%0 Journal Article
%T Altered dopamine release and monoamine transporters in Vps35 p.D620N knock-in mice
%A Austen J. Milnerwood
%A Chelsie Kadgien
%A Emil K. Gustavsson
%A Igor Tatarnikov
%A Jaskaran Khinda
%A Jesse D. Fox
%A Jordan Follett
%A Matthew J. Farrer
%A Stefano Cataldi
%J Archive of "NPJ Parkinson's Disease".
%D 2018
%R 10.1038/s41531-018-0063-3
%X Generation of Vps35 p.D620N knock-in mice (VKI). a Schematic of the targeting design showing the murine Vps35 genomic sequence (Ensembl reference ENSMUSG00000031696), 5¡ä and 3¡ä homology arms (arrowed), exons 14¨C17 (blue), engineered loxP site in intron 14, the g.85,263,520G>A (p.D620N) mutation in exon 15 (encoding p.D620N) and endogenous stop codon in exon 17 (TAA). FlpE-recombinase deletion between FRT sites removed the PKG-neo-pA cassette to yield the cVKI allele (not shown). Subsequent Cre-recombinase deletion between loxP sites created the VKI allele. b cDNA sequencing in wild-type mice (top), heterozygous VKI (middle), and homozygous VKI (bottom), between g.8:85263511¨C85263528 (GRCm38) highlights the g.85,263,520G>A nucleotide mutation in exon 15 that encodes the p.D620N amino acid substitution. c Relative Vps35 mRNA (fold change) expression analysis in cerebellar tissue using quantitative RT-PCR. Data normalized to WT (1-way ANOVA F2,24£¿=£¿0.05, p£¿=£¿0.95). d Total Vps35 protein levels were quantified by western blotting, showing no difference in Het and Homo mice compared to their WT littermates (1-way ANOVA F2,33£¿=£¿0.05, p£¿=£¿0.94
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104078/