ArticleThe Journal of investigative dermatology2015
14-3-3σ regulates keratinocyte proliferation and differentiation by modulating Yap1 cellular localization.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Keratin 15 promotes a progenitor cell state in basal keratinocytes of skin epidermis.The Journal of cell biology · 2026Article
- Article
- Molecular Mechanisms of FAT Atypical Cadherin 1 (FAT1), the Hippo Pathway, and the Yes-Associated Protein (YAP) Signaling Pathways in Some Cancers.Asian Pacific journal of cancer prevention : APJCP · 2026Review
- pH-Responsive Liposome-Hydrogel Composite Accelerates Nasal Mucosa Wound Healing.Pharmaceutics · 2025Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- YAP1 facilitates the pathogenesis of psoriasis via modulating keratinocyte proliferation and inflammation.Cell death & disease · 2025Article
- YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024Review
- Epstein-Barr virus LMP1 protein promotes proliferation and inhibits differentiation of epithelial cells via activation of YAP and TAZ.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Effects of amniotic fluid on human keratinocyte gene expression: Implications for wound healing.Experimental dermatology · 2022Article
- 14-3-3ζ Constrains insulin secretion by regulating mitochondrial function in pancreatic β cells.JCI insight · 2022Article
- Lappaol F, an anticancer agent, inhibits YAP via transcriptional and post-translational regulation.Pharmaceutical biology · 2021Article
- Hippo signaling effectors YAP and TAZ induce Epstein-Barr Virus (EBV) lytic reactivation through TEADs in epithelial cells.PLoS pathogens · 2021Article
- Hippo Signaling Pathway as a New Potential Target in Non-Melanoma Skin Cancers: A Narrative Review.Life (Basel, Switzerland) · 2021Review
- Low-Temperature Argon Plasma Regulates Skin Moisturizing and Melanogenesis-Regulating Markers through Yes-Associated Protein.International journal of molecular sciences · 2021Article
- The role of YAP in the control of the metastatic potential of oral cancer.Oncology research · 2021Review
- Heterozygous Loss of Yap1 in Mice Causes Progressive Cataracts.Investigative ophthalmology & visual science · 2020Article
- Keratin 14-dependent disulfides regulate epidermal homeostasis and barrier function via 14-3-3σ and YAP1.eLife · 2020Article
- Yap1 is required for maintenance of adult RPE differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Hippo Pathway and YAP Signaling Alterations in Squamous Cancer of the Head and Neck.Journal of clinical medicine · 2019Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The homozygous repeated epilation (Er/Er) mouse mutant of the gene encoding 14-3-3σ displays an epidermal phenotype characterized by hyperproliferative keratinocytes and undifferentiated epidermis. Heterozygous Er/+ mice develop spontaneous skin tumors and are highly sensitive to tumor-promoting 7,12-dimethylbenzanthracene/12-O-tetradecanoyl-phorbol-13-acetate induction. The molecular mechanisms underlying 14-3-3σ regulation of epidermal proliferation, differentiation, and tumor formation have not been well elucidated. In this study, we found that Er/Er keratinocytes failed to sequester Yap1 in the cytoplasm, leading to its nuclear localization during epidermal development in vivo and under differentiation-inducing culture conditions in vitro. In addition, enhanced Yap1 nuclear localization was also evident in 7,12-dimethylbenzanthracene/12-O-tetradecanoyl-phorbol-13-acetate-induced tumors from Er/+ skin. Furthermore, short hairpin RNA (shRNA) knockdown of Yap1 expression in Er/Er keratinocytes inhibited their proliferation, suggesting that YAP1 functions as a downstream effector of 14-3-3σ controlling epidermal proliferation. We then demonstrated that keratinocytes express all seven 14-3-3 protein isoforms, some of which form heterodimers with 14-3-3σ, either full-length wild type (WT) or the mutant form found in Er/Er mice. However, Er 14-3-3σ does not interact with Yap1, as demonstrated by coimmunoprecipitation. We conclude that Er 14-3-3σ disrupts the interaction between 14-3-3 and Yap1, and thus fails to block Yap1 nuclear transcriptional function, causing continued progenitor expansion and inhibition of differentiation in the Er/Er epidermis.
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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.