ArticleMolecular and cellular biology2002
CK2 forms a stable complex with TFIIIB and activates RNA polymerase III transcription in human cells.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
- CIGB-300, a novel proapoptotic peptide that impairs the CK2 phosphorylation and exhibits anticancer properties both in vitro and in vivo.Molecular and cellular biochemistry · 2008Trial
- Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus.Molecular cell · 2026Review
- Interactions with multiple inner kinetochore proteins determine mitotic localization of FACT.The Journal of cell biology · 2025Article
- Article
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- Nuclear Actin Dynamics in Gene Expression, DNA Repair, and Cancer.Results and problems in cell differentiation · 2022Article
- Signaling to and from the RNA Polymerase III Transcription and Processing Machinery.Annual review of biochemistry · 2018Review
- Functional interplay between the transcription factors USF1 and PDX-1 and protein kinase CK2 in pancreatic β-cells.Scientific reports · 2017Article
- Gender Specific Differences in RNA Polymerase III Transcription.Journal of carcinogenesis & mutagenesis · 2016Article
- The B-WICH chromatin-remodelling complex regulates RNA polymerase III transcription by promoting Max-dependent c-Myc binding.Nucleic acids research · 2015Article
- Differential phosphorylation of a regulatory subunit of protein kinase CK2 by target of rapamycin complex 1 signaling and the Cdc-like kinase Kns1.The Journal of biological chemistry · 2015Article
- Differential Phosphorylation of RNA Polymerase III and the Initiation Factor TFIIIB in Saccharomyces cerevisiae.PloS one · 2015Article
- Akt activation enhances ribosomal RNA synthesis through casein kinase II and TIF-IA.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Regulation of cell death by transfer RNA.Antioxidants & redox signaling · 2013Review
- Recovery of RNA polymerase III transcription from the glycerol-repressed state: revisiting the role of protein kinase CK2 in Maf1 phosphoregulation.The Journal of biological chemistry · 2012Article
- The functions of TFIIF during initiation and transcript elongation are differentially affected by phosphorylation by casein kinase 2.The Journal of biological chemistry · 2011Article
- RNA polymerase III transcription in cancer: the BRF2 connection.Molecular cancer · 2011Review
- Casein kinase II-mediated phosphorylation of general repressor Maf1 triggers RNA polymerase III activation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Genome stability control by checkpoint regulation of tRNA gene transcription.Transcription · 2010Article
- Inhibition of U6 snRNA Transcription by PTEN.OnLine journal of biological sciences · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
CK2 is a highly conserved protein kinase with growth-promoting and oncogenic properties. It is known to activate RNA polymerase III (PolIII) transcription in Saccharomyces cerevisiae and is shown here to also exert a potent effect on PolIII in mammalian cells. Peptide and chemical inhibitors of CK2 block PolIII transcription in human cell extracts. Furthermore, PolIII transcription in mammalian fibroblasts is decreased significantly when CK2 activity is compromised by chemical inhibitors, antisense oligonucleotides, or kinase-inactive mutants. Coimmunoprecipitation and cofractionation show that endogenous human CK2 associates stably and specifically with the TATA-binding protein-containing factor TFIIIB, which brings PolIII to the initiation site of all class III genes. Serum stimulates TFIIIB phosphorylation in vivo, an effect that is diminished by inhibitors of CK2. Binding to TFIIIC2 recruits TFIIIB to most PolIII promoters; this interaction is compromised specifically by CK2 inhibitors. The data suggest that CK2 stimulates PolIII transcription by binding and phosphorylating TFIIIB and facilitating its recruitment by TFIIIC2. CK2 also activates PolI transcription in mammals and may therefore provide a mechanism to coregulate the output of PolI and PolIII. CK2 provides a rare example of an endogenous activity that operates on the PolIII system in both mammals and yeasts. Such evolutionary conservation suggests that this control may be of fundamental importance.
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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.