ArticleNPJ aging and mechanisms of disease2018
ISGF3 with reduced phosphorylation is associated with constitutive expression of interferon-induced genes in aging cells.
Article in NPJ aging and mechanisms of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Alternative Splicing Constitutes a Transcription-independent Regulatory Layer in Replicative Senescence of Human Umbilical Cord Mesenchymal Stem Cells.Stem cell reviews and reports · 2026Article
- NAMPT activation uncovers a senescence-specific vulnerability and promotes healthy aging in combination with NAM.bioRxiv : the preprint server for biology · 2026Article
- Targeting the chromatin structural changes of antitumor immunity.Journal of pharmaceutical analysis · 2024Review
- Extracellular vesicle‑mediated RNA editing may underlie the heterogeneity and spread of hepatocellular carcinoma in human tissue andOncology reports · 2023Article
- Effects of Betulinic Acid on the Proliferation, Cellular Senescence, and Type 1 Interferon-Related Signaling Pathways in Human Dermal Fibroblasts.Journal of agricultural and food chemistry · 2023Article
- Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis.Nature communications · 2023Article
- The convergence of tumor suppressors on the type I interferon pathway in clear cell renal cell carcinoma and its therapeutic implications.American journal of physiology. Cell physiology · 2022Review
- Article
- Single-cell sequencing of rotavirus-infected intestinal epithelium reveals cell-type specific epithelial repair and tuft cell infection.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Type I Interferon Induction in Cutaneous DNA Damage Syndromes.Frontiers in immunology · 2021Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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Abstract
During cellular aging, many changes in cellular functions occur. A hallmark of aged cells is secretion of inflammatory mediators, which collectively is referred to as the senescence-associated secretory phenotype (SASP). However, the mechanisms underlying such changes are unclear. Canonically, the expression of interferon (IFN)-stimulated genes (ISGs) is induced by IFNs through the formation of the tripartite transcriptional factor ISGF3, which is composed of IRF9 and the phosphorylated forms of STAT1 and STAT2. However, in this study, the constitutive expression of ISGs in human-derived senescent fibroblasts and in fibroblasts from a patient with Werner syndrome, which leads to premature aging, was mediated mainly by the unphosphorylated forms of STATs in the absence of INF production. Under homeostatic conditions, STAT1, STAT2, and IRF9 were localized to the nucleus of aged cells. Although knockdown of JAK1, a key kinase of STAT1 and STAT2, did not affect ISG expression or IFN-stimulated response element (ISRE)-mediated promoter activities in these senescent cells, knockdown of STAT1 or STAT2 decreased ISG expression and ISRE activities. These results suggest that the ISGF3 complex without clear phosphorylation is required for IFN-independent constitutive ISG transcription in senescent cells.
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