ArticleThe Journal of cell biology2001
Keratin attenuates tumor necrosis factor-induced cytotoxicity through association with TRADD.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 200 citations in OpenAlex.
- Article
- The relationship between keratin 18 and epithelial-derived tumors: as a diagnostic marker, prognostic marker, and its role in tumorigenesis.Frontiers in oncology · 2024Review
- APEX2-Mediated Proximity Labeling Resolves the DDIT4-Interacting Proteome.International journal of molecular sciences · 2022Article
- Innovative mouse models for the tumor suppressor activity of Protocadherin-10 isoforms.BMC cancer · 2022Article
- Susceptibility of cytoskeletal-associated proteins for tumor progression.Cellular and molecular life sciences : CMLS · 2021Review
- Integrated genomic and transcriptomic analysis suggestsAnnals of translational medicine · 2021Article
- Heterogeneous responses to low level death receptor activation are explained by random molecular assembly of the Caspase-8 activation platform.PLoS computational biology · 2019Article
- Application of Proteomics to Inflammatory Bowel Disease Research: Current Status and Future Perspectives.Gastroenterology research and practice · 2019Review
- Grouper TRADD Mediates Innate Antiviral Immune Responses and Apoptosis Induced by Singapore Grouper Iridovirus (SGIV) Infection.Frontiers in cellular and infection microbiology · 2019Article
- Intermediate filaments and IF-associated proteins: from cell architecture to cell proliferation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019Review
- Article
- Intermediate Filaments and the Regulation of Cell Motility during Regeneration and Wound Healing.Cold Spring Harbor perspectives in biology · 2017Review
- Autophagy and KRT8/keratin 8 protect degeneration of retinal pigment epithelium under oxidative stress.Autophagy · 2017Article
- Cytokeratin 18 is necessary for initiation of TGF-β1-induced epithelial-mesenchymal transition in breast epithelial cells.Molecular and cellular biochemistry · 2016Article
- The Cohesive Metastasis Phenotype in Human Prostate Cancer.Biochimica et biophysica acta · 2016Review
- Review
- Molecular manipulation of keratin 8/18 intermediate filaments: modulators of FAS-mediated death signaling in human ovarian granulosa tumor cells.Journal of ovarian research · 2016Article
- Article
- Skin Keratins.Methods in enzymology · 2016Article
- Piwil2 inhibits keratin 8 degradation through promoting p38-induced phosphorylation to resist Fas-mediated apoptosis.Molecular and cellular biology · 2014Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keratin 8 and 18 (K8/18) are the major components of intermediate filament (IF) proteins of simple or single-layered epithelia. Recent data show that normal and malignant epithelial cells deficient in K8/18 are nearly 100 times more sensitive to tumor necrosis factor (TNF)-induced cell death. We have now identified human TNF receptor type 1 (TNFR1)-associated death domain protein (TRADD) to be the K18-interacting protein. Among IF proteins tested in two-hybrid systems, TRADD specifically bound K18 and K14, type I (acidic) keratins. The COOH-terminal region of TRADD interacted with the coil Ia of the rod domain of K18. Endogenous TRADD coimmunoprecipitated with K18, and colocalized with K8/18 filaments in human mammary epithelial cells. Overexpression of the NH2 terminus (amino acids 1-270) of K18 containing the TRADD-binding domain as well as overexpression of K8/18 in SW13 cells, which are devoid of keratins, rendered the cells more resistant to killing by TNF. We also showed that overexpressed NH2 termini of K18 and K8/18 were associated with endogenous TRADD in SW13 cells, resulting in the inhibition of caspase-8 activation. These results indicate that K18 may sequester TRADD to attenuate interactions between TRADD and activated TNFR1 and moderate TNF-induced apoptosis in simple epithelial cells.
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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.