ArticleGeroScience2022
DNA damage-induced degradation of Sp1 promotes cellular senescence.
Article in GeroScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Cellular signaling within aged skeletal muscle reveals a dysregulated stress-induced remodeling response following volumetric muscle loss in female mice.Physiological reports · 2026Article
- Letter to the editor 1 on "MET promotes hepatocellular carcinoma development through the promotion of TRIB3-mediated FOXO1 degradation".Clinical and molecular hepatology · 2026Article
- Single-nucleus multiome analysis in the human prefrontal cortex identifies gene expression and cis-regulatory elements associated with aging.Cell reports · 2026Article
- Superenhancer-mediated ferroptosis in age-related hearing loss: cochlear epigenomics.Cellular and molecular life sciences : CMLS · 2026Article
- ATR Deficiency Impairs DNA Damage Repair and Accelerates Cellular Senescence in Bovine Mammary Epithelial Cells, Leading to Lactation Dysfunction.Animals : an open access journal from MDPI · 2025Article
- Review
- Sonic hedgehog restrains the ubiquitin-dependent degradation of SP1 to inhibit neuronal/glial senescence associated phenotypes in chemotherapy-induced peripheral neuropathy via the TRIM25-CXCL13 axis.Journal of advanced research · 2025Article
- Precise Mapping of Physiological DSBs Using In-Suspension Break Labeling In Situ and Sequencing (sBLISS).Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- WTAP increases BMP2 expression to promote osteoblast differentiation and inhibit osteoblast senescence via mMolecular genetics and genomics : MGG · 2024Article
- Review
- Article
- Bioinformatics-based discovery of intervertebral disc degeneration biomarkers and immune-inflammatory infiltrates.JOR spine · 2024Article
- Geroscience and pathology: a new frontier in understanding age-related diseases.Pathology oncology research : POR · 2024Review
- Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent DNA damage (genotoxic stress) triggers signaling cascades that drive cells into apoptosis or senescence to avoid replicating a damaged genome. Sp1 has been found to play a role in double strand break (DSB) repair, and a link between Sp1 and aging has also been established, where Sp1 protein, but not RNA, levels decrease with age. Interestingly, inhibition ATM reverses the age-related degradation of Sp1, suggesting that DNA damage signaling is involved in senescence-related degradation of Sp1. Proteasomal degradation of Sp1 in senescent cells is mediated via sumoylation, where sumoylation of Sp1 on lysine 16 is increased in senescent cells. Taking into consideration our previous findings that Sp1 is phosphorylated by ATM in response to DNA damage and that proteasomal degradation of Sp1 at DSBs is also mediated by its sumoylation and subsequent interaction with RNF4, we investigated the potential contribution of Sp1's role as a DSB repair factor in mediating cellular senescence. We report here that Sp1 expression is decreased with a concomitant increase in senescence markers in response to DNA damage. Mutation of Sp1 at serine 101 to create an ATM phospho-null mutant, or mutation of lysine 16 to create a sumo-null mutant, prevents the sumoylation and subsequent proteasomal degradation of Sp1 and results in a decrease in senescence. Conversely, depletion of Sp1 or mutation of Sp1 to create an ATM phosphomimetic results in premature degradation of Sp1 and an increase in senescence markers. These data link a loss of genomic stability with senescence through the action of a DNA damage repair factor.
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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.