FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022700880> ?p ?o ?g. }

• W2022700880 endingPage "874" @default.
• W2022700880 startingPage "871" @default.
• W2022700880 abstract "The aim of the present work was to estimate the effect of intracellular glutathione depletion on melanogenesis in human melanoma cells. We determined tyrosine hydroxylation activity, the rate-limiting step of the pathway, and 14C-melanin formation, an assay reflecting the global eumelanogenic pathway. Intracellular glutathione was depleted by treatment with buthionine-S-sulfoximine, a well-known inhibitor of gamma-glutamylcysteine synthetase. The intracellular depletion of glutathione was substantial after 20 h of incubation with 50 microM buthionine-S-sulfoximine, although a significant effect could be observed after 6 h. Tyrosine hydroxylase activity increased in parallel with glutathione depletion, to reach 160% with respect to the control values during 24 h of buthionine-S-sulfoximine treatment. We have found the response to buthionine-S-sulfoximine to be dose dependent and the two different human cell lines HBL and LND1 to have similar, if not identical, responses. 14C-melanin formation assay revealed even greater activation, up to 400% of the control values. This indicates that glutathione depletion may have two distinct effects: first, a direct one on tyrosinase activity and, second, an effect on the promotion of eumelanogenesis. The stimulation of tyrosine hydroxylase can be explained by a possible inactivation of the enzyme by endogenous thiol compounds rather than by a direct effect of buthionine-S-sulfoximine itself on tyrosinase. The data suggest that thiol compounds may play a role for stimulation of melanogenesis by ultraviolet radiation." @default.
• W2022700880 created "2016-06-24" @default.
• W2022700880 creator A5003228111 @default.
• W2022700880 creator A5007483917 @default.
• W2022700880 creator A5009257436 @default.
• W2022700880 creator A5014826132 @default.
• W2022700880 creator A5028282419 @default.
• W2022700880 creator A5055634803 @default.
• W2022700880 creator A5072372960 @default.
• W2022700880 date "1993-12-01" @default.
• W2022700880 modified "2023-10-01" @default.
• W2022700880 title "Glutathione Depletion Increases Tyrosinase Activity in Human Melanoma Cells" @default.
• W2022700880 cites W1644644959 @default.
• W2022700880 cites W1775749144 @default.
• W2022700880 cites W1797171289 @default.
• W2022700880 cites W1964952893 @default.
• W2022700880 cites W1975129370 @default.
• W2022700880 cites W1981640796 @default.
• W2022700880 cites W1990980940 @default.
• W2022700880 cites W2001593305 @default.
• W2022700880 cites W2006832623 @default.
• W2022700880 cites W2015153883 @default.
• W2022700880 cites W2020803654 @default.
• W2022700880 cites W2022261965 @default.
• W2022700880 cites W2042280234 @default.
• W2022700880 cites W2053527204 @default.
• W2022700880 cites W2053977768 @default.
• W2022700880 cites W2056792410 @default.
• W2022700880 cites W2062164885 @default.
• W2022700880 cites W2066849510 @default.
• W2022700880 cites W2103832625 @default.
• W2022700880 cites W2118519973 @default.
• W2022700880 cites W2122845914 @default.
• W2022700880 cites W2157667294 @default.
• W2022700880 cites W2158601429 @default.
• W2022700880 cites W2333329865 @default.
• W2022700880 cites W4245957869 @default.
• W2022700880 cites W4298080168 @default.
• W2022700880 doi "https://doi.org/10.1111/1523-1747.ep12371709" @default.
• W2022700880 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7902381" @default.
• W2022700880 hasPublicationYear "1993" @default.
• W2022700880 type Work @default.
• W2022700880 sameAs 2022700880 @default.
• W2022700880 citedByCount "56" @default.
• W2022700880 countsByYear W20227008802012 @default.
• W2022700880 countsByYear W20227008802013 @default.
• W2022700880 countsByYear W20227008802014 @default.
• W2022700880 countsByYear W20227008802015 @default.
• W2022700880 countsByYear W20227008802016 @default.
• W2022700880 countsByYear W20227008802017 @default.
• W2022700880 countsByYear W20227008802018 @default.
• W2022700880 countsByYear W20227008802019 @default.
• W2022700880 countsByYear W20227008802021 @default.
• W2022700880 countsByYear W20227008802022 @default.
• W2022700880 countsByYear W20227008802023 @default.
• W2022700880 crossrefType "journal-article" @default.
• W2022700880 hasAuthorship W2022700880A5003228111 @default.
• W2022700880 hasAuthorship W2022700880A5007483917 @default.
• W2022700880 hasAuthorship W2022700880A5009257436 @default.
• W2022700880 hasAuthorship W2022700880A5014826132 @default.
• W2022700880 hasAuthorship W2022700880A5028282419 @default.
• W2022700880 hasAuthorship W2022700880A5055634803 @default.
• W2022700880 hasAuthorship W2022700880A5072372960 @default.
• W2022700880 hasConcept C107538193 @default.
• W2022700880 hasConcept C153911025 @default.
• W2022700880 hasConcept C181199279 @default.
• W2022700880 hasConcept C185592680 @default.
• W2022700880 hasConcept C2776165026 @default.
• W2022700880 hasConcept C2777476445 @default.
• W2022700880 hasConcept C538909803 @default.
• W2022700880 hasConcept C55493867 @default.
• W2022700880 hasConcept C79879829 @default.
• W2022700880 hasConcept C86803240 @default.
• W2022700880 hasConcept C87554066 @default.
• W2022700880 hasConceptScore W2022700880C107538193 @default.
• W2022700880 hasConceptScore W2022700880C153911025 @default.
• W2022700880 hasConceptScore W2022700880C181199279 @default.
• W2022700880 hasConceptScore W2022700880C185592680 @default.
• W2022700880 hasConceptScore W2022700880C2776165026 @default.
• W2022700880 hasConceptScore W2022700880C2777476445 @default.
• W2022700880 hasConceptScore W2022700880C538909803 @default.
• W2022700880 hasConceptScore W2022700880C55493867 @default.
• W2022700880 hasConceptScore W2022700880C79879829 @default.
• W2022700880 hasConceptScore W2022700880C86803240 @default.
• W2022700880 hasConceptScore W2022700880C87554066 @default.
• W2022700880 hasIssue "6" @default.
• W2022700880 hasLocation W20227008801 @default.
• W2022700880 hasLocation W20227008802 @default.
• W2022700880 hasOpenAccess W2022700880 @default.
• W2022700880 hasPrimaryLocation W20227008801 @default.
• W2022700880 hasRelatedWork W1999810095 @default.
• W2022700880 hasRelatedWork W2022700880 @default.
• W2022700880 hasRelatedWork W2053067513 @default.
• W2022700880 hasRelatedWork W2061008863 @default.
• W2022700880 hasRelatedWork W2079137660 @default.
• W2022700880 hasRelatedWork W2317241531 @default.
• W2022700880 hasRelatedWork W2398131642 @default.
• W2022700880 hasRelatedWork W2402290768 @default.

• next