Biological features of the HTLV-Ip12I protein and its possible role in HTLV-I pathogenesis (Meeting abstract). NLM AIDSLINE Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.

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Biological features of the HTLV-Ip12I protein and its possible role in HTLV-I pathogenesis (Meeting abstract).

Molecular Biology of Hematopoiesis, 8th Symposium. July 9-13, 1993, Basel, Switzerland, p. 44, 1993.. Unique Identifier : AIDSLINE ICDB/95699329
Franchini G; Mulloy J; Koralnik I; Boeri E; Lomonico A; Schlegel R; Leonard W; Gallo RC; Lab. of Tumor Cell Biology, NCI, Bethesda, MD 20892


Abstract: HTLV-I induces T-cell leukemia and transforms human T-cells in vitro. The p12I protein, encoded by the HTLV-I pX region, exhibits significant amino acid sequence similarity to the E5 oncoprotein of bovine papillomavirus (BPV)-1. The p12I protein cooperates with the BPV-1 E5 oncoprotein in neoplastic transformation in vitro and binds to a cellular target of the E5 protein, the 16K component of the vacuolar H+ ATPase. Furthermore, the p12I protein physically binds the beta-chain but not the alpha-chain of the IL-2 receptor. Detail mapping of these proteins' interaction indicated that the binding occurred in the cytoplasmic portion of IL-2 receptor beta-chain, which is termed acidic region and interacts with the Src family PTK (protein tyrosine kinase) including p56lck. Recent reports indicate the lack of expression of p56lck in HTLV-I transformed T-cells, suggesting that alternative pathway for signalling by IL-2 might exist. It is tempting to speculate the p12I protein might play an important role in T-cell proliferation by HTLV-I and might be a key player in HTLV-I transformation of T-cells. The p12I domain involved in this interaction resides between the two putative transmembrane domains of the p12I as is the same portion that interacts also with the 16 kD proteins. Although biological significance of the p12I beta-chain interaction in the IL-2r signalling pathway and T-cell proliferation is not understood at this time, these findings provide new insight for potential mechanisms of HTLV-I transformation.
Keywords: Cell Division Cell Transformation, Neoplastic H(+)-Transporting ATP Synthase/METABOLISM HTLV-I Interleukin-2/METABOLISM Oncogene Proteins, Viral/*PHYSIOLOGY Sequence Homology, Amino Acid Signal Transduction T-Lymphocytes/CYTOLOGY ABSTRACTKWDcelldivisioncelltransformation,neoplastich(+)-transportingatpsynthase/metabolismhtlv-iinterleukin-2/metabolismoncogeneproteins,viral/KWDphysiologysequencehomology,aminoacidsignaltransductiont-lymphocytes/cytologyabstract
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M9521054

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