Human immunodeficiency virus (HIV) transactivator Tat is a potent activator of both viral and cellular genes. Tat has also been implicated in the development of AIDS-related malignancy. Here, we show that Tat physically and functionally is able to sequester the cell cycle check point protein p53. This sequestration results in non-functional promoter activity of cyclin-dependent kinase/cyclin inhibitor, namely p21 (Waf1). Therefore, it is proposed that a Tat/p53 complex in vivo may deregulate p53 responsive genes, hence allowing for deregulation of check point, which may lead to development of malignancies.
Duvall, J. & Kashanchi, F. (1997). Functional and Physical Consequence of Human Immunodefficiency Virus Transactivator TAT Interaction with Human Cell Cycle Regulator p53. Iranian Biomedical Journal, 1(4), 1–9.
MLA
Duvall, J., & Kashanchi, F. "Functional and Physical Consequence of Human Immunodefficiency Virus Transactivator TAT Interaction with Human Cell Cycle Regulator p53", Iranian Biomedical Journal, 1, 4, 1997, 1–9.
HARVARD
Duvall, J., & Kashanchi, F. (1997). 'Functional and Physical Consequence of Human Immunodefficiency Virus Transactivator TAT Interaction with Human Cell Cycle Regulator p53', Iranian Biomedical Journal, 1(4), pp. 1–9.
CHICAGO
Duvall, J. & Kashanchi, F., "Functional and Physical Consequence of Human Immunodefficiency Virus Transactivator TAT Interaction with Human Cell Cycle Regulator p53." Iranian Biomedical Journal, 1 4 (1997): 1–9,
VANCOUVER
Duvall J., Kashanchi F. Functional and Physical Consequence of Human Immunodefficiency Virus Transactivator TAT Interaction with Human Cell Cycle Regulator p53. Iranian Biomedical Journal. 1997;1(4):1–9.
