The heterozygous mutant mice were subsequently intercrossed to generate homozygous mutant mice (Fig. 1C).
LFA-1 FRET CD11a-mYFP/CD18-mCFP CD11a-mYFP/CD18-mCFP CD11a-mYFP/CD18-mCFPing the CD11a-mice and CD18-mYFP knock-in mice.
ELISA data suggested that oral Tat primed for the development of Tat antibodies when mice were subsequently vaccinated with plasmid DNA designed for Tat expression.
C57BL/6 mice were subsequently immunized with engineered Nef DNA constructs, and Nef-specific CD4+ and CD8+ T cell responses were determined.
The mice were subsequently placed on a custom platform, and anesthesia was maintained with isoflurane for restraint and to avoid inflicting psychological stress and pain on the animal during imaging.
Place-conditioned mice were subsequently tested twice weekly for place preference until they demonstrated extinction, defined as the return of the preference response to values statistically similar to initial responses (Brabant et al, 2005; Carey et al, 2007).
To assess proliferation rates and cell division modes of OPC, mice were subsequently treated with 0.1 mg/mL EdU in drinking water for 14 days and resected brains were processed for immunofluorescence.
Effector cells from the immunised mice were subsequently intravenously (i.v).v
The resulting Tek+/CreCD146+/floxed mice were subsequently mated with CD146floxed/floxed mice to generate Tek+/CreCD146floxed/floxed mice (Fig. 1B).
These mice were subsequently backcrossed with CD146floxed/floxed mice to generate endothelial-specific CD146 knockout (Tek+/CreCD146floxed/floxed) and control (Tek+/+CD146floxed/floxed) mice.
When the treated mice were subsequently exposed to HSV-2, the siRNAs thwarted infection by binding to and destroying the RNA of the virus.
