Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Work in the past 8 years, particularly in the past 1-2 years, has greatly expanded our understanding of the mechanisms by which ultraviolet irradiation stimulates melanogenesis in the skin. A direct effect of UV photons on DNA results in up-regulation of the gene for tyrosinase, the rate-limiting enzyme in melanin synthesis, as well as an increase in cell surface expression of receptors for at least one of the several known keratinocyte-derived melanogenic factors, MSH. Direct effects of UV on melanocyte membranes, releasing DAG and arachidonic acid, may also play a role in the tanning response. Diacylglycerol may activate PKC-beta, which in turn phosphorylates and activates tyrosinase protein; the pathways by which products of other inflammatory mediator cascades may act on melanogenesis are unknown. The tanning response also relies heavily on UV-stimulated increased production and release of numerous keratinocyte-derived factors including bFGF, NGF, endothelin-1 and the POMC-derived peptides MSH, ACTH, beta-LPH and beta-endorphin. These factors variably induce melanocyte mitosis, increase melanogenesis, enhance dendricity and prevent apoptotic cell death following the UV injury. Thus, events within the epidermal melanin unit conspire to maintain or increase melanocyte number, increase melanin pigment throughout the epidermis. Overall, ultraviolet-induced melanogenesis may be one part of a eukaryotic SOS response to damaging ultraviolet irradiation that has evolved over time to provide a protective tan in skin at risk of further injury from sun exposure. These recent insights into the mechanisms underlying ultraviolet-induced melanogenesis offer the opportunity for novel therapeutic approaches to minimizing acute and chronic photodamage in human skin.
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PMID:Mechanisms of ultraviolet light-induced pigmentation. 857 60

1. The synthesis and secretion of aldosterone in the adrenal zona glomerulosa in physiologic conditions is controlled by adrenocorticotropin (ACTH), angiotensin II (AII), and extracellular (K+). 2. ACTH effects on aldosterone output are explained by cyclic AMP-(cAMP)- and Ca(2+)-dependent mechanisms. 3. All effects on aldosterone secretion are initiated by an increase in Ca2+ influx through hormone-operated Ca2+ channels and G-protein- and phospholipase C-(PLC) dependent hydrolysis of phosphoinositides leading to the generation of inositol 1,4,5 trisphosphate (IP3) and DAG that induce intracellular Ca2+ release and PKC activation, respectively. 4. ACTH increases DAG formation with marginal or undetectable IP3 generation. The effect of ACTH on DAG levels is discussed. 5. The requirement of external Ca2+ in PLC activation and aldosterone secretion also is discussed.
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PMID:Recent progress in understanding aldosterone secretion. 918 96

The melanocortin 1 (MC-1) receptor is a key control point in the regulation of skin pigmentation. Alpha-MSH is an agonist at this receptor and through its activation regulates melanocyte function. alpha-MSH is cleaved from pro-opiomelanocortin (POMC) in the pituitary, but in humans the skin is a more important source of the peptide. Skin pigmentation is therefore regulated by locally produced alpha-MSH rather than that of pituitary origin. alpha-MSH acts as a paracrine and/or autocrine mediator of UV induced pigmentation. However, the predominant alpha-MSH in human skin is desacetyl alpha-MSH and, compared to the acetylated form, is a relatively weak agonist at the human MC-1 receptor. By acting as a partial agonist desacetyl alpha-MSH may even oppose the actions of acetylated alpha-MSH and other MC-1 receptor agonists. The most abundant MC-1 receptor agonist in human epidermis is ACTH1-17. This POMC peptide, which is produced by keratinocytes, is more potent than acetylated alpha-MSH in stimulating melanogenesis in human melanocytes and, in contrast to the latter, produces a biphasic dose-response curve. This is probably a consequence of its activation of both the cAMP and IP3/DAG signalling pathways. alpha-MSH peptides, on the other hand, selectively activate the cAMP pathway. Compared with alpha-MSH, ACTH1-17 could have the more important role as a paracrine mediator of melanogenesis and other melanocytic processes. However, ACTH1-17 is not the only POMC peptide in the skin and may interact with related peptides at the MC-1 receptor. These interactions are likely to represent important determinants of melanocyte function and skin pigmentation.
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PMID:Skin POMC peptides: their actions at the human MC-1 receptor and roles in the tanning response. 1104 69

This article focuses on recent advances in melanocyte biology and physiology. The major function of this neural crest-derived cell is the production of melanins. A "three enzyme theory" in the initiation of pigmentation is put forward and backed up by recent findings. A receptor-independent role for alpha-MSH and the cofactor (6R)-l-erythro-5,6,7,8-terahydrobiopterin (6BH(4)) in the control of tyrosinase is described. The importance of intramelanosomal pH for melanogenesis is covered. Finally, the redundancy of the cAMP and IP3/DAG/calcium signal in melanocytes together with the downstream events are highlighted. The main message of this article is that the intracellular H(2)O(2)- redox-equilibrium controls melanocyte function in a concentration-dependent manner.
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PMID:Advances in melanocyte basic science research. 1766 94