ArticlePloS one2007
Sp1 is essential for p16 expression in human diploid fibroblasts during senescence.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Bioinformatics-based discovery of intervertebral disc degeneration biomarkers and immune-inflammatory infiltrates.JOR spine · 2024Article
- Article
- Age-associated callus senescent cells produce TGF-β1 that inhibits fracture healing in aged mice.The Journal of clinical investigation · 2022Article
- DNA damage-induced degradation of Sp1 promotes cellular senescence.GeroScience · 2022Article
- Transcriptional regulation of INK4/ARF locus by cis and trans mechanisms.Frontiers in cell and developmental biology · 2022Review
- Obesity Increases Gene Expression of Markers Associated With Immunosenescence in Obese Middle-Aged Individuals.Frontiers in immunology · 2021Article
- Sp3 Transcription Factor Cooperates with the Kaposi's Sarcoma-Associated Herpesvirus ORF50 Protein To Synergistically Activate Specific Viral and Cellular Gene Promoters.Journal of virology · 2020Article
- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Article
- Downregulation of the Apelinergic Axis Accelerates Aging, whereas Its Systemic Restoration Improves the Mammalian Healthspan.Cell reports · 2017Article
- Senescence as a novel mechanism involved in β-adrenergic receptor mediated cardiac hypertrophy.PloS one · 2017Article
- Transcription factor Sp1 prevents TRF2(ΔBΔM)-induced premature senescence in human diploid fibroblasts.Molecular and cellular biochemistry · 2016Article
- Sal-like protein 2 upregulates p16 expression through a proximal promoter element.Cancer science · 2015Article
- Alterations in the Sp1 binding and Fmr-1 gene expression in the cortex of the brain during maturation and aging of mouse.Molecular biology reports · 2014Article
- C-terminal in Sp1-like artificial zinc-finger proteins plays crucial roles in determining their DNA binding affinity.BMC biotechnology · 2013Article
- The role of SIRT6 protein in aging and reprogramming of human induced pluripotent stem cells.The Journal of biological chemistry · 2013Article
- Construction of a computable network model for DNA damage, autophagy, cell death, and senescence.Bioinformatics and biology insights · 2013Article
- Article
- CLCA2 as a p53-inducible senescence mediator.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundp16(INK4a) tumor suppressor protein has been widely proposed to mediate entrance of the cells into the senescent stage. Promoter of p16(INK4a) gene contains at least five putative GC boxes, named GC-I to V, respectively. Our previous data showed that a potential Sp1 binding site, within the promoter region from -466 to -451, acts as a positive transcription regulatory element. These results led us to examine how Sp1 and/or Sp3 act on these GC boxes during aging in cultured human diploid fibroblasts. METHODOLOGY/PRINCIPAL
findingsMutagenesis studies revealed that GC-I, II and IV, especially GC-II, are essential for p16(INK4a) gene expression in senescent cells. Electrophoretic mobility shift assays (EMSA) and ChIP assays demonstrated that both Sp1 and Sp3 bind to these elements and the binding activity is enhanced in senescent cells. Ectopic overexpression of Sp1, but not Sp3, induced the transcription of p16(INK4a). Both Sp1 RNAi and Mithramycin, a DNA intercalating agent that interferes with Sp1 and Sp3 binding activities, reduced p16(INK4a) gene expression. In addition, the enhanced binding of Sp1 to p16(INK4a) promoter during cellular senescence appeared to be the result of increased Sp1 binding affinity, not an alteration in Sp1 protein level. CONCLUSIONS/SIGNIFICANCE: All these results suggest that GC- II is the key site for Sp1 binding and increase of Sp1 binding activity rather than protein levels contributes to the induction of p16(INK4a) expression during cell aging.
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