Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Arg CRISPR/Cas9 KO Plasmid (m): sc-418936
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Arg 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 Arg 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: Arg Antibody (1H1B11): sc-81154
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Arg CRISPR/Cas9 KO Plasmid (m) | sc-418936 | 20 µg | $397.00 |
Overview
Mouse Abl2 encodes the non-receptor tyrosine kinase Arg, a close paralog of ABL1 that integrates signals from growth factor receptors and adhesion complexes to control actin cytoskeleton remodeling. Arg regulates cellular processes including migration, neurite outgrowth, endocytosis, and responses to oxidative and mechanical stress by coupling phosphorylation events to Rho-family GTPase and focal adhesion signaling. Through its roles in cytoskeletal dynamics and cell–cell/cell–matrix interactions, Arg is frequently studied in contexts of invasive cell behavior and aberrant kinase signaling. Dysregulated ABL-family activity and altered Abl2-dependent pathways have been linked to oncogenic phenotypes and neurobiological dysfunction in experimental models.
Arg CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Abl2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Abl2 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 Abl2 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 Arg protein expression.
This CRISPR knockout system enables efficient generation of Abl2-deficient cell models for investigation of Arg signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Abl2 exon(s) critical for Arg 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 Abl2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Arg CRISPR/Cas9 KO Plasmid (m) and Arg CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Abl2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Arg HDR Plasmid (m) and Arg HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Abl2 homology arms to support homology-directed repair at defined Abl2 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.