| pubmed-article:2644141 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2644141 | lifeskim:mentions | umls-concept:C0035696 | lld:lifeskim |
| pubmed-article:2644141 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:2644141 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:2644141 | lifeskim:mentions | umls-concept:C1819634 | lld:lifeskim |
| pubmed-article:2644141 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:2644141 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:2644141 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:2644141 | pubmed:dateCreated | 1989-3-23 | lld:pubmed |
| pubmed-article:2644141 | pubmed:abstractText | The influence of insulin on the downregulation of its receptor was studied in AR42J cultured pancreatic acinar cells, a cell line that has been demonstrated to be metabolically responsive to insulin. Downregulation induced by insulin was time and dose dependent. After a 20-h incubation with 1 microM insulin, Scatchard analysis revealed approximately 80% loss of insulin receptors. Studies of receptor half-life indicated that treatment with insulin accelerated the degradation of both the alpha- and beta-subunits of the insulin receptor by 30-60%. In addition, biosynthetic-labeling studies indicated that insulin inhibited the biosynthesis of the insulin-receptor precursor by greater than 30%. This decreased biosynthesis of the precursor was associated with decreased production of mature receptor subunits. Poly(A)+ RNA was extracted from control cells and cells treated for 24 h with 100 nM insulin. Slot blots and Northern transfers revealed that insulin induced an approximately 50% decrease in insulin-receptor mRNA levels. Therefore, these studies indicate that insulin may diminish the concentration of its receptors in target cells by at least two mechanisms: acceleration of receptor degradation and inhibition of receptor biosynthesis at the level of mRNA. | lld:pubmed |
| pubmed-article:2644141 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2644141 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:2644141 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2644141 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2644141 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:2644141 | pubmed:issn | 0012-1797 | lld:pubmed |
| pubmed-article:2644141 | pubmed:author | pubmed-author:GoldfineI DID | lld:pubmed |
| pubmed-article:2644141 | pubmed:author | pubmed-author:WilliamsJ AJA | lld:pubmed |
| pubmed-article:2644141 | pubmed:author | pubmed-author:OkabayashiYY | lld:pubmed |
| pubmed-article:2644141 | pubmed:author | pubmed-author:MadduxB ABA | lld:pubmed |
| pubmed-article:2644141 | pubmed:author | pubmed-author:LogsdonC DCD | lld:pubmed |
| pubmed-article:2644141 | pubmed:author | pubmed-author:McDonaldA RAR | lld:pubmed |
| pubmed-article:2644141 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2644141 | pubmed:volume | 38 | lld:pubmed |
| pubmed-article:2644141 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2644141 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2644141 | pubmed:pagination | 182-7 | lld:pubmed |
| pubmed-article:2644141 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:meshHeading | pubmed-meshheading:2644141-... | lld:pubmed |
| pubmed-article:2644141 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2644141 | pubmed:articleTitle | Mechanisms of insulin-induced insulin-receptor downregulation. Decrease of receptor biosynthesis and mRNA levels. | lld:pubmed |
| pubmed-article:2644141 | pubmed:affiliation | Cell Biology Laboratory, Mount Zion Hospital, San Francisco, California 94120. | lld:pubmed |
| pubmed-article:2644141 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2644141 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2644141 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2644141 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2644141 | lld:pubmed |
