HIV-1 Capsid Stabilization Assay.
United States. In Methods Mol Biol, Dec 2015
We also found that purified CPSF6 (1-321) protein stabilizes in vitro-assembled HIV-1 CA-NC complexes (Fricke et al., J Virol 87:10587-10597, 2013).
Whole transcriptome sequencing reveals extensive unspliced mRNA in metastatic castration-resistant prostate cancer.
Houston, United States. In Mol Cancer Res, 2015
Using quantitative PCR (qPCR), a series of genes (AR, KLK2, KLK3, STEAP2, CPSF6, and CDK19) were confirmed to have a greater proportion of unspliced RNA in CRPC specimens than in normal prostate epithelium, untreated primary prostate cancer, and cultured prostate cancer cells.
Structural basis of HIV-1 capsid recognition by PF74 and CPSF6.
Charlottesville, United States. In Proc Natl Acad Sci U S A, 2015
Here we report biochemical experiments showing that PF-3450074 (PF74), a drug that inhibits HIV-1 infection, as well as host proteins cleavage and polyadenylation specific factor 6 (CPSF6) and nucleoporin 153 kDa (NUP153), bind to the CA hexamer with at least 10-fold higher affinities compared with nonassembled CA or isolated CA domains.
Impairment of HIV-1 cDNA synthesis by DBR1 knockdown.
Irvine, United States. In J Virol, 2014
When nuclear import of the HIV-1 reverse transcription complex was blocked by expressing a truncated form of the mRNA cleavage and polyadenylation factor CPSF6, the completion of HIV-1 vector cDNA synthesis was detected in the cytoplasm, where it was not inhibited by DBR1 knockdown.
A model for cofactor use during HIV-1 reverse transcription and nuclear entry.
London, United Kingdom. In Curr Opin Virol, 2014
We present a model that may explain how the capsid protein has a fundamental role in the early part of the viral lifecycle by utilising cyclophilin A (CypA), cleavage and polyadenylation specificity factor-6 (CPSF6), Nup358 and TNPO3 to orchestrate a coordinated process of DNA synthesis, capsid uncoating and integration targeting that evades innate responses and promotes integration into preferred areas of chromatin.
HIV-1 evades innate immune recognition through specific cofactor recruitment.
London, United Kingdom. In Nature, 2013
Here we show that HIV-1 capsid mutants N74D and P90A, which are impaired for interaction with cofactors cleavage and polyadenylation specificity factor subunit 6 (CPSF6) and cyclophilins (Nup358 and CypA), respectively, cannot replicate in primary human monocyte-derived macrophages because they trigger innate sensors leading to nuclear translocation of NF-κB and IRF3, the production of soluble type 1 IFN and induction of an antiviral state.