FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1515059043> ?p ?o ?g. }

• W1515059043 endingPage "13497" @default.
• W1515059043 startingPage "13488" @default.
• W1515059043 abstract "The long-term regulatory effect of insulin on glucose transport activity and glucose transporter expression was examined in Chinese hamster ovary (CHO) transfectants that overexpress either human insulin receptors of the wild type (CHO-R cells) or human insulin receptors mutated at two major autophosphorylation sites, Tyr1162 and Tyr1163 (CHO-Y2 cells). Previous studies showed that, when acutely stimulated by insulin, CHO-Y2 cells exhibit decreased receptor kinase activity along with decreased signaling of several pathways, including that for glucose transport, as compared with CHO-R cells. We now report the following. (i) When treated for 24 h with insulin (10(-10) to 10(-6) M), CHO-R and CHO-Y2 cells displayed closely similar concentration-dependent increases in 2-deoxyglucose uptake. In both transfectants, the maximal insulin-induced increase (approximately 3.5-fold) in uptake was cycloheximide-sensitive and was paralleled by equivalent increases in the levels of GLUT-1 immunoreactive protein and mRNA. (ii) By contrast, under similar conditions, CHO-Y2 cells exhibited a marked decrease in their response to insulin for [U-14C]glucose incorporation into glycogen (decreased sensitivity and maximal responsiveness) and for [U-14C]leucine incorporation into protein (decreased sensitivity) as compared with CHO-R cells. (iii) After a 24-h treatment with 10(-7) M insulin, CHO-R (but not CHO-Y2) cells showed a decreased ability to respond to a subsequent acute insulin stimulation of either receptor exogenous kinase activity or 2-deoxyglucose uptake as compared with respective untreated controls. These results indicate that (i) insulin receptors mutated at Tyr1162 and Tyr1163 retain normal signaling of the long-term stimulatory effect of insulin on glucose transport activity and GLUT-1 expression, but not on glycogenesis and overall protein synthesis; (ii) these three insulin signaling pathways may be triggered by distinct domains of the insulin receptor beta-subunit; and (iii) wild-type (but not twin-tyrosine mutant) receptors undergo negative regulation by chronic insulin treatment for subsequent signaling of acute biological actions of insulin." @default.
• W1515059043 created "2016-06-24" @default.
• W1515059043 creator A5007917651 @default.
• W1515059043 creator A5008492739 @default.
• W1515059043 creator A5030245773 @default.
• W1515059043 creator A5035291390 @default.
• W1515059043 creator A5038672868 @default.
• W1515059043 creator A5052417844 @default.
• W1515059043 creator A5064769883 @default.
• W1515059043 creator A5068988380 @default.
• W1515059043 creator A5078442933 @default.
• W1515059043 creator A5009668038 @default.
• W1515059043 date "1992-07-01" @default.
• W1515059043 modified "2023-10-18" @default.
• W1515059043 title "Differential role of insulin receptor autophosphorylation sites 1162 and 1163 in the long-term insulin stimulation of glucose transport, glycogenesis, and protein synthesis." @default.
• W1515059043 cites W1491163588 @default.
• W1515059043 cites W1493815818 @default.
• W1515059043 cites W1496640920 @default.
• W1515059043 cites W1497626374 @default.
• W1515059043 cites W1501935523 @default.
• W1515059043 cites W1503320375 @default.
• W1515059043 cites W1503482502 @default.
• W1515059043 cites W1505075493 @default.
• W1515059043 cites W1513692363 @default.
• W1515059043 cites W1530657391 @default.
• W1515059043 cites W1533778697 @default.
• W1515059043 cites W1534439131 @default.
• W1515059043 cites W1542561369 @default.
• W1515059043 cites W1543750783 @default.
• W1515059043 cites W1549634562 @default.
• W1515059043 cites W1560314955 @default.
• W1515059043 cites W1563180403 @default.
• W1515059043 cites W1567970416 @default.
• W1515059043 cites W1569546742 @default.
• W1515059043 cites W1579383379 @default.
• W1515059043 cites W1603388614 @default.
• W1515059043 cites W1621742514 @default.
• W1515059043 cites W1645918562 @default.
• W1515059043 cites W1871951699 @default.
• W1515059043 cites W1919421236 @default.
• W1515059043 cites W1963840316 @default.
• W1515059043 cites W1964592662 @default.
• W1515059043 cites W1971060217 @default.
• W1515059043 cites W1974473413 @default.
• W1515059043 cites W1976177239 @default.
• W1515059043 cites W1987488904 @default.
• W1515059043 cites W1994214524 @default.
• W1515059043 cites W1997950286 @default.
• W1515059043 cites W2001736800 @default.
• W1515059043 cites W2007796735 @default.
• W1515059043 cites W2008596330 @default.
• W1515059043 cites W2013122740 @default.
• W1515059043 cites W2015707895 @default.
• W1515059043 cites W2016910304 @default.
• W1515059043 cites W2017888726 @default.
• W1515059043 cites W2018751358 @default.
• W1515059043 cites W2030156849 @default.
• W1515059043 cites W2036628453 @default.
• W1515059043 cites W2036650450 @default.
• W1515059043 cites W2036689221 @default.
• W1515059043 cites W2050560415 @default.
• W1515059043 cites W2053849194 @default.
• W1515059043 cites W2072963071 @default.
• W1515059043 cites W2077392184 @default.
• W1515059043 cites W2095262331 @default.
• W1515059043 cites W2100837269 @default.
• W1515059043 cites W2116127446 @default.
• W1515059043 cites W2116968498 @default.
• W1515059043 cites W2122567567 @default.
• W1515059043 cites W2127891186 @default.
• W1515059043 cites W4251494161 @default.
• W1515059043 cites W4293247451 @default.
• W1515059043 cites W80983735 @default.
• W1515059043 doi "https://doi.org/10.1016/s0021-9258(18)42238-7" @default.
• W1515059043 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/1618850" @default.
• W1515059043 hasPublicationYear "1992" @default.
• W1515059043 type Work @default.
• W1515059043 sameAs 1515059043 @default.
• W1515059043 citedByCount "18" @default.
• W1515059043 countsByYear W15150590432012 @default.
• W1515059043 crossrefType "journal-article" @default.
• W1515059043 hasAuthorship W1515059043A5007917651 @default.
• W1515059043 hasAuthorship W1515059043A5008492739 @default.
• W1515059043 hasAuthorship W1515059043A5009668038 @default.
• W1515059043 hasAuthorship W1515059043A5030245773 @default.
• W1515059043 hasAuthorship W1515059043A5035291390 @default.
• W1515059043 hasAuthorship W1515059043A5038672868 @default.
• W1515059043 hasAuthorship W1515059043A5052417844 @default.
• W1515059043 hasAuthorship W1515059043A5064769883 @default.
• W1515059043 hasAuthorship W1515059043A5068988380 @default.
• W1515059043 hasAuthorship W1515059043A5078442933 @default.
• W1515059043 hasBestOaLocation W15150590431 @default.
• W1515059043 hasConcept C109384507 @default.
• W1515059043 hasConcept C112446052 @default.
• W1515059043 hasConcept C11960822 @default.
• W1515059043 hasConcept C126322002 @default.
• W1515059043 hasConcept C134018914 @default.
• W1515059043 hasConcept C150109051 @default.

• next