Date published: 2026-8-31

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p41-ARCb CRISPR/Cas9 KO Plasmid (m): sc-419207

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • p41-ARCb 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 p41-ARCb 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: p41-ARCb Antibody (C-3): sc-137125
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    p41-ARCb CRISPR/Cas9 KO Plasmid (m)

    sc-419207
    20 µg
    $397.00

    Overview

    Arpc1b encodes p41-ARCb, a regulatory subunit of the Arp2/3 complex that nucleates branched actin networks required for dynamic cytoskeletal remodeling. In mouse cells, p41-ARCb supports processes such as lamellipodia formation, cell migration, endocytosis, and immune cell effector functions by coordinating actin polymerization downstream of Rho-family GTPases and nucleation-promoting factors. Arp2/3-dependent actin assembly interfaces with signaling pathways that control adhesion, vesicle trafficking, and immunological synapse organization. Dysregulated ARPC1B/Arp2/3 activity is linked to defects in hematopoietic and immune cell behavior and is relevant to studying immunodeficiency-like phenotypes and inflammatory mechanisms in vivo and in vitro.

    p41-ARCb CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Arpc1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Arpc1b 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 Arpc1b 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 p41-ARCb protein expression.

    This CRISPR knockout system enables efficient generation of Arpc1b-deficient cell models for investigation of p41-ARCb signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Arpc1b exon(s) critical for p41-ARCb 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 Arpc1b genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by p41-ARCb CRISPR/Cas9 KO Plasmid (m) and p41-ARCb CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Arpc1b locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by p41-ARCb HDR Plasmid (m) and p41-ARCb HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Arpc1b homology arms to support homology-directed repair at defined Arpc1b 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.