D
Douglas C. Braaten
Researcher at Washington University in St. Louis
Publications - 20
Citations - 2000
Douglas C. Braaten is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Cyclophilin A & Cyclophilin. The author has an hindex of 15, co-authored 19 publications receiving 1955 citations. Previous affiliations of Douglas C. Braaten include Columbia University.
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Human immunodeficiency virus type 1 Vpr arrests the cell cycle in G2 by inhibiting the activation of p34cdc2-cyclin B.
TL;DR: It is demonstrated that expression of vpr, either in the context of a provirus or from an independent genetic element, induces a discrete cell cycle arrest, with cells containing 4N DNA, indicating vpr's potential contribution to the cellular pathology associated with HIV-1 infection.
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Cyclophilin A is required for an early step in the life cycle of human immunodeficiency virus type 1 before the initiation of reverse transcription.
TL;DR: Results indicate that CyPA is required for an early step in the HIV-1 life cycle following receptor binding and membrane fusion but preceding reverse transcription, the first cellular protein other than the cell surface receptor shown to be required for a early event in the life cycle of a retrovirus.
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Cyclophilin A regulates HIV-1 infectivity, as demonstrated by gene targeting in human T cells
Douglas C. Braaten,Jeremy Luban +1 more
TL;DR: It is formally demonstrated that CypA regulates the infectivity of HIV‐1 virions by deleting the gene encoding CypA in human CD4+ T cells by homologous recombination and stable re‐expression in PPIA−/− cells restored HIV‐ 1 replication to an extent that correlated with steady‐state levels of CypA.
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Cyclophilin A is required for the replication of group M human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus SIV(CPZ)GAB but not group O HIV-1 or other primate immunodeficiency viruses.
TL;DR: These studies identify the first phenotypic difference between HIV-1 group M and group O and are consistent with phylogenetic studies suggesting that the two HIV- 1 groups were introduced into human populations via separate zoonotic transmission events.
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Cyclosporine A-resistant human immunodeficiency virus type 1 mutants demonstrate that Gag encodes the functional target of cyclophilin A.
TL;DR: These experiments demonstrate that, in addition to its ability to package cyclophilin A into virions, gag encodes the functional target of cyclosporine A, indicating that the drug-resistant mutants do not require virion-associated cyclophin A to initiate infection.