{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:02:24Z","timestamp":1791306144741,"version":"4.3.1"},"reference-count":59,"publisher":"American Society of Hematology","issue":"3","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The p12I protein, encoded by the pX open reading frame I of the human T-lymphotropic virus type 1 (HTLV-1), is a hydrophobic protein that localizes to the endoplasmic reticulum and the Golgi. Although p12I contains 4 minimal proline-rich, src homology 3\u2013binding motifs (PXXP), a characteristic commonly found in proteins involved in signaling pathways, it has not been known whether p12I has a role in modulating intracellular signaling pathways. This study demonstrated that p12I binds to the cytoplasmic domain of the interleukin-2 receptor (IL-2R) \u03b2 chain that is involved in the recruitment of the Jak1 and Jak3 kinases. As a result of this interaction, p12I increases signal transducers and activators of transcription 5 (STAT5) DNA binding and transcriptional activity and this effect depends on the presence of both IL-2R \u03b2 and \u03b3c chains and Jak3. Transduction of primary human peripheral blood mononuclear cells (PBMCs) with a human immunodeficiency virus type 1\u2013based retroviral vector expressing p12I also resulted in increased STAT5 phosphorylation and DNA binding. However, p12I could increase proliferation of human PBMCs only after stimulation of T-cell receptors by treatment of cells with low concentrations of \u03b1CD3 and \u03b1CD28 antibodies. In addition, the proliferative advantage of p12I-transduced PBMCs was evident mainly at low concentrations of IL-2. Together, these data indicate that p12I may confer a proliferative advantage on HTLV-1\u2013infected cells in the presence of suboptimal antigen stimulation and that this event may account for the clonal proliferation of infected T cells in vivo.<\/jats:p>","DOI":"10.1182\/blood.v98.3.823","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T08:46:47Z","timestamp":1027759607000},"page":"823-829","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":99,"title":["HTLV-1 p12I protein enhances STAT5 activation and decreases the interleukin-2 requirement for proliferation of primary human peripheral blood mononuclear cells"],"prefix":"10.1182","volume":"98","author":[{"given":"Christophe","family":"Nicot","sequence":"first","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James C.","family":"Mulloy","sequence":"additional","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria G.","family":"Ferrari","sequence":"additional","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie M.","family":"Johnson","sequence":"additional","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaisong","family":"Fu","sequence":"additional","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Risaku","family":"Fukumoto","sequence":"additional","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raffaella","family":"Trovato","sequence":"additional","affiliation":[{"name":"From the National Cancer Institute, Basic Research Laboratory, Bethesda, MD; and the National Heart, Lung, and Blood Institute, Laboratory of Molecular Immunology, Bethesda, 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