ArticleMolecular and cellular biology2009
Regulation of p53 by TopBP1: a potential mechanism for p53 inactivation in cancer.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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
45 citing papers in PubMed, 71 citations in OpenAlex.
- Interaction of polymorphisms in mitotic regulator genes with cigarette smoking and pancreatic cancer risk.Molecular carcinogenesis · 2013Trial
- Development of a structurally distinct TopBP1 inhibitor that enhances PARP blockade and reverses osimertinib resistance.Science advances · 2026Article
- CRISPR/Cas9-mediated knockout of TopBP1 shifts the Bax/Bcl-2 balance toward apoptosis in MCF7 breast cancer cells.Molecular biology reports · 2026Article
- Shining light on drug discovery: optogenetic screening for TopBP1 biomolecular condensate inhibitors.NAR cancer · 2025Article
- The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ.Nature communications · 2025Article
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- TOPBP1 as a potential predictive biomarker for enhanced combinatorial efficacy of olaparib and AZD6738 in PDAC.Cell & bioscience · 2025Article
- A small-molecule inhibitor of TopBP1 exerts anti-MYC activity and synergy with PARP inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Deubiquitinase OTUD6A promotes breast cancer progression by increasing TopBP1 stability and rendering tumor cells resistant to DNA-damaging therapy.Cell death and differentiation · 2022Article
- DNA damage response proteins in canine cancer as potential research targets in comparative oncology.Veterinary and comparative oncology · 2022Review
- Homologous Recombination Deficiency: Cancer Predispositions and Treatment Implications.The oncologist · 2021Review
- Human CTC1 promotes TopBP1 stability and CHK1 phosphorylation in response to telomere dysfunction and global replication stress.Cell cycle (Georgetown, Tex.) · 2020Article
- E2F1 sumoylation as a protective cellular mechanism in oxidative stress response.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
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- Cell Cycle-Dependent Switch of TopBP1 Functions by Cdk2 and Akt.Molecular and cellular biology · 2020Article
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- Joint Transcriptomic Analysis of Lung Cancer and Other Lung Diseases.Frontiers in genetics · 2019Article
- Mutant p53 perturbs DNA replication checkpoint control through TopBP1 and Treslin.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The c.*229C > T gene polymorphism in 3'UTR region of the topoisomerase IIβ binding protein 1 gene and LOH in BRCA1/2 regions and their effect on the risk and progression of human laryngeal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Proper control of the G(1)/S checkpoint is essential for normal proliferation. The activity of p53 must be kept at a very low level under unstressed conditions to allow growth. Here we provide evidence supporting a crucial role for TopBP1 in actively repressing p53. Depletion of TopBP1 upregulates p53 target genes involved in cell cycle arrest and apoptosis and enhances DNA damage-induced apoptosis. The regulation is mediated by an interaction between the seventh and eighth BRCT domains of TopBP1 and the DNA-binding domain of p53, leading to inhibition of p53 promoter binding activity. Importantly, TopBP1 overexpression is found in 46 of 79 primary breast cancer tissues and is associated with high tumor grade and shorter patient survival time. Overexpression of TopBP1 to a level comparable to that seen in breast tumors leads to inhibition of p53 target gene expression and DNA damage-induced apoptosis and G(1) arrest. Thus, a physiological level of TopBP1 is essential for normal G(1)/S transition, but a pathological level of TopBP1 in cancer may perturb p53 function and contribute to an aggressive tumor behavior.
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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.