FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1899385764> ?p ?o ?g. }

• W1899385764 abstract "We have shown previously that low density lipoproteins (LDL) suppressed the synthesis of lactosylceramide in normal human proximal tubular cells, but stimulated such synthesis in proximal tubular cells from LDL receptor negative subjects (Chatterjee, S., Clarke, K., and Kwiterovich, P.O., Jr. (1986) J. Biol. Chem. 261, 13474-13479). To understand the mechanism(s) of this effect of LDL, we have studied here the effects of LDL on the activity of UDP-GalCer:beta-galactosyltransferase (GalT-2). Maximum suppression (70-80%) of the activity of GalT-2 in normal proximal tubular cells at 37 degrees C occurred at a LDL concentration of 25 micrograms/ml medium. Such suppression was not observed either when the cells were incubated with LDL at 4 degrees C, or when the cells were preincubated with leupeptin, followed by incubation with LDL at 37 degrees C. High density lipoproteins and fetuin did not suppress the activity of GalT-2 in normal proximal tubular cells. In contrast LDL modified by reductive methylation (M-LDL, 100 micrograms/ml) stimulated the activity of GalT-2, approximately 3-fold. The effects of LDL and M-LDL were not related to their glycosphingolipid content. Much less suppression and stimulation of the activity of GalT-2 in proximal tubular cells by LDL and M-LDL, respectively, was found in normal human skin fibroblasts, Chinese hamster ovary cells, and bovine smooth muscle cells, suggesting that the LDL-mediated effect may be tissue-specific. In cells grown to very high density, the activity of the LDL receptor is decreased, and there was less suppression of GalT-2 activity by LDL. In normal proximal tubular cells, LDL stimulated the activity of UDP-Gal:LacCer, alpha-galactosyltransferase activity, UDP-Gal:LcOse3Cer, beta-galactosyltransferase, and CMP-NeuAc:LacCer,alpha-sialyltransferase activity but did not alter the activity of sulfotransferase. In conclusion, LDL that entered the normal proximal tubular cells via the LDL receptor-mediated pathway decreased GalT-2 activity, an effect that was dependent upon the binding, internalization, and degradation of receptor-bound LDL. In contrast LDL that entered normal or LDL receptor-negative proximal tubular cells via an LDL receptor-independent pathway failed to suppress GalT-2 activity, and led to a stimulation of LacCer synthesis." @default.
• W1899385764 created "2016-06-24" @default.
• W1899385764 creator A5000104019 @default.
• W1899385764 creator A5034796829 @default.
• W1899385764 creator A5040542097 @default.
• W1899385764 creator A5083406462 @default.
• W1899385764 date "1988-09-01" @default.
• W1899385764 modified "2023-09-29" @default.
• W1899385764 title "Regulation of glycosphingolipid glycosyltransferase by low density lipoprotein receptors in cultured human proximal tubular cells." @default.
• W1899385764 cites W1485806819 @default.
• W1899385764 cites W1487164341 @default.
• W1899385764 cites W1507272843 @default.
• W1899385764 cites W1546449564 @default.
• W1899385764 cites W1559122076 @default.
• W1899385764 cites W1583865009 @default.
• W1899385764 cites W1628167280 @default.
• W1899385764 cites W1775749144 @default.
• W1899385764 cites W1777070967 @default.
• W1899385764 cites W1910396363 @default.
• W1899385764 cites W1964495368 @default.
• W1899385764 cites W1991119501 @default.
• W1899385764 cites W2023544629 @default.
• W1899385764 cites W2025019624 @default.
• W1899385764 cites W2025974151 @default.
• W1899385764 cites W2034052978 @default.
• W1899385764 cites W2064899031 @default.
• W1899385764 cites W2091217736 @default.
• W1899385764 cites W2135503869 @default.
• W1899385764 cites W2156799866 @default.
• W1899385764 cites W2183353649 @default.
• W1899385764 cites W2249421789 @default.
• W1899385764 cites W2416225108 @default.
• W1899385764 cites W28414865 @default.
• W1899385764 cites W4232361916 @default.
