Document 0282 DOCN M95A0282 TI Constitutively activated Jak-STAT pathway in T cells transformed with HTLV-I. DT 9510 AU Migone TS; Lin JX; Cereseto A; Mulloy JC; O'Shea JJ; Franchini G; Leonard WJ; Laboratory of Molecular Immunology, National Heart, Lung, and; Blood Institute, National Institutes of Health, Bethesda, MD; 20892, USA. SO Science. 1995 Jul 7;269(5220):79-81. Unique Identifier : AIDSLINE MED/95327953 AB Human T cell lymphotropic virus I (HTLV-I) is the etiological agent for adult T cell leukemia and tropical spastic paraparesis (also termed HTLV-I-associated myelopathy). HTLV-I-infected peripheral blood T cells exhibit an initial phase of interleukin-2 (IL-2)-dependent growth; over time, by an unknown mechanism, the cells become IL-2-independent. Whereas the Jak kinases Jak1 and Jak3 and the signal transducer and activator of transcription proteins Stat3 and Stat5 are activated in normal T cells in response to IL-2, this signaling pathway was constitutively activated in HTLV-I-transformed cells. In HTLV-I-infected cord blood lymphocytes, the transition from IL-2-dependent to IL-2-independent growth correlated with the acquisition of a constitutively activated Jak-STAT pathway, which suggests that this pathway participates in HTLV-I-mediated T cell transformation. DE Base Sequence Cell Line, Transformed *Cell Transformation, Viral Cells, Cultured DNA-Binding Proteins/*METABOLISM Enzyme Activation Fetal Blood/CYTOLOGY Human HTLV-I/*PHYSIOLOGY Interleukin-2/PHARMACOLOGY Molecular Sequence Data Phosphorylation Protein-Tyrosine Kinase/*METABOLISM Receptors, Interleukin-2/METABOLISM Signal Transduction Support, Non-U.S. Gov't T-Lymphocytes/METABOLISM/*VIROLOGY Trans-Activators/*METABOLISM JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).