Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 10, Issue -, Pages 919-930Publisher
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/1586
Keywords
HTLV-1; p53; tax; cancer; cell-cycle; review
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Funding
- NATIONAL CANCER INSTITUTE [Z01BC005691, ZIABC005691] Funding Source: NIH RePORTER
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Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia and tropical spastic paraparesis/ HTLV-1 associated myelopathy (TSP/HAM). Although the precise mechanism of HTLV-1 oncogenesis remains unclear, the pathogenesis has been linked to the pleiotropic activity of the viral transcriptional activator protein Tax. Tax has been shown to regulate viral and cellular gene expression and to functionally interfere with proteins involved in cell-cycle progression and DNA repair. This review will concentrate on the ability of Tax to promote cellular proliferation through activation of the NF-kappa B pathway while inhibiting the cell-cycle checkpoint and apoptotic function of the tumor suppressor gene p53.
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