{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:42:06Z","timestamp":1791276126761,"version":"4.1.0"},"reference-count":55,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2001,2,1]],"date-time":"2001-02-01T00:00:00Z","timestamp":980985600000},"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":[[2001,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IL-15 mRNA levels are increased in diseases caused by human T cell lymphotropic virus type I (HTLV-I). In this study, we demonstrated that IL-15R\u03b1, the IL-15-specific binding receptor, mRNA and protein levels were also elevated in HTLV-I-infected cells. We showed that transient HTLV-I Tax expression lead to increased IL-15R\u03b1 mRNA levels. In addition, by using a reporter construct that bears the human IL-15R\u03b1 promoter, we demonstrated that Tax expression increased promoter activity by at least 4-fold. Furthermore, using promoter deletion constructs and gel shift analysis, we defined a functional NF-\u03baB-binding motif in the human IL-15R\u03b1 promoter, suggesting that Tax activation of IL-15R\u03b1 is due, in part, to the induction of NF-\u03baB. These data indicate that IL-15R\u03b1 is transcriptionally regulated by the HTLV-I Tax protein through the action of NF-\u03baB. These findings suggest a role for IL-15R\u03b1 in aberrant T cell proliferation observed in HTLV-I-associated diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.166.4.2602","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T22:56:08Z","timestamp":1398034568000},"page":"2602-2609","source":"Crossref","is-referenced-by-count":88,"title":["Human T Cell Lymphotropic Virus Type I Tax Activates IL-15R\u03b1 Gene Expression Through an NF-\u03baB Site"],"prefix":"10.1093","volume":"166","author":[{"given":"Jennifer M","family":"Mariner","sequence":"first","affiliation":[{"name":"Metabolism Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"},{"name":"Graduate Genetics Program, Institute of Biomedical Sciences, George Washington University , Washington, DC 20052"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valerie","family":"Lantz","sequence":"additional","affiliation":[{"name":"Metabolism Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A","family":"Waldmann","sequence":"additional","affiliation":[{"name":"Metabolism Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nazli","family":"Azimi","sequence":"additional","affiliation":[{"name":"Metabolism Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,2,15]]},"reference":[{"key":"2026020209152754300_R1","first-page":"4935","volume-title":"Proc. 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