ArticleCell death and differentiation2018
Oncoprotein Tudor-SN is a key determinant providing survival advantage under DNA damaging stress.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- ACSS1 co-opts acetyl-CoA metabolism to drive DNA repair and undermine radiotherapy efficacy in breast cancer.Cell death & disease · 2025Article
- Translational regulation of SND1 governs endothelial homeostasis during stress.The Journal of clinical investigation · 2025Article
- A novel partnership between lncTCF7 and SND1 regulates the expression of the TCF7 gene via recruitment of the SWI/SNF complex.Scientific reports · 2024Article
- KDM6A-SND1 interaction maintains genomic stability by protecting the nascent DNA and contributes to cancer chemoresistance.Nucleic acids research · 2024Article
- Vascular injury activates the ELK1/SND1/SRF pathway to promote vascular smooth muscle cell proliferative phenotype and neointimal hyperplasia.Cellular and molecular life sciences : CMLS · 2024Article
- ELFN1-AS1 promotes GDF15-mediated immune escape of colorectal cancer from NK cells by facilitating GCN5 and SND1 association.Discover oncology · 2023Article
- Molecular Design, Spectroscopic, DFT, Pharmacological, and Molecular Docking Studies of Novel Ruthenium(III)-Schiff Base Complex: An Inhibitor of Progression in HepG2 Cells.International journal of environmental research and public health · 2022Article
- Impact of hepatocyte-specific deletion of staphylococcal nuclease and tudor domain containing 1 (SND1) on liver insulin resistance and acute liver failure of mice.Bioengineered · 2021Article
- Translation ofRNA biology · 2021Article
- The Role of the PRMT5-SND1 Axis in Hepatocellular Carcinoma.Epigenomes · 2021Article
- SND1 promotes Th1/17 immunity against chlamydial lung infection through enhancing dendritic cell function.PLoS pathogens · 2021Article
- The E2F1 transcription factor and RB tumor suppressor moonlight as DNA repair factors.Cell cycle (Georgetown, Tex.) · 2020Review
- The interactome of the prostate-specific protein Anoctamin 7.Cancer biomarkers : section A of Disease markers · 2020Article
- The novel chromatin architectural regulator SND1 promotes glioma proliferation and invasion and predicts the prognosis of patients.Neuro-oncology · 2019Article
- SND1 acts as an anti-apoptotic factor via regulating the expression of lncRNA UCA1 in hepatocellular carcinoma.RNA biology · 2018Article
- The multifaceted oncogene SND1 in cancer: focus on hepatocellular carcinoma.Hepatoma research · 2018Article
- Insights IntoFrontiers in oncology · 2018Review
- Circ SMARCA5 Inhibited Tumor Metastasis by Interacting with SND1 and Downregulating the YWHAB Gene in Cervical Cancer.Cell transplantationArticle
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
Herein, Tudor-SN was identified as a DNA damage response (DDR)-related protein that plays important roles in the early stage of DDR. X-ray or laser irradiation could evoke the accumulation of Tudor-SN to DNA damage sites in a poly(ADP-ribosyl)ation-dependent manner via interaction with PARP-1. Additionally, we illustrated that the SN domain of Tudor-SN mediated the association of these two proteins. The accumulated Tudor-SN further recruited SMARCA5 (ATP-dependent chromatin remodeller) and GCN5 (histone acetyltransferase) to DNA damage sites, resulting in chromatin relaxation, and consequently activating the ATM kinase and downstream DNA repair signalling pathways to promote cell survival. Consistently, the loss-of-function of Tudor-SN attenuated the enrichment of SMARCA5, GCN5 and acetylation of histone H3 (acH3) at DNA break sites and abolished chromatin relaxation; as a result, the cells exhibited DNA repair and cell survival deficiency. As Tudor-SN protein is highly expressed in different tumours, it is likely to be involved in the radioresistance of cancer treatment.
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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.