Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific antisera to alpha-melanotropin (alpha-MSH) and corticotropin (ACTH 1-39) were used to obtain immunocytochemical evidence for the differential localization of alpha-MSH and ACTH in the secretory granules of corticotropes of rat anterior pituitary. The specificity of the antisera was established by binding 131I-labeled alpha-MSH and ACTH 1-39 to their respective antisera. Double-labeling immunocytochemistry (for alpha-MSH, ferritin; for ACTH, colloidal gold) was performed. Some secretory granules were labeled with ferritin particles (alpha-MSH), whereas others contained gold particles (ACTH). Only a few granules showed both ACTH and alpha-MSH. In typical corticotropes (stellate in form with a small number of secretory granules aligned along the cell periphery) only some of the secretory granules that were labeled with anti-ACTH serum were also immunoreactive to anti-alpha-MSH. In atypical corticotropes (polygonal in shape and containing a large number of secretory granules) almost all of the immunoreactive ACTH secretory granules were also positive to anti-alpha-MSH serum. An intermediate type of corticotrope was observed containing a small number of secretory granules, almost all of which were labeled with anti-alpha-MSH. Thus, rat anterior pituitary corticotropes may be classified into three types according to the distribution and content of alpha-MSH. The light-microscopic immunocytochemistry provided similar results.
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PMID:Differential subcellular localization of ACTH and alpha-MSH in corticotropes of the rat anterior pituitary. 300 31

Cultured cells from adult rat anterior pituitaries and intermediate lobes were treated with proteinase inhibitor substrate analogues (Boc-DPhe-Pro-Arginal [BOC-DPPA], DPhe-Pro-Arginal [DPPA], BOC-DPhe-Leu-Lysinal [BOC-DPLL], BOC-DPhe-Phe-Lysinal [BOC-DPPL]) to elucidate their effect on cell morphology. It was established that BOC-DPPA and DPPA (which in previous studies stimulated alpha-MSH release [6]) caused a slight decrease in the number of immunoreactive secretory granules in melanotrophs. BOC-DPLL, which inhibited growth hormone and prolactin release, did not alter the fine structural features of cultured cells. No difference was observed in the membrane turnover traced by cationic ferritin when cells were treated with BOC-DPPL. We suggest that substrate analogues used are harmless to pituitary cells.
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PMID:Proteinase inhibitors while influencing hormone release do not affect cell morphology of hypophyseal cultures. 313 79

Exposure of cultured human melanocytes to ultraviolet radiation (UV) results in DNA damage. In melanoma, UV-signature mutations resulting from unrepaired photoproducts are rare, suggesting the possible involvement of oxidative DNA damage in melanocyte malignant transformation. Here we present data demonstrating immediate dose-dependent generation of hydrogen peroxide in UV-irradiated melanocytes, which correlated directly with a decrease in catalase activity. Pretreatment of melanocytes with alpha-melanocortin (alpha-MSH) reduced the UV-induced generation of 7,8-dihydro-8-oxyguanine (8-oxodG), a major form of oxidative DNA damage. Pretreatment with alpha-MSH also increased the protein levels of catalase and ferritin. The effect of alpha-MSH on 8-oxodG induction was mediated by activation of the melanocortin 1 receptor (MC1R), as it was absent in melanocytes expressing loss-of-function MC1R, and blocked by concomitant treatment with an analog of agouti signaling protein (ASIP), ASIP-YY. This study provides unequivocal evidence for induction of oxidative DNA damage by UV in human melanocytes and reduction of this damage by alpha-MSH. Our data unravel some mechanisms by which alpha-MSH protects melanocytes from oxidative DNA damage, which partially explain the strong association of loss-of-function MC1R with melanoma.
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PMID:alpha-MSH activates immediate defense responses to UV-induced oxidative stress in human melanocytes. 1965 42