keloid/phosphatase

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Alpha-naphthyl acid phosphatase activity in normal human skin and keloids.

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Pleiotrophin is downregulated in human keloids.

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Keloid is an abnormal hyperproliferative scarring process with involvement of complex genetic and triggering environmental factors. Previously published dysregulated gene expression profile of keloids includes genes involved in tumor formation. Pleiotrophin (PTN) is a secreted, heparin-binding

Inhibition of microRNA-21-5p reduces keloid fibroblast autophagy and migration by targeting PTEN after electron beam irradiation.

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Electron beam (EB) irradiation is useful to reduce the recurrence of keloids; however, the underlying mechanism remains unknown. MicroRNA-21 (miR-21), which regulates autophagy during cancer radiation therapy, was identified as a potential therapeutic target for keloids. Here, we investigate the

MiR-181a Targets PHLPP2 to Augment AKT Signaling and Regulate Proliferation and Apoptosis in Human Keloid Fibroblasts.

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OBJECTIVE Keloids are fibrous overgrowths induced by cutaneous injury. MicroRNAs (miRNAs) have recently emerged as post-transcriptional gene repressors and participants in a diverse array of pathophysiological processes leading to skin disease. The purpose of the current study was to explore the

MicroRNA-21 affects proliferation and apoptosis by regulating expression of PTEN in human keloid fibroblasts.

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BACKGROUND MicroRNAs (miRNAs) are small noncoding RNA molecules that regulate gene expression in the progress of proliferation, differentiation, and apoptosis. A keloid is considered to be a type of benign tumor. The exact contribution of miRNAs in keloid fibroblasts remains largely

Enzyme activity in human scars, hypertrophic scars and keloids.

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Biopsies from non-hypertrophic and hypertrophic scars and from normal skin have been studied histochemically for activities of nicotanamide adenine dinucleotide diaphorase, lactate dehydrogenase, acid phosphatase, beta-D glucuronidase and alkaline phosphatase. The activities of all enzymes studied

Ocular Pathology of Oculocerebrorenal Syndrome of Lowe: Novel Mutations and Genotype-Phenotype Analysis.

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Mutations in the OCRL1 gene result in the oculocerebrorenal syndrome of Lowe, with symptoms including congenital bilateral cataracts, glaucoma, renal failure, and neurological impairments. OCRL1 encodes an inositol polyphosphate 5-phosphatase which preferentially dephosphorylates

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