| First Author | Ninkina N | Year | 2015 |
| Journal | Sci Rep | Volume | 5 |
| Pages | 16615 | PubMed ID | 26564109 |
| Mgi Jnum | J:227400 | Mgi Id | MGI:5700383 |
| Doi | 10.1038/srep16615 | Citation | Ninkina N, et al. (2015) A novel resource for studying function and dysfunction of alpha-synuclein: mouse lines for modulation of endogenous Snca gene expression. Sci Rep 5:16615 |
| abstractText | Pathological modification of alpha-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 alpha-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 alpha-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 alpha-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 alpha-synuclein normal function and the role of this protein in disease pathogenesis. |
