Functional cross-talk of HIV-1 Tat with p53 through its C-terminal domain

被引：33

作者：

Ariumi, Y ^{[1
]}

Kaida, A ^{[1
]}

Hatanaka, M ^{[1
]}

Shimotohno, K ^{[1
]}

机构：

[1] Kyoto Univ, Inst Virus Res, Sakyo Ku, Kyoto 6068507, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 287卷 / 02期

关键词：

AIDS; HIV-1; Tat; p53; NF-kappa B; CBP/p300; replication;

D O I：

10.1006/bbrc.2001.5626

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：

Human immunodeficiency virus type 1 (HIV-1) Tat repressed the p53-dependent gene expression through its C-terminal domain of Tat (amino acid residues 73-86) independent of the involvement of NF-kappaB and coactivator CBP/p300. Although Tat did not directly bind to p53, this repression required the N-terminal domain of p53. In contrast, Tat and p53 cooperated in the activation of HIV-1 gene expression. Thus, the crosstalk between Tat and p53 may be linked with cellular transformation by HIV-1 infection or activation of HIV-1 replication. (C) 2001 Academic Press.

引用

收藏

页码：556 / 561

页数：6

相关论文

共 30 条

[1] HTLV-1 Tax oncoprotein represses the p53-mediated trans-activation function through coactivator CBP sequestration [J].

Ariumi, Y ;

Kaida, A ;

Lin, JY ;

Hirota, M ;

Masui, O ;

Yamaoka, S ;

Taya, Y ;

Shimotohno, K .

ONCOGENE, 2000, 19 (12) :1491-1499

[2] Recruitment of p300/CBP in p53-dependent signal pathways [J].

Avantaggiati, ML ;

Ogryzko, V ;

Gardner, K ;

Giordano, A ;

Levine, AS ;

Kelly, K .

CELL, 1997, 89 (07) :1175-1184

[3] Activation of integrated provirus requires histone acetyltransferase - p300 AND P/CAF are coactivators for HIV-1 Tat [J].

Benkirane, M ;

Chun, RF ;

Xiao, H ;

Ogryzko, VV ;

Howard, BH ;

Nakatani, Y ;

Jeang, KT .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (38) :24898-24905

[4] The Tat protein of human immunodeficiency virus type 1 is a substrate and inhibitor of the interferon-induced, virally activated protein kinase, PKR [J].

Brand, SR ;

Kobayashi, R ;

Mathews, MB .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (13) :8388-8395

[5] Loss of G1/S checkpoint in human immunodeficiency virus type 1-infected cells is associated with a lack of cyclin-dependent kinase inhibitor p21/Waf1 [J].

Clark, E ;

Santiago, F ;

Deng, LW ;

Chong, SY ;

de la Fuente, C ;

Wang, L ;

Fu, P ;

Stein, D ;

Denny, T ;

Lanka, V ;

Mozafari, F ;

Okamoto, T ;

Kashanchi, F .

JOURNAL OF VIROLOGY, 2000, 74 (11) :5040-5052

[6]

CORALLINI A, 1993, CANCER RES, V53, P5569

[7] Human immunodeficiency virus type 1 Tat protein activates transcription factor NF-κB through the cellular interferon-inducible, double-stranded RNA-dependent protein kinase, PKR [J].

Demarchi, F ;

Gutierrez, MI ;

Giacca, M .

JOURNAL OF VIROLOGY, 1999, 73 (08) :7080-7086

[8] THE TUMOR-SUPPRESSOR PROTEIN P53 STRONGLY ALTERS HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REPLICATION [J].

DUAN, LX ;

OZAKI, I ;

OAKES, JW ;

TAYLOR, JP ;

KHALILI, K ;

POMERANTZ, RJ .

JOURNAL OF VIROLOGY, 1994, 68 (07) :4302-4313

[9]

Endo S, 1989, Virus Genes, V3, P99

[10] SYNERGY BETWEEN BASIC FIBROBLAST GROWTH-FACTOR AND HIV-I TAT PROTEIN IN INDUCTION OF KAPOSIS-SARCOMA [J].

ENSOLI, B ;

GENDELMAN, R ;

MARKHAM, P ;

FIORELLI, V ;

COLOMBINI, S ;

RAFFELD, M ;

CAFARO, A ;

CHANG, HK ;

BRADY, JN ;

GALLO, RC .

NATURE, 1994, 371 (6499) :674-680