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Pathological modification of α-synuclein is believed to be an important event in pathogenesis of Parkinson's disease and several other neurodegenerative diseases. In normal cells this protein has been linked to many intracellular processes and pathways. However, neither normal function of α-synuclein in neuronal and certain other types of cells nor its exact role in the disease pathogenesis is well understood, which is largely due to limitations of animal models used for studying this protein. We produced and validated several novel mouse lines for manipulating expression of the endogenous Snca gene coding for α-synuclein. These include a line for conditional Cre-recombinase-driven inactivation of the gene; a line for conditional Flp-driven restoration of a neo-cassete-blocked α-synuclein expression; a new line with a "clean" constituent knockout of the gene as well as a line carrying this knockout locus and Rosa26-stop-lacZ reporter locus linked at the same mouse chromosome 6. Altogether these lines represent a set of new useful tools for studies of α-synuclein normal function and the role of this protein in disease pathogenesis.

Original publication

DOI

10.1038/srep16615

Type

Journal article

Journal

Sci Rep

Publication Date

13/11/2015

Volume

5

Keywords

Animals, Base Sequence, Blotting, Southern, Blotting, Western, Cerebral Cortex, Gene Expression, Gene Targeting, Integrases, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Molecular Sequence Data, alpha-Synuclein