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Assia Derfoul

Researcher at National Institutes of Health

Publications -  16
Citations -  1662

Assia Derfoul is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Myositis & Aggrecan. The author has an hindex of 12, co-authored 16 publications receiving 1344 citations.

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The NAD+-Dependent SIRT1 Deacetylase Translates a Metabolic Switch into Regulatory Epigenetics in Skeletal Muscle Stem Cells

TL;DR: It is reported that during the transition from quiescence to proliferation, skeletal muscle stem cells experience a metabolic switch from fatty acid oxidation to glycolysis, revealing how metabolic cues can be mechanistically translated into epigenetic modifications that regulate skeletal muscle cell biology.
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eRNAs Promote Transcription by Establishing Chromatin Accessibility at Defined Genomic Loci

TL;DR: The data suggest that eRNAs contribute to establishing a cell-type-specific transcriptional circuitry by directing chromatin-remodeling events by regulating genomic access of the transcriptional complex to defined regulatory regions.
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Polycomb EZH2 controls self-renewal and safeguards the transcriptional identity of skeletal muscle stem cells

TL;DR: It is reported that EZH2, the enzymatic subunit of the Polycomb-repressive complex 2 (PRC2), is expressed in both Pax7+/Myf5⁻ stem cells and Pax7/My f5+ committed myogenic precursors and is required for homeostasis of the adult SC pool.
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Glucosamine promotes chondrogenic phenotype in both chondrocytes and mesenchymal stem cells and inhibits MMP-13 expression and matrix degradation

TL;DR: It is suggested that GlcN treatment enhances hMSC chondrogenesis and maintains cartilage matrix gene expression in chondrocytes, which may account for some of the reported chONDroprotective properties of Glcn on cartilage.
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Decreased microRNA-214 levels in breast cancer cells coincides with increased cell proliferation, invasion and accumulation of the Polycomb Ezh2 methyltransferase.

TL;DR: Findings indicate that reduced miR-214 levels may contribute to breast tumorigenesis by allowing abnormally elevated Ezh2 accumulation and subsequent unchecked cell proliferation and invasion.