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Cited by 485

The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.

HIV-1 infection of nondividing cells through the recognition of integrase by the importin/karyopherin pathway

Open access
Gallay, Philippe, Hope, Thomas, Chin, Daniel, Trono, Didier·1997·Proceedings of the National Academy of Sciences

Abstract

The karyophilic properties of the HIV-1 nucleoprotein complex facilitate infection of nondividing cells such as macrophages and quiescent T lymphocytes, and allow the in vivo delivery of transgenes by HIV-derived retroviral vectors into terminally differentiated cells such as neurons. Although the viral matrix (MA) and Vpr proteins have previously been shown to play important roles in this process, we demonstrate here that integrase, the enzyme responsible for mediating the integration of the viral genome in the host cell chromosome, can suffice to connect the HIV-1 preintegration complex with the cell nuclear import machinery. This novel function of integrase reflects the recognition of an atypical bipartite nuclear localization signal by the importin/karyopherin pathway.

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Crossref · 10.1073/pnas.94.18.9825

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Metadata

Authors
Gallay, P., Hope, T., Chin, D., & Trono, D.
Venue
Proceedings of the National Academy of Sciences
Published
1997-09-02
Volume
94
Issue
18
Pages
9825-9830
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1982537658
Cited by
485
References
34
FWCI
10.42
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: HIV-1 infection of nondividing cells through the recognition of integrase by the importin/karyopherin pathway. https://app.cochat.ai/papers/10.1073/pnas.94.18.9825
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Gallay, P., Hope, T., Chin, D., & Trono, D. (1997). HIV-1 infection of nondividing cells through the recognition of integrase by the importin/karyopherin pathway. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.94.18.9825

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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