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Journal of Virology, December 2004, p. 14033-14038, Vol. 78, No. 24
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.24.14033-14038.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Takashi Komatsu,
,
Mary E. Ballestas,
and
Kenneth M. Kaye*
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
Received 4 March 2004/ Accepted 27 July 2004
In latent infection, Kaposi's sarcoma-associated herpesvirus (KSHV) latency-associated nuclear antigen 1 (LANA1)-specific binding to KSHV terminal repeat DNA mediates multicopy episome persistence. We now use electrophoretic mobility shift assays to investigate LANA1 binding to its 20-bp cognate sequence. Mutations at positions 6, 7, and 8 (6CCC8) severely reduced LANA1 binding, whereas mutations at other positions only modestly reduced binding. Since 6CCC8 is in the 5' half of an inverted repeat sequence, these results are consistent with an asymmetric role for the inverted repeat in LANA1 binding.
V.S. and T.K. contributed equally to this work.
Present address: PTC Therapeutics, South Plainfield, NJ 07080.
Present address: Human Genetics Program and Department of Biochemistry, Tulane Medical School, New Orleans, LA 70112.
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