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Bryan R. Cullen

Researcher at Duke University

Publications -  376
Citations -  52946

Bryan R. Cullen is an academic researcher from Duke University. The author has contributed to research in topics: RNA & Gene. The author has an hindex of 121, co-authored 371 publications receiving 50901 citations. Previous affiliations of Bryan R. Cullen include Hoffmann-La Roche & University of Medicine and Dentistry of New Jersey.

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Characterization of Staphylococcus aureus Cas9: a smaller Cas9 for all-in-one adeno-associated virus delivery and paired nickase applications

TL;DR: The results reveal an S. aureus Cas9 that is effective for a variety of genome engineering purposes, including paired nickase approaches and all-in-one delivery of Cas9 and multiple gRNA expression cassettes with AAV vectors.
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Human APOBEC3B is a potent inhibitor of HIV-1 infectivity and is resistant to HIV-1 Vif.

TL;DR: It is reported that a third human protein, APOBEC3B, is able to suppress the infectivity of both Vif-deficient and wild-type HIV-1 with equal efficiency.
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Trans-activation of human immunodeficiency virus gene expression is mediated by nuclear events

TL;DR: Results suggest that tat could play a role in human immunodeficiency virus replication essentially similar to that proposed for the trans-acting nuclear gene products described for several other virus species.
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Mutational analysis of the trans-activation-responsive region of the human immunodeficiency virus type I long terminal repeat.

TL;DR: Site-directed mutagenesis allows more precise delineation of the sequences important for TAR function and suggest that the TAR may be recognized by a host-specific DNA-binding protein rather than by the tat protein directly.
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Inactivation of the Human Papillomavirus E6 or E7 Gene in Cervical Carcinoma Cells by Using a Bacterial CRISPR/Cas RNA-Guided Endonuclease

TL;DR: It is demonstrated that the recently described bacterial CRISPR/Cas RNA-guided endonuclease can be reprogrammed to target and destroy the E6 or E7 gene in cervical carcinoma cells transformed by HPV, resulting in cell cycle arrest and eventual cell death.