{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T16:37:52Z","timestamp":1789749472020,"version":"4.0.1"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"1","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":["eur j endocrinol"],"published-print":{"date-parts":[[2005,7]]},"abstract":"<jats:p><jats:italic>Objective<\/jats:italic>: Thyrotropin activates the cAMP pathway in thyroid cells, and stimulates cell cycle progression in cooperation with insulin or insulin-like growth factor-I. Because p38 mitogen-activated protein kinases (p38 MAPKs) were stimulated by cAMP in the FRTL-5 rat thyroid cell line, we investigated (i) the effect of the specific inhibition of p38 MAPKs on FRTL-5 cell proliferation and (ii) the mechanism of action of p38 MAPKs on cell cycle control, by studying the expression and\/or the activity of several cell cycle regulatory proteins in FRTL-5 cells.<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>: DNA synthesis was monitored by incorporation of [<jats:sup>3<\/jats:sup>H]thymidine into DNA and the cell cycle distribution was assessed by fluorescence-activated cell sorter analysis. Expression of cell cycle regulatory proteins was determined by Western blot analysis. Cyclin-dependent kinase 2 (Cdk2) activity associated to cyclin E was immunoprecipitated and was measured by an<jats:italic>in vitro<\/jats:italic>kinase assay.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>: SB203580, an inhibitor of \u03b1 and \u03b2 isoforms of p38 MAPKs, but not its inactive analog SB202474, inhibited DNA synthesis and the G1-S transition induced by forskolin plus insulin. SB203580 inhibited specifically p38 MAPK activity but not other kinase activities such as Akt and p70-S6 kinase. Treatment of FRTL-5 cells with SB203580 decreased total and cyclin E-associated Cdk2 kinase activity stimulated with forskolin and insulin. However, inhibition of p38 MAPKs by SB203580 was without effect on total cyclin E and Cdk2 levels. The decrease in Cdk2 kinase activity caused by SB203580 treatment was not due to an increased expression of p21<jats:sup>Cip1<\/jats:sup>or p27<jats:sup>Kip1<\/jats:sup>inhibitory proteins. In addition, SB203580 affected neither Cdc25A phosphatase expression nor Cdk2 Tyr-15 phosphorylation. Inhibition of p38 MAPKs decreased Cdk2-cyclin E activation by regulating the subcellular localization of Cdk2 and its phosphorylation on Thr-160.<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>: These results indicate that p38 MAPK activity is involved in the regulation of cell cycle progression in FRTL-5 thyroid cells, at least in part by increasing nuclear Cdk2 activity.<\/jats:p>","DOI":"10.1530\/eje.1.01942","type":"journal-article","created":{"date-parts":[[2005,7,1]],"date-time":"2005-07-01T03:43:31Z","timestamp":1120189411000},"page":"123-133","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":16,"title":["p38 mitogen-activated protein kinase contributes to cell cycle regulation by cAMP in FRTL-5 thyroid 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