<prompt> All of the following are true statements regarding the regulation of cholesterol synthesis, EXCEPT?Binding of SREBP to SRE enhances the transcription of HMG-CoA reductaseHMG-CoA reductase is active in phosphorylated formInsig1 is involved in the degradation of HMG-CoA reductaseMevalonate inhibit the HMG-CoA reductase  <response>: 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 biosynthesisOption 4 is True. Cholesterol synthesis is an anabolic pathways and anabolic enzymes are active in dephosphorylated state Option 2 is false. 