ArticleJournal of cell science2017
Nuclear α-catenin mediates the DNA damage response via β-catenin and nuclear actin.
Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Rewired DDR-TGF-β-β-catenin-PD-L1 axis accelerates progression and shapes therapy in human papillomavirus-driven cancer.Frontiers in immunology · 2026Review
- Review
- Identification of potential biomarkers for aging diagnosis of mesenchymal stem cells derived from the aged donors.Stem cell research & therapy · 2024Article
- Crosstalk between Wnt/β-catenin signaling pathway and DNA damage response in cancer: a new direction for overcoming therapy resistance.Frontiers in pharmacology · 2023Review
- Filamentous nuclear actin regulation of PML NBs during the DNA damage response is deregulated by prelamin A.Cell death & disease · 2022Article
- Pan-cancer Analysis of Homologous Recombination Repair-associated Gene Alterations and Genome-wide Loss-of-Heterozygosity Score.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Premetastatic shifts of endogenous and exogenous mutational processes support consolidative therapy in EGFR-driven lung adenocarcinoma.Cancer letters · 2022Article
- Mechanisms of mutant β-catenin in endometrial cancer progression.Frontiers in oncology · 2022Review
- Adherens junction proteins on the move-From the membrane to the nucleus in intestinal diseases.Frontiers in cell and developmental biology · 2022Review
- Genotoxic stress-triggered β-catenin/JDP2/PRMT5 complex facilitates reestablishing glutathione homeostasis.Nature communications · 2019Article
- β-Catenin: A Metazoan Filter for Biological Noise?Frontiers in genetics · 2019Review
- Multiple Pools of Nuclear Actin.Anatomical record (Hoboken, N.J. : 2007) · 2018Article
- Nuclear Actin: From Discovery to Function.Anatomical record (Hoboken, N.J. : 2007) · 2018Review
- Protein sequestration at the nuclear periphery as a potential regulatory mechanism in premature aging.The Journal of cell biology · 2018Review
- Overexpression of lamin B1 induces mitotic catastrophe in colon cancer LoVo cells and is associated with worse clinical outcomes.International journal of oncology · 2018Article
- NBPF7 promotes the proliferation of α-catenin-knockdown HaCaT cells via functional interaction with the NF-κB pathway.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
α-Catenin is an F-actin-binding protein widely recognized for its role in cell-cell adhesion. However, a growing body of literature indicates that α-catenin is also a nuclear protein. In this study, we show that α-catenin is able to modulate the sensitivity of cells to DNA damage and toxicity. Furthermore, nuclear α-catenin is actively recruited to sites of DNA damage. This recruitment occurs in a β-catenin-dependent manner and requires nuclear actin polymerization. These findings provide mechanistic insight into the WNT-mediated regulation of the DNA damage response and suggest a novel role for the α-catenin-β-catenin complex in the nucleus.
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What OpenQuestion holds
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.