AN EBNA-1-DEPENDENT ENHANCER ACTS FROM A DISTANCE OF 10-KILOBASE PAIRS TO INCREASE EXPRESSION OF THE EPSTEIN-BARR-VIRUS LMP GENE

被引：162

作者：

GAHN, TA ^{[1
]}

SUGDEN, B ^{[1
]}

机构：

[1] UNIV WISCONSIN, MCARDLE LAB CANC RES, MADISON, WI 53706 USA

来源：

JOURNAL OF VIROLOGY | 1995年 / 69卷 / 04期

关键词：

D O I：

10.1128/JVI.69.4.2633-2636.1995

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Upon infection of human B lymphocytes, the 172-kbp Epstein-Barr virus genome forms a covalently closed circle via its terminal repeats. This event brings all of the promoters that control expression of the latent gene products, and the viral origin of plasmid replication, oriP, within a 20-kbp stretch of contiguous DNA. We have found that the EBNA-1-dependent transcriptional enhancer FR, located in oriP, increased the expression of a tagged viral oncogene encoding the latent membrane protein (LMP) up to 200-fold in normal Epstein-Barr virus-positive cells. The effect of FR was exerted across 10 kbp of viral DNA that spans the circularized ends of the viral genome. Enhancement of the tagged LMP gene by FR/EBNA-1 did not require the EBNA-2-responsive element.

引用

页码：2633 / 2636

页数：4

共 24 条

[11] EBNA-2 UP-REGULATION OF EPSTEIN-BARR-VIRUS LATENCY PROMOTERS AND THE CELLULAR CD23 PROMOTER UTILIZES A COMMON TARGETING INTERMEDIATE, CBF1 [J].

LING, PD ;

HSIEH, JJD ;

RUF, IK ;

RAWLINS, DR ;

HAYWARD, SD .

JOURNAL OF VIROLOGY, 1994, 68 (09) :5375-5383

[12] THE EPSTEIN-BARR-VIRUS IMMORTALIZING PROTEIN EBNA-2 IS TARGETED TO DNA BY A CELLULAR ENHANCER-BINDING PROTEIN [J].

LING, PD ;

RAWLINS, DR ;

HAYWARD, SD .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (20) :9237-9241

[13]

MIDDLETON T, 1991, ADV VIRAL RES, P19

[14]

Pallesen Gorm, 1993, V62, P179

[15] SEQUENCE-SPECIFIC DNA-BINDING OF THE EPSTEIN-BARR VIRUS NUCLEAR ANTIGEN (EBNA-1) TO CLUSTERED SITES IN THE PLASMID MAINTENANCE REGION [J].

RAWLINS, DR ;

MILMAN, G ;

HAYWARD, SD ;

HAYWARD, GS .

CELL, 1985, 42 (03) :859-868

[16] TRANS ACTIVATION OF AN EPSTEIN-BARR VIRAL TRANSCRIPTIONAL ENHANCER BY THE EPSTEIN-BARR VIRAL NUCLEAR ANTIGEN-1 [J].

REISMAN, D ;

SUGDEN, B .

MOLECULAR AND CELLULAR BIOLOGY, 1986, 6 (11) :3838-3846

[17] A PUTATIVE ORIGIN OF REPLICATION OF PLASMIDS DERIVED FROM EPSTEIN-BARR VIRUS IS COMPOSED O 2 CIS-ACTING COMPONENTS [J].

REISMAN, D ;

YATES, J ;

SUGDEN, B .

MOLECULAR AND CELLULAR BIOLOGY, 1985, 5 (08) :1822-1832

[18] INFLUENCES OF BURKITTS-LYMPHOMA AND PRIMARY B-CELLS ON LATENT GENE-EXPRESSION BY THE NONIMMORTALIZING P3J-HR-1 STRAIN OF EPSTEIN-BARR VIRUS [J].

ROONEY, C ;

HOWE, JG ;

SPECK, SH ;

MILLER, G .

JOURNAL OF VIROLOGY, 1989, 63 (04) :1531-1539

[19] HOST-CELL AND EBNA-2 REGULATION OF EPSTEIN-BARR-VIRUS LATENT-CYCLE PROMOTER ACTIVITY IN LYMPHOCYTES-B [J].

ROONEY, CM ;

BRIMMELL, M ;

BUSCHLE, M ;

ALLAN, G ;

FARRELL, PJ ;

KOLMAN, JL .

JOURNAL OF VIROLOGY, 1992, 66 (01) :496-504

[20]

SPECK SH, 1989, ADV VIRAL ONCOL, V8, P133

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