Upregulation of survivin by HIV-1 Vpr

被引:45
作者
Zhu, Y
Roshall, M
Li, F
Blackett, J
Planelles, V
机构
[1] Univ Utah, Sch Med, Dept Pathol, Salt Lake City, UT 84132 USA
[2] Univ Rochester, Dept Microbiol & Immunol, Rochester, NY 14642 USA
[3] Roswell Pk Canc Inst, Grace Canc Drug Ctr, Buffalo, NY 14263 USA
关键词
apoptosis; cell cycle; HIV-1; survivin; Vpr;
D O I
10.1023/A:1021653119934
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The human survivin gene belongs to the family of inhibitor of apoptosis proteins (IAP) and is involved in apoptosis inhibition and regulation of cell division. The survivin gene is the only member of the IAP family whose expression is known to be regulated through the cell cycle. Survivin expression reaches the highest levels during the G(2)/M transition and then is rapidly degraded during the G(1) phase. Here we report that the human immunodeficiency virus type 1 (HIV-1) upregulates Survivin expression via survivin promoter transactivation. Vpr, an HIV-1 accessory protein that induces cell cycle arrest in G(2)/M, is necessary and sufficient for this effect. Blocking Vpr-induced G(2)/M arrest leads to elimination of the survivin promoter transactivation by Vpr. Our results suggest that Survivin may be actively involved in regulating cell viability during HIV-1 infection.
引用
收藏
页码:71 / 79
页数:9
相关论文
共 40 条
[1]   The molecular basis and potential role of survivin in cancer diagnosis and therapy [J].
Altieri, DC .
TRENDS IN MOLECULAR MEDICINE, 2001, 7 (12) :542-547
[2]   A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma [J].
Ambrosini, G ;
Adida, C ;
Altieri, DC .
NATURE MEDICINE, 1997, 3 (08) :917-921
[3]   An inducible human immunodeficiency virus type 1 (HIV-1) vector which effectively suppresses HIV-1 replication [J].
An, DS ;
Morizono, K ;
Li, QX ;
Mao, SH ;
Lu, S ;
Chen, ISY .
JOURNAL OF VIROLOGY, 1999, 73 (09) :7671-7677
[4]   VESICULAR STOMATITIS-VIRUS G GLYCOPROTEIN PSEUDOTYPED RETROVIRAL VECTORS - CONCENTRATION TO VERY HIGH-TITER AND EFFICIENT GENE-TRANSFER INTO MAMMALIAN AND NONMAMMALIAN CELLS [J].
BURNS, JC ;
FRIEDMANN, T ;
DRIEVER, W ;
BURRASCANO, M ;
YEE, JK .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :8033-8037
[5]   Differential apoptosis effects of primate lentiviral Vpr and Vpx in mammalian cells [J].
Chang, LJ ;
Chen, CH ;
Urlacher, V ;
Lee, TF .
JOURNAL OF BIOMEDICAL SCIENCE, 2000, 7 (04) :322-333
[6]   Down-regulation of survivin by antisense oligonucleotides increases apoptosis, inhibits cytokinesis and anchorage-independent growth [J].
Chen, J ;
Wu, W ;
Tahir, SK ;
Kroeger, PE ;
Rosenberg, SH ;
Cowsert, LM ;
Bennett, F ;
Krajewski, S ;
Krajewska, M ;
Welsh, K ;
Reed, JC ;
Ng, SC .
NEOPLASIA, 2000, 2 (03) :235-241
[7]   PREVENTION OF APOPTOSIS BY A BACULOVIRUS GENE DURING INFECTION OF INSECT CELLS [J].
CLEM, RJ ;
FECHHEIMER, M ;
MILLER, LK .
SCIENCE, 1991, 254 (5036) :1388-1390
[8]  
COHEN EA, 1990, J ACQ IMMUN DEF SYND, V3, P11
[9]   Dual role of the HIV-1 vpr protein in the modulation of the apoptotic response of T cells [J].
Conti, L ;
Matarrese, P ;
Varano, B ;
Gauzzi, MC ;
Sato, A ;
Malorni, W ;
Belardelli, F ;
Gessani, S .
JOURNAL OF IMMUNOLOGY, 2000, 165 (06) :3293-3300
[10]   Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition [J].
Du, CY ;
Fang, M ;
Li, YC ;
Li, L ;
Wang, XD .
CELL, 2000, 102 (01) :33-42