FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2032576132> ?p ?o ?g. }

• W2032576132 endingPage "12541" @default.
• W2032576132 startingPage "12536" @default.
• W2032576132 abstract "The sodium-dependent glucose transporter SGLT1 is expressed on the apical plasma membrane of fully differentiated enterocytes. Recently, we have found that the cotransport function appears gradually during the process of differentiation of the human intestinal epithelial cell clone HT-29-D4. However, the SGLT1 protein was detected in both undifferentiated and differentiated HT-29-D4 cells suggesting that sodium-glucose cotransport was dependent on post-translational events controlling the efficient targeting of the protein in the plasma membrane. In the present study, we have analyzed the molecular mechanisms controlling the functional expression of the SGLT1 protein during the course of HT-29-D4 differentiation. We show that the appearance of the cotransport function in the apical membrane is blocked by 1-5-isoquinolinesulfonyl)-2-methylpiperazine-HCl (H-7), a potent inhibitor of protein kinase C activity. Moreover, H-7 treatment was associated with an unability of HT-29-D4 cells to organize into a polarized monolayer of differentiated cells. Reciprocally, short term treatment (15 min) of undifferentiated cells by 0.1 μM phorbol myristyl acetate resulted in the appearance of the cotransport function. In contrast, inhibition of cAMP and cGMP-dependent protein kinases by N-(2-guanidinoethyl)-5-isoquinolinesulfonamide-HCl did not prevent the development of sodium-glucose cotransport during the differentiation of HT-29-D4 cells. In addition, stimulation of cAMP-dependent protein kinases by 8-Cl-cAMP did not induce the cotransport function in undifferentiated HT-29-D4 cells. By using immunogold labeling at the electron microscopy level, we demonstrated that phorbol myristyl acetate induced the redistribution of SGLT1 protein from intracellular sites to the plasma membrane. In conclusion, our data show that the appearance of a functional sodium-glucose cotransporter in HT-29-D4 cells is controlled, at least in part, by intracellular pathways regulated by the activity of protein kinase C. The sodium-dependent glucose transporter SGLT1 is expressed on the apical plasma membrane of fully differentiated enterocytes. Recently, we have found that the cotransport function appears gradually during the process of differentiation of the human intestinal epithelial cell clone HT-29-D4. However, the SGLT1 protein was detected in both undifferentiated and differentiated HT-29-D4 cells suggesting that sodium-glucose cotransport was dependent on post-translational events controlling the efficient targeting of the protein in the plasma membrane. In the present study, we have analyzed the molecular mechanisms controlling the functional expression of the SGLT1 protein during the course of HT-29-D4 differentiation. We show that the appearance of the cotransport function in the apical membrane is blocked by 1-5-isoquinolinesulfonyl)-2-methylpiperazine-HCl (H-7), a potent inhibitor of protein kinase C activity. Moreover, H-7 treatment was associated with an unability of HT-29-D4 cells to organize into a polarized monolayer of differentiated cells. Reciprocally, short term treatment (15 min) of undifferentiated cells by 0.1 μM phorbol myristyl acetate resulted in the appearance of the cotransport function. In contrast, inhibition of cAMP and cGMP-dependent protein kinases by N-(2-guanidinoethyl)-5-isoquinolinesulfonamide-HCl did not prevent the development of sodium-glucose cotransport during the differentiation of HT-29-D4 cells. In addition, stimulation of cAMP-dependent protein kinases by 8-Cl-cAMP did not induce the cotransport function in undifferentiated HT-29-D4 cells. By using immunogold labeling at the electron microscopy level, we demonstrated that phorbol myristyl acetate induced the redistribution of SGLT1 protein from intracellular sites to the plasma membrane. In conclusion, our data show that the appearance of a functional sodium-glucose cotransporter in HT-29-D4 cells is controlled, at least in part, by intracellular pathways regulated by the activity of protein kinase C." @default.
• W2032576132 created "2016-06-24" @default.
• W2032576132 creator A5003514981 @default.
• W2032576132 creator A5047254221 @default.
• W2032576132 creator A5070951004 @default.
• W2032576132 date "1995-05-01" @default.
• W2032576132 modified "2023-10-14" @default.
• W2032576132 title "The Development of Na+-dependent Glucose Transport during Differentiation of an Intestinal Epithelial Cell Clone Is Regulated by Protein Kinase C" @default.
• W2032576132 cites W1512501096 @default.
• W2032576132 cites W1517822715 @default.
• W2032576132 cites W1875077626 @default.
• W2032576132 cites W1883544415 @default.
• W2032576132 cites W1971748855 @default.
• W2032576132 cites W2009086732 @default.
• W2032576132 cites W2027284791 @default.
