LRRK2 CRISPR/Cas9 KO Plasmid (m): sc-426167
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRRK2 CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the LRRK2 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LRRK2 Antibody (133AT1218): sc-130159
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LRRK2 CRISPR/Cas9 KO Plasmid (m) | sc-426167 | 20 µg | $397.00 |
Overview
Lrrk2 encodes leucine-rich repeat kinase 2 (LRRK2), a multidomain serine/threonine kinase with GTPase activity that integrates signaling at endomembrane compartments. In mouse cells, LRRK2 modulates vesicle trafficking and endolysosomal homeostasis through phosphorylation of Rab GTPases, influencing autophagy, cytoskeletal dynamics, and organelle transport. Lrrk2 function intersects with innate immune and inflammatory signaling in myeloid lineages, shaping responses to cellular stress. Dysregulation of LRRK2-linked pathways is widely studied in neurodegeneration, particularly mechanisms relevant to Parkinson’s disease, as well as in models of altered lysosomal function and neuroinflammation.
LRRK2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Lrrk2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Lrrk2 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Lrrk2 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish LRRK2 protein expression.
This CRISPR knockout system enables efficient generation of Lrrk2-deficient cell models for investigation of LRRK2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Lrrk2 exon(s) critical for LRRK2 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple Lrrk2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LRRK2 CRISPR/Cas9 KO Plasmid (m) and LRRK2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Lrrk2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LRRK2 HDR Plasmid (m) and LRRK2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Lrrk2 homology arms to support homology-directed repair at defined Lrrk2 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.