ArticleThe Journal of investigative dermatology2010
PKC-delta and -eta, MEKK-1, MEK-6, MEK-3, and p38-delta are essential mediators of the response of normal human epidermal keratinocytes to differentiating agents.
Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
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- Reconstructing and comparing signal transduction networks from single-cell protein quantification data.Bioinformatics (Oxford, England) · 2026Article
- The C2 Domain of PKC‑δ as a Dominant-Negative Modulator of Breast Cancer Cell Survival and Chemosensitivity.ACS omega · 2025Article
- MCPIP3 orchestrates the balance of epidermal proliferation and differentiation.Cell communication and signaling : CCS · 2025Article
- A Novel Immune-Related Three-Gene Signature and Immune Infiltration Insights in Psoriasis and Chronic Kidney Disease.Clinical, cosmetic and investigational dermatology · 2025Article
- IRF6 Enhances IFN-β Expression and Inhibits Viral Replication to Reduce the Severity of Herpetic Stromal Keratitis.Journal of inflammation research · 2025Article
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- The impact of signaling pathways on the desmosome ultrastructure in pemphigus.Frontiers in immunology · 2024Article
- Mesothelioma cancer cells are glutamine addicted and glutamine restriction reduces YAP1 signaling to attenuate tumor formation.Molecular carcinogenesis · 2023Article
- CDK9 activity switch associated with AFF1 and HEXIM1 controls differentiation initiation from epidermal progenitors.Nature communications · 2022Article
- Transglutaminase 2 enhances hepatocyte growth factor signaling to drive the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2022Article
- Transglutaminase 2 Maintains Hepatocyte Growth Factor Signaling to Enhance the Cancer Cell Phenotype.Molecular cancer research : MCR · 2021Article
- ACTL6A suppresses p21Oncogenesis · 2021Article
- VGLL4 inhibits YAP1/TEAD signaling to suppress the epidermal squamous cell carcinoma cancer phenotype.Molecular carcinogenesis · 2021Article
- Sulforaphane inhibits PRMT5 and MEP50 function to suppress the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2021Article
- Effects ofMolecules (Basel, Switzerland) · 2021Article
- GRHL3 Promotes Tumor Growth and Metastasis via the MEK Pathway in Colorectal Cancer.Analytical cellular pathology (Amsterdam) · 2021Article
- Mammalian Epidermis: A Compendium of Lipid Functionality.Frontiers in physiology · 2021Review
- Role of FGFR2b expression and signaling in keratinocyte differentiation: sequential involvement of PKCδ and PKCα.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies suggest that the novel protein kinase C (PKC) isoforms initiate a mitogen-activated protein kinase (MAPK) signaling cascade that regulates keratinocyte differentiation. However, assigning these functions has relied on treatment with pharmacologic inhibitors and/or manipulating kinase function using overexpression of wild-type or dominant-negative kinases. As these methods are not highly specific, an obligatory regulatory role for individual kinases has not been assigned. In this study, we use small interfering RNA knockdown to study the role of individual PKC isoforms as regulators of keratinocyte differentiation induced by the potent differentiating stimulus, 12-O-tetradecanoylphorbol-13-acetate (TPA). PKC-delta knockdown reduces TPA-activated involucrin promoter activity, nuclear activator protein-1 factor accumulation and binding to DNA, and cell morphology change. Knockdown of PKC downstream targets, including MEKK-1, MEK-6, MEK-3, or p38-delta, indicates that these kinases are required for these responses. Additional studies indicate that knockdown of PKC-eta inhibits TPA-dependent involucrin promoter activation. In contrast, knockdown of PKC-alpha (a classical PKC isoform) or PKC-epsilon (a novel isoform) does not inhibit these TPA-dependent responses. Further studies indicate that PKC-delta is required for calcium and green tea polyphenol-dependent regulation of end responses. These findings are informative as they suggest an essential role for selected PKC and MAPK cascade enzymes in mediating a range of end responses to a range of differentiation stimuli in keratinocytes.
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