ArticleBritish journal of cancer2013
Role of multifunctional transcription factor TFII-I and putative tumour suppressor DBC1 in cell cycle and DNA double strand damage repair.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Gtf2i-encoded transcription factor Tfii-i regulates myelination via Sox10 and Mbp regulatory elements.Nature communications · 2025Article
- Cellular transcription factor TFII-I represses adenovirus gene expression.Journal of virology · 2025Article
- CCAR2 functions downstream of the Shieldin complex to promote double-strand break end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A novel form of Deleted in breast cancer 1 (DBC1) lacking the N-terminal domain does not bind SIRT1 and is dynamically regulated in vivo.Scientific reports · 2019Article
- Phosphoprotein profiles of candidate markers for early cellular responses to low-dose γ-radiation in normal human fibroblast cells.Journal of radiation research · 2017Article
- CCAR2 Is Required for Proliferation and Tumor Maintenance in Human Squamous Cell Carcinoma.The Journal of investigative dermatology · 2017Article
- A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection.Nature communications · 2016Article
- DBC1/CCAR2 is involved in the stabilization of androgen receptor and the progression of osteosarcoma.Scientific reports · 2015Article
- CCAR2/DBC1 is required for Chk2-dependent KAP1 phosphorylation and repair of DNA damage.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn multicellular organisms, precise control of cell cycle and the maintenance of genomic stability are crucial to prevent chromosomal alterations. The accurate function of the DNA damage pathway is maintained by DNA repair mechanisms including homologous recombination (HR). Herein, we show that both TFII-I and DBC1 mediate cellular mechanisms of cell-cycle regulation and DNA double strand damage repair.
methodsRegulation of cell cycle by TFII-I and DBC1 was investigated using Trypan blue dye exclusion test, luciferase assay, and flow cytometry analysis. We also analysed the role of TFII-I and DBC1 in DNA double strand damage repair after irradiation by immunofluorescence study, clonogenicity assay, and HR assay.
resultsFlow cytometry analysis revealed a novel function that siRNA-mediated knockdown of endogenous DBC1 resulted in G2/M phase arrest. We also have shown that both endogenous TFII-I and DBC1 activate DNA repair mechanisms after irradiation because irradiation-induced foci formation of TFII-I-γH2AX was observed, and the depletion of endogenous TFII-I or DBC1 resulted in the inhibition of normal HR efficiency.
conclusionThese results reveal novel mechanisms by which TFII-I and DBC1 can modulate cellular fate by affecting cell-cycle control as well as HR pathway.
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