{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T04:00:02Z","timestamp":1790913602508,"version":"4.1.0"},"reference-count":49,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p> Calcineurin mediates repression of plasma membrane Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup>-ATPase-4 (PMCA4) expression in neurons, whereas c-Myb is known to repress PMCA1 expression in vascular smooth muscle cells (VSMC). Here, we describe a novel mouse VSMC line (MOVAS) in which <jats:sup>45<\/jats:sup>Ca efflux rates decreased 50%, fura 2-AM-based intracellular Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup> concentrations ([Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>) increased twofold, and real-time RT-PCR and Western blot revealed a \u223c40% decrease in PMCA4 expression levels from G<jats:sub>0<\/jats:sub> to G<jats:sub>1<\/jats:sub>\/S in the cell cycle, where PMCA4 constituted \u223c20% of total PMCA protein. Although calcineurin activity increased fivefold as MOVAS progressed from G<jats:sub>0<\/jats:sub> to G<jats:sub>1<\/jats:sub>\/S, inhibition of this increase with either BAPTA or retroviral transduction with peptide inhibitors of calcineurin (CAIN), or its downstream target nuclear factor of activated T cells (NFAT) (VIVIT), had no effect on the repression of PMCA4 mRNA expression at G<jats:sub>1<\/jats:sub>\/S. By contrast, Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup>-independent activity of the calmodulin-dependent protein kinase-II (CaMK-II) increased eightfold as MOVAS progressed from G<jats:sub>0<\/jats:sub> to G<jats:sub>1<\/jats:sub>\/S, and treatment with an inhibitor of CaMK-II (KN-93) or transduction of a c-Myb-neutralizing antibody significantly alleviated the G<jats:sub>1<\/jats:sub>\/S-associated repression of PMCA4. These data show that G<jats:sub>1<\/jats:sub>\/S-specific PMCA4 repression in proliferating VSMC is brought about by c-Myb and CaMK-II and that calcineurin may regulate cell cycle-associated [Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub> through alternate targets. <\/jats:p>","DOI":"10.1152\/ajpcell.00518.2002","type":"journal-article","created":{"date-parts":[[2013,5,14]],"date-time":"2013-05-14T00:15:05Z","timestamp":1368490505000},"page":"C88-C95","source":"Crossref","is-referenced-by-count":46,"title":["Calcineurin-independent regulation of plasma membrane  Ca<sup>2<\/sup><sup>+<\/sup> ATPase-4 in the vascular smooth muscle cell  cycle"],"prefix":"10.1152","volume":"285","author":[{"given":"Talat","family":"Afroze","sequence":"first","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li L.","family":"Yang","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changsen","family":"Wang","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Gros","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Waseem","family":"Kalair","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abu N.","family":"Hoque","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Imran N.","family":"Mungrue","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziping","family":"Zhu","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mansoor","family":"Husain","sequence":"additional","affiliation":[{"name":"Heart and Stroke Richard Lewar Centre of Excellence, University of  Toronto, Division of Cell and Molecular Biology, Toronto General Hospital  Research Institute, and Department of Medicine, University of Toronto,  Toronto, Ontario, Canada M5G-2C4"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"crossref","unstructured":"Afroze T and  Husain M. c-Myb-binding sites mediate G1\/S-associated  repression of the plasma membrane Ca2+-ATPase-1  promoter. 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Circ Res 92: 314\u2013321,  2003.","DOI":"10.1161\/01.RES.0000056758.73215.5A"}],"container-title":["American Journal of Physiology-Cell Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajpcell.00518.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:05:42Z","timestamp":1718651142000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajpcell.00518.2002"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2003,7]]},"references-count":49,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2003,7]]}},"alternative-id":["10.1152\/ajpcell.00518.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajpcell.00518.2002","relation":{},"ISSN":["0363-6143","1522-1563"],"issn-type":[{"value":"0363-6143","type":"print"},{"value":"1522-1563","type":"electronic"}],"subject":[],"published":{"date-parts":[[2003,7]]}}}