All of the following are true statements regarding the regulation of cholesterol synthesis, EXCEPT?
Transcription of HMG-CoA reductase gene is regulated by a transcription factor known as sterol regulatory element binding protein (SREBP).Binding of this protein to DNA sequences known as sterol regulatory element (SRE) which is located 5' to the HMG-CoA reductase gene increases the transcription (option 1 is true). When the amount of cellular cholesterol is adequate, SREBP remains inactive in endoplasmic reticulum (ER) bound to SREBP cleavage activating protein (SCAP). Binding of SCAP to SREBP is facilitated by another transmembrane protein known as Insig (Insulin induced gene). SCAP is a cholesterol sensor. When cholesterol levels fall, SCAP escos SREBP to the Golgi complex In golgi, SREBP is cleaved by proteases. This releases the DNA-binding domain of SREBP which can go to nucleus and increase the HMG-CoA reductase transcription. Insig1 helps in degradation of HMG-CoA reductase by ubiquitin degradation system (Option 3 is true). Mevalonate is feedback inhibitor of HMG-CoA reductase (RLE of cholesterol biosynthesis)(Option 4 is True). Cholesterol synthesis is an anabolic pathways and anabolic enzymes are active in dephosphorylated state (Option 2 is false).
Binding of SREBP to SRE enhances the transcription of HMG-CoA reductase
HMG-CoA reductase is active in phosphorylated form
Insig1 is involved in the degradation of HMG-CoA reductase
Mevalonate inhibit the HMG-CoA reductase
Cholesterol synthesis and bile acids