ArticleNucleus (Austin, Tex.)2015
Akt promotes tumorigenesis in part through modulating genomic instability via phosphorylating XLF.
Article in Nucleus (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Interactions between the DNA Damage Response and the Telomere Complex in Carcinogenesis: A Hypothesis.Current issues in molecular biology · 2023Review
- Article
- ITCH nuclear translocation and H1.2 polyubiquitination negatively regulate the DNA damage response.Nucleic acids research · 2019Article
- UBE2S, a novel substrate of Akt1, associates with Ku70 and regulates DNA repair and glioblastoma multiforme resistance to chemotherapy.Oncogene · 2017Article
- Cloning, localization and focus formation at DNA damage sites of canine XLF.The Journal of veterinary medical science · 2017Article
- PKIB promotes cell proliferation and the invasion-metastasis cascade through the PI3K/Akt pathway in NSCLC cells.Experimental biology and medicine (Maywood, N.J.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
To maintain genome stability, mammalian cells have developed a delicate, yet efficient, system to sense and repair damaged DNA, including two evolutionarily conserved DNA damage repair (DDR) pathways: homologous recombination (HR) and non-homologous-end-joining (NHEJ). Deregulation in these repair pathways may lead to genomic instability and subsequent human diseases, including cancer. On the other hand, hyper-activation of the oncogenic Akt signaling pathway has been observed in almost all solid tumors. Emerging evidence has begun to reveal a possible role of active Akt in regulating DDR, possibly through suppression of HR. However, whether and how Akt regulates NHEJ remains largely undefined. To this end, we recently reported that Akt impairs NHEJ by phosphorylating XLF at T181, to trigger its dissociation from the functional DNA ligase IV (LIG4)/XRCC4 complex. Here, we provide an additional perspective discussing how Akt is activated upon DNA damage to regulate DNA repair pathways as well as the cellular apoptotic responses.
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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.