ArticleThe Journal of biological chemistry2012
Delayed cell cycle progression in selenoprotein W-depleted cells is regulated by a mitogen-activated protein kinase kinase 4-p38/c-Jun NH2-terminal kinase-p53 pathway.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The trial behind it
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
15 citing papers in PubMed, 32 citations in OpenAlex.
- Current Advances in the Physiological Roles of the Thioredoxin-Like Family of Selenoproteins.Biological trace element research · 2026Review
- Redox Modulation of Erythropoiesis by Selenoproteins.Biological trace element research · 2026Review
- Selenium and Skeletal Muscle Health in Sports Nutrition.Nutrients · 2025Review
- Loss of SELENOW aggravates muscle loss with regulation of protein synthesis and the ubiquitin-proteasome system.Science advances · 2024Article
- Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023Review
- Article
- PIWI-interacting RNA-36712 restrains breast cancer progression and chemoresistance by interaction with SEPW1 pseudogene SEPW1P RNA.Molecular cancer · 2019Article
- Article
- Orai3 calcium channel and resistance to chemotherapy in breast cancer cells: the p53 connection.Cell death and differentiation · 2018Article
- Tannic acid inhibits EGFR/STAT1/3 and enhances p38/STAT1 signalling axis in breast cancer cells.Journal of cellular and molecular medicine · 2017Article
- Accessing human selenoproteins through chemical protein synthesis.Chemical science · 2017Article
- p38δ MAPK: Emerging Roles of a Neglected Isoform.International journal of cell biology · 2014Review
- Simple and sensitive detection of HBsAg by using a quantum dots nanobeads based dot-blot immunoassay.Theranostics · 2014Article
- Selenoprotein W expression and regulation in mouse brain and neurons.Brain and behavior · 2013Article
- Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenoprotein W (SEPW1) is a ubiquitous, highly conserved thioredoxin-like protein whose depletion causes a transient p53- and p21(Cip1)-dependent G(1)-phase cell cycle arrest in breast and prostate epithelial cells. SEPW1 depletion increases phosphorylation of Ser-33 in p53, which is associated with decreased p53 ubiquitination and stabilization of p53. We report here that delayed cell cycle progression, Ser-33 phosphorylation, and p53 nuclear accumulation from SEPW1 depletion require mitogen-activated protein kinase kinase 4 (MKK4). Silencing MKK4 rescued G(1) arrest, Ser-33 phosphorylation, and nuclear accumulation of p53 induced by SEPW1 depletion, but silencing MKK3, MKK6, or MKK7 did not. SEPW1 silencing did not change the phosphorylation state of MKK4 but increased total MKK4 protein. Silencing p38γ, p38δ, or JNK2 partially rescued G(1) arrest from SEPW1 silencing, suggesting they signal downstream from MKK4. These results imply that SEPW1 silencing increases MKK4, which activates p38γ, p38δ, and JNK2 to phosphorylate p53 on Ser-33 and cause a transient G(1) arrest.
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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.