{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T01:14:41Z","timestamp":1793236481736,"version":"4.5.0"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>PMA and ionomycin cause T cell cytokine production. We report that ionomycin alone induces IL-4 and IFN-\u03b3, but not IL-2, from in vivo- and in vitro-generated murine Th2 and Th1 cells. Ionomycin-induced cytokine production requires NFAT, p38, and calmodulin-dependent kinase IV (CaMKIV). Ionomycin induces p38 phosphorylation through a calcium-dependent, cyclosporine A-inhibitable pathway. Knocking down ASK1 inhibits ionomycin-induced p38 phosphorylation and IL-4 production. Ionomycin also activates CaMKIV, which, together with p38, induces AP-1. Cooperation between AP-1 and NFAT leads to Il4 gene transcription. p38 also regulates IL-4 production by mRNA stabilization. TCR stimulation also phosphorylates p38, partially through the calcium-dependent pathway; activated p38 is required for optimal IL-4 and IFN-\u03b3.<\/jats:p>","DOI":"10.4049\/jimmunol.181.6.3984","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:24:33Z","timestamp":1397849073000},"page":"3984-3993","source":"Crossref","is-referenced-by-count":31,"title":["Elevating Calcium in Th2 Cells Activates Multiple Pathways to Induce IL-4 Transcription and mRNA Stabilization"],"prefix":"10.1093","volume":"181","author":[{"given":"Liying","family":"Guo","sequence":"first","affiliation":[{"name":"Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph F","family":"Urban","sequence":"additional","affiliation":[{"name":"Nutrient Requirements & Functions Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture , Beltsville, MD 20705"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinfang","family":"Zhu","sequence":"additional","affiliation":[{"name":"Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William E","family":"Paul","sequence":"additional","affiliation":[{"name":"Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2008,9,15]]},"reference":[{"key":"2026012807101234200_R1","first-page":"101","article-title":"The T cell receptor: critical role of the membrane environment in receptor assembly and function","volume-title":"Annu. 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