Date published: 2026-10-7

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ABR CRISPR/Cas9 KO Plasmid (m): sc-430977

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ABR 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 ABR 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ABR CRISPR/Cas9 KO Plasmid (m)

    sc-430977
    20 µg
    $397.00

    Overview

    Abr encodes ABR, a Rho family GTPase-activating protein (RhoGAP) that attenuates signaling by small GTPases such as Rac and Cdc42, thereby shaping cytoskeletal remodeling, cell adhesion, and migration. In mouse cells, ABR contributes to regulation of actin dynamics and downstream pathways linked to immune cell trafficking and inflammatory responses. Through its negative control of GTPase-driven signaling cascades, ABR influences processes including endocytosis, cell polarity, and stress-responsive signaling. Dysregulated Rho GTPase signaling is broadly relevant to phenotypes involving aberrant motility and tissue organization, making Abr a useful node for mechanistic studies of signaling-network balance.

    ABR CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Abr gene in mouse 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.

    Key Features

    • sgRNAs targeting Abr exon(s) critical for ABR 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 Abr genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by ABR CRISPR/Cas9 KO Plasmid (m) and ABR CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Abr locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by ABR HDR Plasmid (m) and ABR HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Abr homology arms to support homology-directed repair at defined Abr 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.