- 作者: Dorothy Trihn; Kuan-Teh Jeang; Oliver J. Semmes
- 作者服務機構: a Molecular Virology Section, Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Md., and; b Department of Microbiology, Myles H. Thaler Center, University of Virginia, Charlottesville, Va., USA
- 中文摘要: --
- 英文摘要: Human T cell leukemia virus type I (HTLV-I) has been linked to the development of an aggressive lymphoproliferative disorder (adult T cell leukemia), a chronic neurodegenerative presentation (HTLV-I-associated myelopathy/ tropical spastic paraparesis) and numerous less well-defined inflammatory conditions. The viral regulatory protein Tax has been implicated in cellular transformation events leading to the onset of adult T cell leukemia. Details on the stepwise processes through which Tax induces morphological changes in cells are poorly understood. We show here that Tax can bind to a class of intermediate filaments, the cytokeratins (Ker). Tax interacts with the 1B helical coil of keratin 8, a domain critical for higher-order intermediate filament matrix formation. Expression of Tax in epithelial cells visibly altered the structural pattern of the Ker network. In a T lymphocyte cell line, induction of Tax expression resulted in increased cellular adherence/invasion of Matrigel filters. We propose that one aspect of Tax function is the induction of morphological changes in cellular cytoskeletal structures. This finding for Tax-expressing cells might be one factor contributing directly to the pathogenesis of HTLV-I disease(s).
- 中文關鍵字: --
- 英文關鍵字: HTLV-I; Cytokeratin ; Invasive ; Motility ; HAM/TSP ; Regulatory protein