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Here, we report the effects of dex in regulating the interaction between Lamin A\/C and HDAC2 in WT and A\u2010T cells. Upon administration of dex to A\u2010T cells, we first observed that the accumulation of HDAC2 on the <jats:italic>CDKN1A<\/jats:italic> promoter did not exert a repressive role on p21<jats:sup>cip1\/waf1<\/jats:sup> expression, and second, we established that HDAC2 accumulation was not dependent on Lamin A\/C. Both of these results are contrary to previous reported outcomes in other cellular models. Furthermore, large amounts of LAP2\u03b1 and FoxO3a were found to occupy the <jats:italic>CDKN1A<\/jats:italic> promoter with matched p21<jats:sup>cip1\/waf1<\/jats:sup> overexpression. Hence, in A\u2010T cells p21 could be activated as a result of a dex\u2010induced rearrangement of a multicomponent complex, composed of Lamin A\/C, HDAC2, LAP2\u03b1, pRb, E2F1, and FoxO3a, at the <jats:italic>CDKN1A<\/jats:italic> gene promoter.<\/jats:p>","DOI":"10.1002\/2211-5463.13663","type":"journal-article","created":{"date-parts":[[2023,6,24]],"date-time":"2023-06-24T10:02:41Z","timestamp":1687600961000},"page":"1459-1468","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Dexamethasone induces p21<sup>cip1\/waf1<\/sup> expression via <scp>FoxO3a<\/scp> independently of the Lamin A\/<scp>C\u2010HDAC2<\/scp> interaction in Ataxia Telangiectasia"],"prefix":"10.1002","volume":"13","author":[{"given":"Anastasia","family":"Ricci","sequence":"first","affiliation":[{"name":"Department of Biomolecular Sciences University of Urbino \u2018Carlo Bo\u2019  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