Term
| 2 sites of cholesterol synthesis in mammals |
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Definition
-liver (major site)
-intestine (significant) |
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Term
| how the rate of cholesterol formation is regulated |
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Definition
| primarily by changes in the amount and activity of 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase) |
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Term
| 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase) |
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Definition
| helps regulate the rate of cholesterol formation |
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Term
| the committed step in cholesterol biosynthesis |
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Definition
| the formation of mevalonate |
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Term
| some ways HMG-CoA reductase is controlled |
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Definition
1: rate of synthesis of HMG-CoA reductase mRNA is controlled by the sterol regulatory element binding protein (SREBP)
2: the rate of translation of HMG-CoA reductase nRNA is inhibited by nonsterol metabolites derived from mevalonate as well as by dietary cholesterol
3: the degradation of HMG-CoA reductase is stringently controlled by interactions involving the cytoplasmic and membrane domains
4: phosphorylation decreases the activity of HMG-CoA reductase |
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Term
| the rate of synthesis of HMG-CoA reductase mRNA is controlled by... |
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Definition
| the sterol regulatory element binding protein (SREBP) |
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Term
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Definition
| a short DNA sequence called the sterol regulatory element (SRE) on the 5' side of the reductase gene |
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Term
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Definition
| when cholesterol levels are low |
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Term
| when SREBP binding to SRE does for transcription |
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Definition
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Term
| membrane protein that acts as the cholesterol sensor |
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Definition
| SREB cleavage activating protein (SCAP) |
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Term
| what SCAP does when cholesterol levels are low |
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Definition
| escorts SREBP in small membrane vesicles to the Golgi complex, where it is released from the membrane |
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Term
| how SREBP enhances transcription |
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Definition
| migrates to nucleus and binds to the SRE of the HMG-CoA reductase gene, as well as several other genes in the cholesterol biosynthetic pathway |
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Term
| what happens to SREBP when cholesterol levels are high? |
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Definition
| release of SREBP is blocked and SREBP in nucleus is rapidly degraded |
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Term
| what SCAP in the endoplasmic reticulum does when cholesterol is low |
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Definition
| binds to vesicular proteins that facilitate the transport of SCAP-SREBP to the Golgi apparatus |
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Term
| what SCAP in the endoplasmic reticulum does when cholesterol is present |
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Definition
| binds cholesterol, which causes a structural change in SCAP so that it binds to insig (insulin-induced gene), another endoplasmic reticulum protein |
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Term
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Definition
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Term
| the importance of insig when cholesterol is present |
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Definition
| it is the anchor that retains SCAP and thus SREBP in the endoplasmic reticulum in the presence of cholesterol |
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Term
| depiction of the site of cholesterol synthesis |
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Definition
[image]
the arrow points to a vesicle that is releasing its content of VLDL particles |
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Term
| depiction of the SREBP pathway |
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Definition
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Term
| the rate of translation of HMG-CoA reductase nRNA is inhibited by... |
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Definition
| nonsterol metabolites derived from mevalonate as well as by dietary cholesterol |
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Term
| the 2 domains of HMG-CoA reductase |
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Definition
-cytoplasmic domain, which carries out catalysis
-membrane domain, which senses signals that lead to its degradation |
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Term
| function of the cytoplasmic domain of HMG-CoA reductase |
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Definition
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Term
| function of the membrane domain of HMG-CoA reductase |
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Definition
| senses signals that lead to its degradation |
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Term
| effect of phosphorylation on the activity of HMG-CoA reductase |
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Definition
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Term
| why cholesterol synthesis ceases when ATP is low |
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Definition
| because HMG-CoA reductase is switched off by an AMP-activated protein kinase |
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