ArticleScientific reports2025
Dysregulation of STS in keratinocytes promotes calcium signaling and differentiation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Central precocious puberty as the initial manifestation of multisystem involvement caused byFrontiers in endocrinology · 2026Article
- Dysregulated cholesterol metabolism in genodermatoses: implications for systemic disease and therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Gapmer Antisense Oligonucleotide Targeting E-Cadherin Rescues Abnormal Keratinization in X-Linked Ichthyosis Models.Biomolecules & therapeutics · 2026Article
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5 authors.
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Abstract
Steroid sulfatase (STS) is a key enzyme for the desulfation of steroid sulfates, converting them into their biologically active forms. Notably, X-linked ichthyosis (XLI), a genetic disorder characterized by hyperkeratinization, arises as a direct result of STS deficiency. Keratinocyte differentiation is essential for proper keratinization. In this study, gene ontology analysis from STS-deficient mice revealed enhanced differentiation and upregulation of calcium-related signaling. Calcium plays a key role in regulating keratinocyte differentiation, with STS-deficient cells showing a marked increase in intracellular calcium influx. Additionally, these cells significantly upregulated calcium-sensing receptors (CasR), leading to elevated tyrosine phosphorylation, increased differentiation signaling, and the upregulation of early differentiation markers, including keratin 1 and keratin 10, as seen in HaCaT cells and mouse primary keratinocytes. Furthermore, STS inhibitors enhanced the expression of E-cadherin and terminal differentiation markers such as involucrin and loricrin. Due to increased calcium sensitivity, STS-deficient cells treated with calcium exhibited a significant upregulation of differentiation markers and reduced sensitivity to calcium chelation. Collectively, our findings demonstrate that reduced STS expression and inhibition of its activity enhance calcium responsiveness, induce CasR expression, and amplify calcium signaling, thereby promoting keratinocyte differentiation. These findings offer valuable insights into the mechanisms underlying STS deficiency-induced hyperkeratinization.
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