Exclusion of Int-6 from PML Nuclear Bodies by Binding to the HTLV-I Tax Oncoprotein

• Published in: Science (American Association for the Advancement of Science) 1996-08, Vol.273 (5277), p.951-953
• Main Authors: Desbois, Christelle, Rousset, Raphaël, Bantignies, Frédéric, Jalinot, Pierre
• Format: Article
• Language: English
• Subjects: AIDS/HIV; Amino acids; Animals; Antibodies; Biological and medical sciences; Cancer cells; Cell Line; Cell Nucleus - chemistry; Cell physiology; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes; Complementary DNA; Cytoplasm; Cytoplasm - chemistry; Delta cells; Epitopes; Eukaryotic Initiation Factor-3; Fundamental and applied biological sciences. Psychology; Gene Products, tax - analysis; Gene Products, tax - metabolism; HeLa Cells; HTLV-I (Virus); Humans; Laboratory staining techniques; Mice; Molecular and cellular biology; Neoplasm Proteins; Nuclear Proteins; Plasmids; Promyelocytic Leukemia Protein; Property taxes; Proto-Oncogene Proteins - analysis; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism; Recombinant Fusion Proteins - metabolism; Transcription Factors - analysis; Transfection; Tumor Suppressor Proteins
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.273.5277.951

The Tax transactivator of the human T cell leukemia virus type I (HTLV-I) exhibits oncogenic properties. A screen for proteins interacting with Tax yielded a complementary DNA (cDNA) encoding the human Int-6 protein. In mice, the Int-6 gene can be converted into a putative dominant negative oncogene after retroviral insertion. Here, Int-6 was localized in the cell nucleus to give a speckled staining pattern superposed to that of the promyelocytic leukemia (PML) protein. The binding of Tax to Int-6 caused its redistribution from the nuclear domains to the cytoplasm. Thus, Int-6 is a component of the PML nuclear bodies and Tax disrupts its normal cellular localization by binding to it.