• W1899385764 doi "https://doi.org/10.1016/s0021-9258(18)37665-8" @default.
• W1899385764 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/2458339" @default.
• W1899385764 hasPublicationYear "1988" @default.
• W1899385764 type Work @default.
• W1899385764 sameAs 1899385764 @default.
• W1899385764 citedByCount "18" @default.
• W1899385764 countsByYear W18993857642014 @default.
• W1899385764 countsByYear W18993857642016 @default.
• W1899385764 countsByYear W18993857642021 @default.
• W1899385764 crossrefType "journal-article" @default.
• W1899385764 hasAuthorship W1899385764A5000104019 @default.
• W1899385764 hasAuthorship W1899385764A5034796829 @default.
• W1899385764 hasAuthorship W1899385764A5040542097 @default.
• W1899385764 hasAuthorship W1899385764A5083406462 @default.
• W1899385764 hasBestOaLocation W18993857641 @default.
• W1899385764 hasConcept C126322002 @default.
• W1899385764 hasConcept C134018914 @default.
• W1899385764 hasConcept C170493617 @default.
• W1899385764 hasConcept C185592680 @default.
• W1899385764 hasConcept C22222904 @default.
• W1899385764 hasConcept C24998067 @default.
• W1899385764 hasConcept C2776931407 @default.
• W1899385764 hasConcept C2778163477 @default.
• W1899385764 hasConcept C2779620165 @default.
• W1899385764 hasConcept C2780072125 @default.
• W1899385764 hasConcept C2910328161 @default.
• W1899385764 hasConcept C43554185 @default.
• W1899385764 hasConcept C55493867 @default.
• W1899385764 hasConcept C71924100 @default.
• W1899385764 hasConcept C86803240 @default.
• W1899385764 hasConceptScore W1899385764C126322002 @default.
• W1899385764 hasConceptScore W1899385764C134018914 @default.
• W1899385764 hasConceptScore W1899385764C170493617 @default.
• W1899385764 hasConceptScore W1899385764C185592680 @default.
• W1899385764 hasConceptScore W1899385764C22222904 @default.
• W1899385764 hasConceptScore W1899385764C24998067 @default.
• W1899385764 hasConceptScore W1899385764C2776931407 @default.
• W1899385764 hasConceptScore W1899385764C2778163477 @default.
• W1899385764 hasConceptScore W1899385764C2779620165 @default.
• W1899385764 hasConceptScore W1899385764C2780072125 @default.
• W1899385764 hasConceptScore W1899385764C2910328161 @default.
• W1899385764 hasConceptScore W1899385764C43554185 @default.
• W1899385764 hasConceptScore W1899385764C55493867 @default.
• W1899385764 hasConceptScore W1899385764C71924100 @default.
• W1899385764 hasConceptScore W1899385764C86803240 @default.
• W1899385764 hasLocation W18993857641 @default.
• W1899385764 hasOpenAccess W1899385764 @default.
• W1899385764 hasPrimaryLocation W18993857641 @default.
• W1899385764 hasRelatedWork W1552202055 @default.
• W1899385764 hasRelatedWork W1628167280 @default.
• W1899385764 hasRelatedWork W1985199555 @default.
• W1899385764 hasRelatedWork W1989506971 @default.
• W1899385764 hasRelatedWork W1994075911 @default.
• W1899385764 hasRelatedWork W2028683797 @default.
• W1899385764 hasRelatedWork W2042584293 @default.
• W1899385764 hasRelatedWork W2067792922 @default.
• W1899385764 hasRelatedWork W2073645536 @default.
• W1899385764 hasRelatedWork W2076812453 @default.
• W1899385764 hasRelatedWork W2086176714 @default.
• W1899385764 hasRelatedWork W2109467404 @default.
• W1899385764 hasRelatedWork W2125232915 @default.
• W1899385764 hasRelatedWork W2159177651 @default.
• W1899385764 hasRelatedWork W2166316651 @default.
• W1899385764 hasRelatedWork W2188927525 @default.
• W1899385764 hasRelatedWork W2404641809 @default.
• W1899385764 hasRelatedWork W2409437392 @default.

• next