Cholesterol Homeostasis: Methods and Protocols by Ingrid C. Gelissen, Andrew J. Brown

By Ingrid C. Gelissen, Andrew J. Brown

This quantity presents state of the art ideas for learning a variety of facets of ldl cholesterol homeostasis, together with its uptake, synthesis and efflux from the cellphone, in addition to its trafficking in the cellphone. Chapters additionally disguise thoughts for learning the rules of ldl cholesterol homeostasis at either the transcriptional and post-translational degrees, in addition to learning the membrane topology and constitution of cholesterol-related proteins. Written within the hugely profitable Methods in Molecular Biology series layout, chapters contain introductions to their respective issues, lists of the required fabrics and reagents, step by step, conveniently reproducible laboratory protocols, and tips about troubleshooting and warding off recognized pitfalls.

Authoritative and sensible, Cholesterol Homeostasis: tools and Protocols aims to supply key concepts in tackling the research of ldl cholesterol homeostasis.

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The underlying message here is that even subtle changes in sterol structure may be crucial for receptor function, thereby reinforcing the stringency associated with receptor-cholesterol interaction. Adapted from ref. 89. See text for more details 30 Md. Jafurulla and Amitabha Chattopadhyay Structural Stringency of Cholesterol for Protein Function 31 requirement of membrane cholesterol for its function has been demonstrated [23]). Taken together, these results demonstrate the stringent requirement of cholesterol structure for the function of GPCRs.

Adapted from [8] that excess cellular cholesterol inhibits SREBP-2 activation, inhibiting cholesterol synthesis and uptake, and promoting efflux. In this chapter, we describe ways in which cellular cholesterol status can be manipulated in cell culture studies for the study of cholesterol homeostasis, including sterol starvation and sterol enrichment. 3); for example, lowering basal cellular cholesterol status before a treatment to upregulate the expression of cholesterol synthesis genes. One way to do this is to pretreat and/or treat cells with a class of drugs that target HMGCR called the statins.

Importantly, ent-­cholesterol induced the conformational change in the cholesterol-sensing protein Scap like its natural counterpart, which would result in retention of SREBP-2 in ER. Taken together, these results show that ent-cholesterol exhibits similarly homeostatic responses as natural cholesterol. On this basis, it has been suggested that cholesterol could also maintain its homeostasis through alterations in membrane properties beyond those specific cholesterol–protein interactions currently recognized [103].

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