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  • 1
    Keywords: CELLS ; CELL ; Germany ; INHIBITION ; PROTEIN ; PROTEINS ; COMPLEX ; MECHANISM ; DOMAIN ; FORM ; PARTICLES ; DEGRADATION ; ANTIVIRAL ACTIVITY ; HIV-1 VIF ; LEUKEMIA-VIRUS ; VIF ; 2 DISTINCT ; ANTIRETROVIRAL DEFENSE ; CYTIDINE DEAMINASES ; EDITING ENZYME APOBEC3G ; MURINE APOBEC3 ; SOCS-BOX ; TYPE-1 VIF
    Abstract: The APOBEC3 cytidine deaminases are part of the intrinsic defense of cells against retroviruses. Lentiviruses and spumaviruses have evolved essential accessory proteins, Vif and Bet, respectively, which counteract the APOBEC3 proteins. We show here that Bet of the Prototype foamy virus inhibits the antiviral APOBEC3C activity by a mechanism distinct to Vif: Bet forms a complex with APOBEC3C without inducing its degradation. Bet abolished APOBEC3C dimerization as shown by co-immunoprecipitation and cross-linking experiments. These findings implicate a physical interaction between Bet and the APOBEC3C. Subsequently, we identified the Bet interaction domain in human APOBEC3C in the predicted APOBEC3C dimerization site. Taken together, these data support the hypothesis that Bet inhibits incorporation of APOBEC3Cs into retroviral particles. Bet likely achieves this by trapping APOBEC3C protein in complexes rendering them unavailable for newly generated viruses due to direct immobilization
    Type of Publication: Journal article published
    PubMed ID: 19074429
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  • 2
    Keywords: CELLS ; EXPRESSION ; proliferation ; SURVIVAL ; tumor ; BLOOD ; CELL ; Germany ; IN-VIVO ; KINASE ; THERAPY ; VIVO ; FOLLOW-UP ; SITE ; SITES ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; PROTEINS ; transcription ; METABOLISM ; TRANSDUCTION ; gene transfer ; GENE-TRANSFER ; PATIENT ; DONOR ; TRANSPLANTATION ; CONTRAST ; SUFFICIENT ; treatment ; FREQUENCY ; FREQUENCIES ; TARGET ; CELL-SURVIVAL ; PATTERNS ; gene expression ; VECTOR ; LYMPHOCYTES ; HUMAN GENOME ; REGION ; REGIONS ; PROGENITOR CELLS ; IMMUNITY ; T-LYMPHOCYTES ; T lymphocyte ; CHILDREN ; PERIPHERAL-BLOOD ; T lymphocytes ; INTEGRATION ; PATTERN ; SEVERE COMBINED IMMUNODEFICIENCY ; LEVEL ; LONG ; progenitor ; EVENTS ; USA ; in vivo ; progenitor cell ; TRANSDUCED CELLS ; RECONSTITUTION ; RETROVIRAL GENE MARKING ; RETROVIRAL INTEGRATION ; MEDICINE ; VECTOR INTEGRATION ; PROGENITOR-CELL ; SCID-X1 ; ADA
    Abstract: We treated 10 children with X-linked SCID (SCID-X1) using gammaretrovirus-mediated gene transfer. Those with sufficient follow-up were found to have recovered substantial immunity in the absence of any serious adverse events up to 5 years after treatment. To determine the influence of vector integration on lymphoid reconstitution, we compared retroviral integration sites (RISs) from peripheral blood CD3(+) T lymphocytes of 5 patients taken between 9 and 30 months after transplantation with transduced CD34(+) progenitor cells derived from 1 further patient and I healthy donor. Integration occurred preferentially in gene regions on either side of transcription start sites, was clustered, and correlated with the expression level in CD34(+) progenitors during transduction. In contrast to those in CD34(+) cells, RISs recovered from engrafted CD3(+)T cells were significantly overrepresented within or near genes encoding proteins with kinase or transferase activity or involved in phosphorus metabolism. Although gross patterns of gene expression were unchanged in transduced cells, the divergence of RIS target frequency between transduced progenitor cells and post-thymic T lymphocytes indicates that vector integration influences cell survival, engraftment, or proliferation
    Type of Publication: Journal article published
    PubMed ID: 17671654
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