ArticleThe Journal of cell biology2018
Cell polarity and adherens junction formation inhibit epithelial Fas cell death receptor signaling.
Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Fas acts as a T cell co-stimulatory receptor via both death domain-independent and -dependent mechanisms.Cell death and differentiation · 2026Article
- Rho/ROCK signaling and α-catenin mediate β-catenin-driven hyperplasia in the adrenal cortex via adherens junctions.The Journal of clinical investigation · 2026Article
- The Fas-FasL system: from apoptosis regulator to therapeutic target in autoimmunity, cancer, and transplantation.Immunologic research · 2026Review
- Antibody-Targeted Artificial T Cell and Natural Killer Cell Derived Vesicles for Cancer Immunotherapy.Journal of extracellular vesicles · 2026Article
- Visualizing androgen signaling and assessing its interaction with canonical Wnt signaling pathways in prostate development, morphogenesis, and regeneration.PLoS genetics · 2025Article
- LncRNAs and IgA nephropathy: underlying molecular pathways and clinical applications.Clinical and experimental medicine · 2025Review
- Impact of LIN7A silencing on U87 cell invasion and its clinical significance in glioblastoma.Scientific reports · 2025Article
- Role of mucosal immunity and epithelial-vascular barrier in modulating gut homeostasis.Internal and emergency medicine · 2023Review
- A DLG1-ARHGAP31-CDC42 axis is essential for the intestinal stem cell response to fluctuating niche Wnt signaling.Cell stem cell · 2023Article
- Dual role of E-cadherin in cancer cells.Tissue barriers · 2022Review
- Integrin-ECM interactions and membrane-associated Catalase cooperate to promote resilience of the Drosophila intestinal epithelium.PLoS biology · 2022Article
- CD95/Fas suppresses NF-κB activation through recruitment of KPC2 in a CD95L/FasL-independent mechanism.iScience · 2021Article
- Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS.Computational and mathematical methods in medicine · 2021Article
- Dual Role of the PTPN13 Tyrosine Phosphatase in Cancer.Biomolecules · 2020Review
- PTPN13 induces cell junction stabilization and inhibits mammary tumor invasiveness.Theranostics · 2020Article
- CD95 Structure, Aggregation and Cell Signaling.Frontiers in cell and developmental biology · 2020Review
- E-cadherin Beyond Structure: A Signaling Hub in Colon Homeostasis and Disease.International journal of molecular sciences · 2019Review
- TRAIL and FasL Functions in Cancer and Autoimmune Diseases: Towards an Increasing Complexity.Cancers · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Finely tuned regulation of epithelial cell death maintains tissue integrity and homeostasis. At the cellular level, life and death decisions are controlled by environmental stimuli such as the activation of death receptors. We show that cell polarity and adherens junction formation prevent proapoptotic signals emanating from the Fas death receptor. Fas is sequestered in E-cadherin actin-based adhesion structures that are less able to induce downstream apoptosis signaling. Using a proteomic-based approach, we find that the polarity molecule Dlg1 interacts with the C-terminal PDZ-binding site in Fas and that this interaction decreases formation of the death-inducing complex upon engagement with Fas ligand (FasL), thus acting as an additional cell death protection mechanism. We propose that E-cadherin and Dlg1 inhibit FasL-induced cell death by two complementary but partially independent mechanisms that help to maintain epithelial homeostasis by protecting normal polarized epithelia from apoptosis. When polarity is lost, the Fas-cadherin-Dlg1 antiapoptotic complex is disrupted, and FasL can promote the elimination of compromised nonpolarized 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.