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- W3028566036 abstract "To investigate molecular mechanisms of nicastrin (NCSTN) mutations inducing acne inversa (AI).New and old lesional and non-lesional skin samples were obtained from an AI patient. Healthy skin samples were obtained from the buttocks of 100 non-AI patients. Hematoxylin-eosin staining and immunohistochemistry of NCSTN protein were examined. All exon-intron and exon boundary sequences were polymerase chain reaction (PCR) -amplified and sequenced. Bioinformatic analyses of NCSTN 3'-untranslated regions (3'UTR) were conducted using RegRNA2.0. 3'UTR of NCSTN was cloned vector of psiCHECK-2 vector; the mutant 3'UTR NCSTN-psiCHECK-2 was constructed on a template of NCSTN 3'UTR. A dual-luciferase reporter gene assay, real-time reverse transcription (qRT)-PCR and Western blot analysis were conducted to evaluate functional changes associated with the mutation.We identified a novel deletion mutation of the NCSTN gene in the NCSTN 3'UTR region (designated c.2584-2585del CA) at the binding site of human micro-RNA-155 (hsa-miR-155). Levels of NCSTN protein were potently lower in epidermis and hair follicles of AI patients with lesions than in healthy skin. The hsa-miR-155+mutant NCSTN significantly downregulated in dual luciferase assay, qRT-PCR, and Western blot. The novel deletion mutation was confirmed to be a pathological cause of AI.miR-155 downregulates the expression of NCSTN by binding NCSTN 3'UTR, providing a possible new mechanism of loss of NCSTN function in AI patients. hsa-miR-155 functions as a promoter in AI, and is a potential therapy target for AI." @default.
- W3028566036 created "2020-05-29" @default.
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- W3028566036 date "2018-01-01" @default.
- W3028566036 modified "2023-09-27" @default.
- W3028566036 title "hsa-miR-155 targeted NCSTN 3'UTR mutation promotes the pathogenesis and development of acne inversa." @default.
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