Cholesterol Transporters of the START Domain Protein Family by Barbara J. Clark, Douglas M. Stocco PDF

By Barbara J. Clark, Douglas M. Stocco

ISBN-10: 1493911112

ISBN-13: 9781493911110

ISBN-10: 1493911120

ISBN-13: 9781493911127

Non-vesicular intracellular ldl cholesterol shipping is a vital mechanism for retaining membrane ldl cholesterol homeostasis. contemporary experiences of reports directed at soluble ldl cholesterol delivery proteins point out that aberrant expression of the beginning proteins may well give a contribution to disorder states linked to problems in ldl cholesterol homeostasis. this can be a thrilling new course within the box and the aim of this publication can be to spotlight the present examine directed at strength roles for the beginning relatives in diabetes, melanoma and atherogenesis.

This booklet additionally presents a private and old point of view of the discovery-to-publication trip that the authors had for his or her specific commence area friend. The target should be to supply views to graduate scholars, post-doctoral fellows and endocrinology fellows at the examine discovery process.

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Extra resources for Cholesterol Transporters of the START Domain Protein Family in Health and Disease: START Proteins - Structure and Function

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Clark and D. M. Stocco mitochondria for cholesterol transport into the organelle. Thus, relatively quickly, key data confirmed StAR’s role as the acute regulator of steroidogenesis. Given the importance of the criteria for new protein synthesis for the acute regulation of steroidogenesis, understanding the molecular mechanisms that control the increase in StAR expression following trophic hormone stimulation would be important for understanding the mechanisms that control steroidogenesis. The cAMP responsive region of mouse and human StAR promoter is a non-consensus CRE/AP-1 element with overlapping specificity for members of the CREB/CREM and AP-1 protein families.

I was discussing some of our results with Jerry and eventually the discussion came around to the enigma of searching for the cause of the disease, lipoid congenital adrenal hyperplasia (lipoid CAH). Lipoid CAH results from an almost complete inability of the afflicted patients to synthesize steroid hormones. Lipoid CAH was originally thought to be a result of a mutation in the CYP11A1 gene, but this proved to be incorrect once the human gene was cloned and later sequenced from the tissue of patients having this disease [54].

CYP11A1, cytochrome P450 side chain cleavage enzyme; CYP17, cytochrome P450 17a-hydroxylase, 17, 20 lyase; CYP19, cytochrome P450 aromatase are used as examples of regulated genes within the steroid hormone biosynthetic pathway H hypothalamus, CRH corticotrophin-releasing hormone, GnRH gonadotropin-releasing hormone, Ant. Pit. anterior pituitary, ACTH adrenocorticotropin hormone, LH luteinizing hormone, FSH follicle stimulating hormone, StAR steroidogenic acute regulatory protein, cAMP cyclic adenosine-3′,5′-monophosphate, DAG diacylglycerol 28 B.

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Cholesterol Transporters of the START Domain Protein Family in Health and Disease: START Proteins - Structure and Function by Barbara J. Clark, Douglas M. Stocco


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