The above actions of ACTH increased the available cholesterol pool for steroidogenesis. PKA modifies the activity of specific transcription factors via phosphorylation.ĪCTH actions include, the activation of HMG CoA reductase (the rate-limiting enzyme in cholesterol synthesis), increased LDL-C esters uptake (that are either stored or converted into cholesterol), activation of hormone-sensitive lipase (HSL) and lastly inhibition of acyl-coenzyme A (CoA): cholesterol acyltransferase (ACAT). This binding results in the activation of adenylyl cyclase, cAMP production, and activation of protein kinase A (PKA). ACTH acts by binding to a G protein-coupled receptor (the melanocortin two receptor- MC2R). Corticotrophin-releasing hormone (CRH) is released from the hypothalamus and stimulates the adrenocorticotropic hormone (ACTH). The release of cortisol is under the feed-back control of the hypothalamic-pituitary-adrenal (HPA) axis.
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