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.
c-Abl CRISPR/Cas9 KO Plasmid (m): sc-418935
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- c-Abl 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 c-Abl 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 | |
c-Abl CRISPR/Cas9 KO Plasmid (m) | sc-418935 | 20 µg | $397.00 |
Overview
Mouse Abl1 encodes the non-receptor tyrosine kinase c-Abl, a multifunctional signaling protein that integrates cues from growth factor receptors, integrins, and genotoxic stress to regulate proliferation, cytoskeletal remodeling, adhesion, and apoptosis. c-Abl activity influences pathways controlling actin dynamics and focal adhesion turnover, and it participates in DNA damage response signaling through phosphorylation-dependent protein interactions in the nucleus. Dysregulated Abl1 signaling and altered c-Abl kinase activity are broadly relevant to oncogenic transformation and aberrant cell survival programs, making Abl1 a key node for studying kinase-driven signaling networks. In mouse models, Abl1 perturbation supports mechanistic investigation of development, immune cell function, and stress-response phenotypes linked to tyrosine kinase signaling.
c-Abl CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Abl1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Abl1 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 Abl1 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 c-Abl protein expression.
This CRISPR knockout system enables efficient generation of Abl1-deficient cell models for investigation of c-Abl signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Abl1 exon(s) critical for c-Abl 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 Abl1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by c-Abl CRISPR/Cas9 KO Plasmid (m) and c-Abl CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Abl1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by c-Abl HDR Plasmid (m) and c-Abl HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Abl1 homology arms to support homology-directed repair at defined Abl1 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.