
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABR CRISPR/Cas9 KO Plasmid (h) | sc-407250 | 20 µg | $397.00 |
ABR (active BCR-related) encodes a multidomain Rho GTPase-activating protein that modulates small GTPases such as RAC1 and CDC42, thereby influencing actin cytoskeleton dynamics, cell adhesion, membrane ruffling, and vesicular trafficking. Through its GAP activity and signaling scaffolding functions, ABR participates in pathways that couple receptor-driven cues to cytoskeletal remodeling and cell motility. Altered ABR-regulated Rho GTPase signaling has been associated with dysregulated proliferation and migration phenotypes relevant to oncogenic transformation and invasive behavior. ABR is also studied in the context of immune cell signaling and neurodevelopmental processes where precise control of Rho-family GTPases is required.
ABR CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ABR gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ABR 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 ABR 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 ABR protein expression.
This CRISPR knockout system enables efficient generation of ABR-deficient cell models for investigation of ABR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.