Regulated step in cholesterol feedback localized to budding of SCAP from ER membranes

Article Abstract:

Results demonstrate that in sterol-treated mammalian cells, the polytopic membrane SREBP Cleaving-Activating-Protein budding is reduced. Data further point out that the budding is from endoplasm reticulum of the sterol treated cells.

Japan, Analysis, Endoplasmic reticulum, Metabolic regulation

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SREBP cleavage-activating protein (SCAP) is required for increased lipid synthesis in liver induced by cholesterol deprivation and insulin elevation

Article Abstract:

Sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) has been found to be necessary for increased lipid synthesis in liver brought on by cholesterol deprivation and insulin elevation. The SCAP gene was targeted by flanking exon1 with loxP sites, targets for bacteriophage P1Cre recombinase. Mice homozygous for the loxP-tagged SCAP allele were generated. They carry a transgene encoding Cre under control of the interferon-inducible MX1 promoter. The mice have a major lowering in synthesis of cholesterol and fatty acids. They do not have normal increase in the processes in response to insulin or to cholesterol deprivation.

Statistical Data Included, Research, Liver, Cytochemistry, Fatty acids, Proteolysis, Insulin

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Sterol resistance in CHO cells traced to point mutation in SREBP cleavage-activating protein

Article Abstract:

Sterol regulatory element binding proteins-1 and -2 (SREBP) are key molecules in the cholesterol feedback system. Cleavage of transcription factors SREBP-1 and -2 causes the release of the NH2-terminal segment into the cytosol via the proteolytic pathway. Studies on Chinese hamster ovary cells with defects in feedback regulation have shown that sterols play an important role in the regulation of the feedback system. The accumulation of sterols turns off the protease which clips SREBP activity.

Carrier proteins, Transport proteins, Cholesterol metabolism

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