Nuclear receptors at the crossroads of inflammation and atherosclerosis [electronic resource] / Christopher K. Glass.

By: Glass, Christopher K, 1955- [spk]Material type: FilmFilmSeries: Henry Stewart talksBiomedical & life sciences collection. Innate immunity : host recognition and response in health and disease: Publisher: London : Henry Stewart Talks, 2009Description: 1 online resource (1 streaming video file (41 min.) : color, sound)Subject(s): Atherosclerosis -- etiology | Diabetes Mellitus, Type 2 -- etiology | Immunity, Innate | Inflammation | Metabolism | Receptors, Cytoplasmic and NuclearOnline resources: Click here to access online | Series
Contents:
Contents: Nuclear receptors comprise a superfamily of ligand- and signal-dependent transcription factors that regulate diverse aspects of reproduction, development, metabolism and immunity -- Recent studies have demonstrated that a subset of nuclear receptors can co-ordinately regulate aspects of inflammation and metabolism that impact on the development of atherosclerosis and type 2 diabetes by inhibiting transcriptional responses to toll like receptors -- The nuclear receptor co-repressor NCoR plays a key role in maintaining inflammatory response genes in a repressed state under basal conditions -- PPARg inhibits inflammatory responses by preventing the removal of NCoR from target genes.
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Animated audio-visual presentation with synchronized narration.

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Contents: Nuclear receptors comprise a superfamily of ligand- and signal-dependent transcription factors that regulate diverse aspects of reproduction, development, metabolism and immunity -- Recent studies have demonstrated that a subset of nuclear receptors can co-ordinately regulate aspects of inflammation and metabolism that impact on the development of atherosclerosis and type 2 diabetes by inhibiting transcriptional responses to toll like receptors -- The nuclear receptor co-repressor NCoR plays a key role in maintaining inflammatory response genes in a repressed state under basal conditions -- PPARg inhibits inflammatory responses by preventing the removal of NCoR from target genes.

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