transcription.Journal of carcinogenesis & mutagenesis · 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
- Regulation of human RNA polymerase III transcription by DNMT1 and DNMT3a DNA methyltransferases.The Journal of biological chemistry · 2012Article
- RNA polymerase III drives alternative splicing of the potassium channel-interacting protein contributing to brain complexity and neurodegeneration.The Journal of cell biology · 2011Article
- Cell growth- and differentiation-dependent regulation of RNA polymerase III transcription.Cell cycle (Georgetown, Tex.) · 2010Review
- Transcriptional repression: conserved and evolved features.Current biology : CB · 2010Review
- Regulation of TFIIIB during F9 cell differentiation.BMC molecular biology · 2010Article
- Structure and activity of putative intronic miRNA promoters.RNA (New York, N.Y.) · 2010Article
- TLS inhibits RNA polymerase III transcription.Molecular and cellular biology · 2010Article
- Down-regulation of the transcriptional mediator subunit Med1 contributes to the loss of expression of metastasis-associated dapk1 in human cancers and cancer cells.International journal of cancer · 2009Article
- The JNKs differentially regulate RNA polymerase III transcription by coordinately modulating the expression of all TFIIIB subunits.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Enhanced RNA polymerase III-dependent transcription is required for oncogenic transformation.The Journal of biological chemistry · 2008Article
- PTEN represses RNA polymerase III-dependent transcription by targeting the TFIIIB complex.Molecular and cellular biology · 2008Article
- Transcriptional regulation of human small nuclear RNA genes.Biochimica et biophysica acta · 2008Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
The retinoblastoma (RB) protein represses global RNA polymerase III transcription of genes that encode nontranslated RNAs, potentially to control cell growth. However, RNA polymerase III-transcribed genes exhibit diverse promoter structures and factor requirements for transcription, and a universal mechanism explaining global repression is uncertain. We show that RB represses different classes of RNA polymerase III-transcribed genes via distinct mechanisms. Repression of human U6 snRNA (class 3) gene transcription occurs through stable promoter occupancy by RB, whereas repression of adenovirus VAI (class 2) gene transcription occurs in the absence of detectable RB-promoter association. Endogenous RB binds to a human U6 snRNA gene in both normal and cancer cells that maintain functional RB but not in HeLa cells whose RB function is disrupted by the papillomavirus E7 protein. Both U6 promoter association and transcriptional repression require the A/B pocket domain and C region of RB. These regions of RB contribute to U6 promoter targeting through numerous interactions with components of the U6 general transcription machinery, including SNAP(C) and TFIIIB. Importantly, RB also concurrently occupies a U6 promoter with RNA polymerase III during repression. These observations suggest a novel mechanism for RB function wherein RB can repress U6 transcription at critical steps subsequent to RNA polymerase III recruitment.
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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.