ArticleMolecular and cellular biology2012
Sp1 facilitates DNA double-strand break repair through a nontranscriptional mechanism.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Links between the unfolded protein response and the DNA damage response in hypoxia: a systematic review.Biochemical Society transactions · 2021Pooled it
- DHODH-Mediated Suppression of Ferroptosis Supports Radioresistance and Represents a Therapeutic Vulnerability in Lung Cancer.Cancer research · 2026Article
- Targeting the DNA damage response through TBL1X in mantle cell lymphoma.Blood advances · 2025Article
- 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
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- EPI-DynFusion: enhancer-promoter interaction prediction model based on sequence features and dynamic fusion mechanisms.Frontiers in genetics · 2025Article
- Crosstalk between BER and NHEJ in XRCC4-Deficient Cells Depending on hTERT Overexpression.International journal of molecular sciences · 2024Article
- DNA damage remodels the MITF interactome to increase melanoma genomic instability.Genes & development · 2024Article
- Translation regulatory long non-coding RNA 1 negatively regulates cell radiosensitivity via the miR-22-3p/SP1 axis in non-small cell lung cancer.The clinical respiratory journal · 2024Article
- Zinc finger transcription factor CASZ1b is involved in the DNA damage response in live cells.Biochemical and biophysical research communications · 2023Article
- Article
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- UVB-mediated DNA damage induces matrix metalloproteinases to promote photoaging in an AhR- and SP1-dependent manner.JCI insight · 2022Article
- DNA damage-induced degradation of Sp1 promotes cellular senescence.GeroScience · 2022Article
- Human exposure to low dose ionizing radiation affects miR-21 and miR-625 expression levels.Molecular biology reports · 2022Article
- Bioinformatics network analyses of growth differentiation factor 11.Open life sciences · 2022Article
- Immediate-Early, Early, and Late Responses to DNA Double Stranded Breaks.Frontiers in genetics · 2022Review
- miR-9 modulates and predicts the response to radiotherapy and EGFR inhibition in HNSCC.EMBO molecular medicine · 2021Article
- Double strand breaks (DSBs) as indicators of genomic instability in PATRR-mediated translocations.Human molecular genetics · 2021Article
- Sweet Melody or Jazz? Transcription Around DNA Double-Strand Breaks.Frontiers in molecular biosciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sp1 is a ubiquitously expressed transcription factor that is phosphorylated by ataxia telangiectasia mutated kinase (ATM) in response to ionizing radiation and H(2)O(2). Here, we show by indirect immunofluorescence that Sp1 phosphorylated on serine 101 (pSp1) localizes to ionizing radiation-induced foci with phosphorylated histone variant γH2Ax and members of the MRN (Mre11, Rad50, and Nbs1) complex. More precise analysis of occupancy of DNA double-strand breaks (DSBs) by chromatin immunoprecipitation (ChIP) shows that Sp1, like Nbs1, resides within 200 bp of DSBs. Using laser microirradiation of cells, we demonstrate that pSp1 is present at DNA DSBs by 7.5 min after induction of damage and remains at the break site for at least 8 h. Depletion of Sp1 inhibits repair of site-specific DNA breaks, and the N-terminal 182-amino-acid peptide, which contains targets of ATM kinase but lacks the zinc finger DNA binding domain, is phosphorylated, localizes to DSBs, and rescues the repair defect resulting from Sp1 depletion. Together, these data demonstrate that Sp1 is rapidly recruited to the region immediately adjacent to sites of DNA DSBs and is required for DSB repair, through a mechanism independent of its sequence-directed transcriptional effects.
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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.