• W2032576132 cites W2027457570 @default.
• W2032576132 cites W2042315603 @default.
• W2032576132 cites W2066875479 @default.
• W2032576132 cites W2067907729 @default.
• W2032576132 cites W2071277783 @default.
• W2032576132 cites W2080483966 @default.
• W2032576132 cites W2089909903 @default.
• W2032576132 cites W2101108802 @default.
• W2032576132 cites W2137171440 @default.
• W2032576132 cites W2153373667 @default.
• W2032576132 cites W73570518 @default.
• W2032576132 doi "https://doi.org/10.1074/jbc.270.21.12536" @default.
• W2032576132 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7759499" @default.
• W2032576132 hasPublicationYear "1995" @default.
• W2032576132 type Work @default.
• W2032576132 sameAs 2032576132 @default.
• W2032576132 citedByCount "36" @default.
• W2032576132 countsByYear W20325761322013 @default.
• W2032576132 countsByYear W20325761322014 @default.
• W2032576132 countsByYear W20325761322017 @default.
• W2032576132 countsByYear W20325761322018 @default.
• W2032576132 crossrefType "journal-article" @default.
• W2032576132 hasAuthorship W2032576132A5003514981 @default.
• W2032576132 hasAuthorship W2032576132A5047254221 @default.
• W2032576132 hasAuthorship W2032576132A5070951004 @default.
• W2032576132 hasConcept C104317684 @default.
• W2032576132 hasConcept C134018914 @default.
• W2032576132 hasConcept C148738053 @default.
• W2032576132 hasConcept C153911025 @default.
• W2032576132 hasConcept C161573976 @default.
• W2032576132 hasConcept C178790620 @default.
• W2032576132 hasConcept C184235292 @default.
• W2032576132 hasConcept C185592680 @default.
• W2032576132 hasConcept C188053792 @default.
• W2032576132 hasConcept C195794163 @default.
• W2032576132 hasConcept C2779306644 @default.
• W2032576132 hasConcept C3018436504 @default.
• W2032576132 hasConcept C41625074 @default.
• W2032576132 hasConcept C537181965 @default.
• W2032576132 hasConcept C55493867 @default.
• W2032576132 hasConcept C86803240 @default.
• W2032576132 hasConcept C95444343 @default.
• W2032576132 hasConcept C97029542 @default.
• W2032576132 hasConceptScore W2032576132C104317684 @default.
• W2032576132 hasConceptScore W2032576132C134018914 @default.
• W2032576132 hasConceptScore W2032576132C148738053 @default.
• W2032576132 hasConceptScore W2032576132C153911025 @default.
• W2032576132 hasConceptScore W2032576132C161573976 @default.
• W2032576132 hasConceptScore W2032576132C178790620 @default.
• W2032576132 hasConceptScore W2032576132C184235292 @default.
• W2032576132 hasConceptScore W2032576132C185592680 @default.
• W2032576132 hasConceptScore W2032576132C188053792 @default.
• W2032576132 hasConceptScore W2032576132C195794163 @default.
• W2032576132 hasConceptScore W2032576132C2779306644 @default.
• W2032576132 hasConceptScore W2032576132C3018436504 @default.
• W2032576132 hasConceptScore W2032576132C41625074 @default.
• W2032576132 hasConceptScore W2032576132C537181965 @default.
• W2032576132 hasConceptScore W2032576132C55493867 @default.
• W2032576132 hasConceptScore W2032576132C86803240 @default.
• W2032576132 hasConceptScore W2032576132C95444343 @default.
• W2032576132 hasConceptScore W2032576132C97029542 @default.
• W2032576132 hasIssue "21" @default.
• W2032576132 hasLocation W20325761321 @default.
• W2032576132 hasOpenAccess W2032576132 @default.
• W2032576132 hasPrimaryLocation W20325761321 @default.
• W2032576132 hasRelatedWork W157765740 @default.
• W2032576132 hasRelatedWork W1979850765 @default.
• W2032576132 hasRelatedWork W2019595537 @default.
• W2032576132 hasRelatedWork W2041386649 @default.
• W2032576132 hasRelatedWork W2051086962 @default.
• W2032576132 hasRelatedWork W2059389639 @default.
• W2032576132 hasRelatedWork W2062741205 @default.
• W2032576132 hasRelatedWork W2129314512 @default.
• W2032576132 hasRelatedWork W2395684592 @default.
• W2032576132 hasRelatedWork W2395972093 @default.
• W2032576132 hasVolume "270" @default.
• W2032576132 isParatext "false" @default.
• W2032576132 isRetracted "false" @default.
• W2032576132 magId "2032576132" @default.
• W2032576132 workType "article" @default.