ArticleGenes & development2004
Smurf2 up-regulation activates telomere-dependent senescence.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 98 citations in OpenAlex.
- SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics.International journal of molecular sciences · 2026Review
- Citronellal improves endothelial dysfunction by affecting the stability of the GCH1 protein.Acta biochimica et biophysica Sinica · 2024Article
- Escape from oncogene-induced senescence is controlled by POU2F2 and memorized by chromatin scars.Cell genomics · 2023Article
- Article
- Smurf2 inhibition enhances chemotherapy and radiation sensitivity in non-small-cell lung cancer.Scientific reports · 2022Article
- Stress response decay with aging visualized using a dual-channel logic-based fluorescent probe.Chemical science · 2021Article
- Mdm2 phosphorylation by Akt regulates the p53 response to oxidative stress to promote cell proliferation and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Stress reactivity elicits a tissue-specific reduction in telomere length in aging zebrafish (Danio rerio).Scientific reports · 2021Article
- Enhancing the regenerative effectiveness of growth factors by local inhibition of interleukin-1 receptor signaling.Science advances · 2020Article
- SMURF2 prevents detrimental changes to chromatin, protecting human dermal fibroblasts from chromosomal instability and tumorigenesis.Oncogene · 2020Article
- The ubiquitination ligase SMURF2 reduces aerobic glycolysis and colorectal cancer cell proliferation by promoting ChREBP ubiquitination and degradation.The Journal of biological chemistry · 2019Article
- E3 ubiquitin ligases in B-cell malignancies.Cellular immunology · 2019Review
- Article
- Regulation of CNKSR2 protein stability by the HECT E3 ubiquitin ligase Smurf2, and its role in breast cancer progression.BMC cancer · 2018Article
- Redox control of senescence and age-related disease.Redox biology · 2017Review
- Impaired osteogenesis of T1DM bone marrow-derived stromal cells and periosteum-derived cells and their differential in-vitro responses to growth factor rescue.Stem cell research & therapy · 2017Article
- Intervertebral Disc Aging, Degeneration, and Associated Potential Molecular Mechanisms.Journal of head, neck & spine surgery · 2017Article
- Telomeres in aging and disease: lessons from zebrafish.Disease models & mechanisms · 2016Review
- The ubiquitin ligase Smurf2 suppresses TGFβ-induced epithelial-mesenchymal transition in a sumoylation-regulated manner.Cell death and differentiation · 2016Article
- Two Degradation Pathways of the p35 Cdk5 (Cyclin-dependent Kinase) Activation Subunit, Dependent and Independent of Ubiquitination.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive telomere shortening activates replicative senescence, which prevents somatic cells from being propagated indefinitely in culture. The limitation of proliferative capacity imposed by replicative senescence is thought to contribute to both organismal aging and the prevention of tumor development. Here we report that up-regulation of Smurf2, an E3 ubiquitin ligase previously implicated in TGF-beta signaling, is a specific consequence of telomere attrition in human fibroblasts and that such up-regulation is sufficient to produce the senescence phenotype. Adventitious production of the Smurf2 protein in early passage fibroblasts at the same physiological level observed during telomere-mediated senescence resulted in proliferative arrest in a viable state, morphological and biochemical alterations characteristic of senescence, acquisition of senescence-specific alterations in gene expression, and reversal of cellular immortalization by telomerase. We show that the senescence-inducing actions of Smurf2 occur in the absence of detectable DNA damage or stress response, that Smurf2's effects require a novel function distinct from its E3 activity, that Smurf2 recruits the Rb and p53 pathways for senescence induction, and that while p21 is elevated by Smurf2, Smurf2-mediated senescence is independent of p21. Smurf2 is the first gene found to be both up-regulated by telomere attrition and sufficient to induce senescence.
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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.