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The cellular function of SCAP in metabolic signaling
Abstract
Sterol regulatory element binding protein (SREBP) cleavage activating protein (SCAP) is a key regulator of SREBP maturation. SCAP induces translocation of SREBP from the endoplasmic reticulum to the Golgi apparatus, allowing it to regulate cellular triglyceride and cholesterol levels. Previous studies have shown that suppression of SREBP activation in SCAP conditional knockout mice reduced the accumulation of intracellular triglycerides, which eventually causes the development of metabolic diseases such as atherosclerosis, diabetes, hepatic steatosis, and insulin resistance. However, despite the significance of SCAP as a regulator of SREBP, its function has not been thoroughly discussed. In this review, we have summarized the function of SCAP and its regulatory proteins. Furthermore, we discuss recent studies regarding SCAP as a possible therapeutic target for hypertriglyceridemia and hyperlipidemia.
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“Complement proteins, including C1q and C3, are upregulated in AD brain tissues36 and cerebrospinal fluid87,91, where they are pivotal in neuroinflammation and synapse elimination88,92.”
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“Consistently, a metabolic study noted that the loss of SCAP attenuates lipopolysaccharide -induced IκBα phosphorylation and p65 nuclear entry, indicating that SCAP is essential for NF-κB activation independent of its lipid metabolism role87.”
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Metadata
- Authors
- Lee, S. H., Lee, J.-H., & Im, S.-S.
- ORCID
- Im, Seung-Soon
- Venue
- Experimental & Molecular Medicine
- Published
- 2020-05
- Volume
- 52
- Issue
- 5
- Pages
- 724-729
- ISSN
- 1226-3613
- 2092-6413
- PMC
- PMC7272406
- Cited by
- 96
- References
- 4
- Language
- en
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