pubmed-article:12126481 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0288472 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0034792 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0249197 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C1420626 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0237477 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:12126481 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:12126481 | pubmed:issue | Pt 2 | lld:pubmed |
pubmed-article:12126481 | pubmed:dateCreated | 2002-10-4 | lld:pubmed |
pubmed-article:12126481 | pubmed:abstractText | We have assessed the growth response of Chinese-hamster ovary (CHO) cells to activation of recombinantly expressed G-protein-coupled muscarinic M(2) or M(3) acetylcholine receptors (AChRs). We show that activation of these receptors leads to divergent growth responses: M(2) AChR activation causes an increase in DNA synthesis, whereas M(3) AChR activation causes a dramatic decrease in DNA synthesis. We have characterized the M(3) AChR-mediated growth inhibition and show that it involves a G(1) phase cell-cycle arrest. Further analysis of this arrest indicates that it involves an increase in expression of the cyclin-dependent kinase (CDK) inhibitor, p21(Cip1/Waf1) (where Cip1 is CDK-interacting protein 1 and Waf1 is wild-type p53-associated fragment 1), in response to M(3) AChR activation. This increase in protein expression leads to an increase in p21(Cip1/Waf1) association with CDK2, a decrease in CDK2 activity and an accumulation of hypophosphorylated retinoblastoma protein. The increased p21(Cip1/Waf1) expression is due, at least in part, to an increase in p21(Cip1/Waf1) mRNA, and receptor-mediated changes in phosphorylation of c-Jun provide a mechanism to account for this p21(Cip1/Waf1) transcriptional regulation. Evaluation of the extracellular signal-regulated protein kinase and c-Jun N-terminal kinase activities has shown striking differences in the profiles of activation of these mitogen-activated protein kinases by the M(2) and M(3) AChRs, and their potential involvement in mediating growth arrest by the M(3) AChR is discussed. | lld:pubmed |
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pubmed-article:12126481 | pubmed:language | eng | lld:pubmed |
pubmed-article:12126481 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12126481 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12126481 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:12126481 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12126481 | pubmed:month | Oct | lld:pubmed |
pubmed-article:12126481 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:12126481 | pubmed:author | pubmed-author:ChallissR A... | lld:pubmed |
pubmed-article:12126481 | pubmed:author | pubmed-author:BurdonDrewD | lld:pubmed |
pubmed-article:12126481 | pubmed:author | pubmed-author:PatelRajnikan... | lld:pubmed |
pubmed-article:12126481 | pubmed:author | pubmed-author:BlankJonathan... | lld:pubmed |
pubmed-article:12126481 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12126481 | pubmed:day | 15 | lld:pubmed |
pubmed-article:12126481 | pubmed:volume | 367 | lld:pubmed |
pubmed-article:12126481 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12126481 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12126481 | pubmed:pagination | 549-59 | lld:pubmed |
pubmed-article:12126481 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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