SCAP: Proteins and Enzymes
Sterol regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) is a molecular chaperone that plays a role in the biosynthesis of cholesterol and triglycerides (1). SCAP is a membrane protein that helps shuttle SREBP from the endoplasmic reticulum (ER) via coat protein II (COPII) vesicles to the golgi where SREBP is cleaved via protease S1P and S2P, becomes activated, and is translocated to the nucleus for transcription (1-3). The SCAP protein has a theoretical molecular weight of 140 kDa and is comprised of 1276 amino acids with an N-terminal domain containing 8 transmembrane alpha helices, where transmembrane 2-6 consist of a sterol-sensing domain, and a C-terminal domain with WD40 motif repeats (1,3). The SCAP-SREBP association plays a pivotal role in regulating lipid metabolism and lipogenesis (1,4). SREBP activation via SCAP is associated with accumulation of triglycerides and cholesterol leading to metabolic disorders including diabetes, atherosclerosis, and nonalcoholic fatty liver disease (NAFLD) (1,4). Animal models have revealed that inhibition or blocking of SCAP using antagonists may be a potential therapeutic target for hyperlipidemia and hypertriglyceridemia (1,4).
References
1. Lee, S. H., Lee, J. H., & Im, S. S. (2020). The cellular function of SCAP in metabolic signaling. Experimental & molecular medicine, 52(5), 724-729. https://doi.org/10.1038/s12276-020-0430-0
2. Cheng, X., Li, J., & Guo, D. (2018). SCAP/SREBPs are Central Players in Lipid Metabolism and Novel Metabolic Targets in Cancer Therapy. Current topics in medicinal chemistry, 18(6), 484-493. https://doi.org/10.2174/1568026618666180523104541
3. Brown, M. S., Radhakrishnan, A., & Goldstein, J. L. (2018). Retrospective on Cholesterol Homeostasis: The Central Role of Scap. Annual review of biochemistry, 87, 783-807. https://doi.org/10.1146/annurev-biochem-062917-011852
4. Moon Y. A. (2017). The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis. Endocrinology and metabolism (Seoul, Korea), 32(1), 6-10. https://doi.org/10.3803/EnM.2017.32.1.6
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References
1. Lee, S. H., Lee, J. H., & Im, S. S. (2020). The cellular function of SCAP in metabolic signaling. Experimental & molecular medicine, 52(5), 724-729. https://doi.org/10.1038/s12276-020-0430-0
2. Cheng, X., Li, J., & Guo, D. (2018). SCAP/SREBPs are Central Players in Lipid Metabolism and Novel Metabolic Targets in Cancer Therapy. Current topics in medicinal chemistry, 18(6), 484-493. https://doi.org/10.2174/1568026618666180523104541
3. Brown, M. S., Radhakrishnan, A., & Goldstein, J. L. (2018). Retrospective on Cholesterol Homeostasis: The Central Role of Scap. Annual review of biochemistry, 87, 783-807. https://doi.org/10.1146/annurev-biochem-062917-011852
4. Moon Y. A. (2017). The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis. Endocrinology and metabolism (Seoul, Korea), 32(1), 6-10. https://doi.org/10.3803/EnM.2017.32.1.6
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1 result for "SCAP Proteins and Enzymes" in Products
SCAP: Proteins and Enzymes
Sterol regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) is a molecular chaperone that plays a role in the biosynthesis of cholesterol and triglycerides (1). SCAP is a membrane protein that helps shuttle SREBP from the endoplasmic reticulum (ER) via coat protein II (COPII) vesicles to the golgi where SREBP is cleaved via protease S1P and S2P, becomes activated, and is translocated to the nucleus for transcription (1-3). The SCAP protein has a theoretical molecular weight of 140 kDa and is comprised of 1276 amino acids with an N-terminal domain containing 8 transmembrane alpha helices, where transmembrane 2-6 consist of a sterol-sensing domain, and a C-terminal domain with WD40 motif repeats (1,3). The SCAP-SREBP association plays a pivotal role in regulating lipid metabolism and lipogenesis (1,4). SREBP activation via SCAP is associated with accumulation of triglycerides and cholesterol leading to metabolic disorders including diabetes, atherosclerosis, and nonalcoholic fatty liver disease (NAFLD) (1,4). Animal models have revealed that inhibition or blocking of SCAP using antagonists may be a potential therapeutic target for hyperlipidemia and hypertriglyceridemia (1,4).
References
1. Lee, S. H., Lee, J. H., & Im, S. S. (2020). The cellular function of SCAP in metabolic signaling. Experimental & molecular medicine, 52(5), 724-729. https://doi.org/10.1038/s12276-020-0430-0
2. Cheng, X., Li, J., & Guo, D. (2018). SCAP/SREBPs are Central Players in Lipid Metabolism and Novel Metabolic Targets in Cancer Therapy. Current topics in medicinal chemistry, 18(6), 484-493. https://doi.org/10.2174/1568026618666180523104541
3. Brown, M. S., Radhakrishnan, A., & Goldstein, J. L. (2018). Retrospective on Cholesterol Homeostasis: The Central Role of Scap. Annual review of biochemistry, 87, 783-807. https://doi.org/10.1146/annurev-biochem-062917-011852
4. Moon Y. A. (2017). The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis. Endocrinology and metabolism (Seoul, Korea), 32(1), 6-10. https://doi.org/10.3803/EnM.2017.32.1.6
Show More
References
1. Lee, S. H., Lee, J. H., & Im, S. S. (2020). The cellular function of SCAP in metabolic signaling. Experimental & molecular medicine, 52(5), 724-729. https://doi.org/10.1038/s12276-020-0430-0
2. Cheng, X., Li, J., & Guo, D. (2018). SCAP/SREBPs are Central Players in Lipid Metabolism and Novel Metabolic Targets in Cancer Therapy. Current topics in medicinal chemistry, 18(6), 484-493. https://doi.org/10.2174/1568026618666180523104541
3. Brown, M. S., Radhakrishnan, A., & Goldstein, J. L. (2018). Retrospective on Cholesterol Homeostasis: The Central Role of Scap. Annual review of biochemistry, 87, 783-807. https://doi.org/10.1146/annurev-biochem-062917-011852
4. Moon Y. A. (2017). The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis. Endocrinology and metabolism (Seoul, Korea), 32(1), 6-10. https://doi.org/10.3803/EnM.2017.32.1.6
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