leupaxin CRISPR/Cas9 KO Plasmid (m): sc-430706
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- leupaxin 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 leupaxin 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
leupaxin CRISPR/Cas9 KO Plasmid (m) | sc-430706 | 20 µg | $397.00 |
Overview
Mouse Lpxn encodes leupaxin, a LIM domain–containing focal adhesion adaptor that associates with integrin-linked complexes and actin-regulatory proteins to coordinate cytoskeletal remodeling. Leupaxin participates in adhesion-dependent signaling pathways involving focal adhesion kinase (FAK) and Src family kinases, influencing cell spreading, migration, and mechanotransduction. In immune and mesenchymal contexts, it can modulate transcriptional programs through interactions with nuclear receptors and other co-regulators. Dysregulated focal adhesion signaling and altered leupaxin expression have been connected to invasive cell behavior and inflammatory microenvironment dynamics, supporting its relevance in studies of cancer biology and immune cell trafficking.
leupaxin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Lpxn gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Lpxn 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 Lpxn 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 leupaxin protein expression.
This CRISPR knockout system enables efficient generation of Lpxn-deficient cell models for investigation of leupaxin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Lpxn exon(s) critical for leupaxin 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 Lpxn genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by leupaxin CRISPR/Cas9 KO Plasmid (m) and leupaxin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Lpxn locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by leupaxin HDR Plasmid (m) and leupaxin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Lpxn homology arms to support homology-directed repair at defined Lpxn 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.