| pubmed-article:9139693 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C0014597 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C0003018 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C1882726 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C0021547 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C1752727 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:9139693 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:9139693 | pubmed:issue | 19 | lld:pubmed |
| pubmed-article:9139693 | pubmed:dateCreated | 1997-6-16 | lld:pubmed |
| pubmed-article:9139693 | pubmed:abstractText | Chronic stimulation of WB rat liver epithelial cells by angiotensin II (Ang II) resulted in the down-regulation of both type I and type III myo-inositol 1,4,5-trisphosphate receptors (IP3Rs). Stimulation with vasopressin, bradykinin, epidermal growth factor, or 12-O-tetradecanoylphorbol-13-acetate was without effect. Ang II-induced down-regulation of IP3Rs could be detected within 2 h and resulted in an inhibition of IP3-induced Ca2+ release from permeabilized cells. IP3R down-regulation was reversible, and both homo- and heterooligomers of IP3Rs were equally susceptible to Ang II-induced degradation. Chloroquine and NH4Cl increased the basal levels of IP3Rs by 2-fold, suggesting that the basal turnover of IP3Rs occurs via a lysosomal pathway. However, Ang II-induced degradation of IP3R was not affected by these inhibitors, suggesting that stimulated degradation of IP3Rs occurs via a non-lysosomal pathway. The cysteine protease and proteasomal inhibitor N-acetyl-Leu-Leu-norleucinal completely prevented Ang II-mediated down-regulation of IP3Rs, whereas the structural analog N-acetyl-Leu-Leu-methioninal was without effect. Lactacystin, a highly specific proteasome inhibitor, also blocked Ang II-mediated IP3R degradation. Stimulation with Ang II increased the amount of IP3R immunoprecipitated by anti-ubiquitin antibodies. We conclude that Ang II-stimulated IP3R degradation involves enhanced ubiquitination of the protein and degradation by the proteasome pathway. | lld:pubmed |
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| pubmed-article:9139693 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9139693 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9139693 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9139693 | pubmed:month | May | lld:pubmed |
| pubmed-article:9139693 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9139693 | pubmed:author | pubmed-author:JosephS KSK | lld:pubmed |
| pubmed-article:9139693 | pubmed:author | pubmed-author:BokkalaSS | lld:pubmed |
| pubmed-article:9139693 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9139693 | pubmed:day | 9 | lld:pubmed |
| pubmed-article:9139693 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9139693 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9139693 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9139693 | pubmed:pagination | 12454-61 | lld:pubmed |
| pubmed-article:9139693 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9139693 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9139693 | pubmed:articleTitle | Angiotensin II-induced down-regulation of inositol trisphosphate receptors in WB rat liver epithelial cells. Evidence for involvement of the proteasome pathway. | lld:pubmed |
| pubmed-article:9139693 | pubmed:affiliation | Department of Pathology, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania 19107, USA. | lld:pubmed |
| pubmed-article:9139693 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9139693 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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