期刊
VIROLOGY
卷 357, 期 1, 页码 79-90出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2006.08.011
关键词
HIV-1; integrase; integration; LEDGF/p75; protein interaction; AIDS
类别
资金
- NIAID NIH HHS [AI70042, AI52014, AI60354] Funding Source: Medline
LEDGF/p75 binding-defective IN mutant viruses were previously characterized as replication-defective, yet RNAi did not reveal an essential role for the host factor in HIV-1 replication. Correlative analyses of protein binding and viral fitness were expanded here by targeting 12 residues at the IN-LEDGF/p75 binding interface. Whereas many of the resultant viruses were defective, the majority of the INs displayed wild-type in vitro integration activities. Though an overall trend of parallel loss of LEDGF/p75 binding and HIV-1 infectivity was observed, a strict correlation was not. His-tagged INA128Q, derived from a phenotypically wild-type virus, failed to pull-down LEDGF/p75, but INA128Q was effectively recovered in a reciprocal GST pull-down assay. Under these conditions, INH171A, also derived from a phenotypically wild-type virus, interacted less efficiently than a previously described interaction-defective mutant, INQ168A. Thus, the relative affinity of the in vitro IN-LEDGF/p75 interaction is not a universal predictor of IN mutant viral fitness. (c) 2006 Elsevier Inc. All rights reserved.
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