Christina Raupp

TL;DR: Comparing the capsid assembly of several AAV serotypes with AAP protein from AAV2 (AAP-2), it is shown that AAP-2 is able to efficiently stimulate capsid formation of VP3 derived from several serotypes, as demonstrated for AAV1, Aav2, AAV8, and AAV9.

TL;DR: One obvious trend in the quantitative data was the degree of variation between institutions for each assay despite the relatively tight correlation of assay results within an institution, which emphasize the need in the field for universal reference standards.

TL;DR: A structure-directed strategy for characterizing the antigenic regions of AAVs can thus generate useful information to help re-engineer vectors that escape host neutralization and are hence more efficacious.

TL;DR: It is shown that the impaired hepatic expression of transcriptional cofactor transducin beta-like (TBL) 1 represents a common feature of mono- and multigenic fatty liver mouse models, and the lack of hepatic TBL1/TBLR1 cofactor activity may represent a molecular rationale for hepatic steatosis in subjects with obesity and the metabolic syndrome.

TL;DR: A multifunctional role of the 3-fold region of AAV capsids in the infection process is supported and a neutralizing monoclonal antibody that binds to amino acids 588QQNTA592 of A AV8 does not prevent cell binding and virus uptake, indicating that this region is not necessary for receptor binding.