Date published: 2026-7-8

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CD79B CRISPR/Cas9 KO Plasmid (m): sc-421055

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CD79B 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 CD79B 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: CD79B Antibody (B29/123): sc-53210
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CD79B CRISPR/Cas9 KO Plasmid (m)

    sc-421055
    20 µg
    $397.00

    Overview

    Cd79b encodes CD79B (Igβ), an essential signaling subunit of the B cell antigen receptor (BCR) complex that pairs with CD79A to couple surface immunoglobulin engagement to intracellular signaling. Through its ITAM motif, CD79B coordinates recruitment of kinases and adaptor proteins to propagate BCR-dependent pathways that regulate B cell development, activation, antigen processing, and survival. CD79B function is tightly linked to downstream cascades including SYK/BTK-mediated signaling and NF-κB and MAPK pathway activation, shaping immune responses and tolerance. Dysregulated BCR signaling and altered CD79B expression or function are commonly studied in the context of B cell malignancy mechanisms and immune dysregulation, making Cd79b a useful locus for interrogating B cell signaling networks.

    CD79B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cd79b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cd79b 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 Cd79b 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 CD79B protein expression.

    This CRISPR knockout system enables efficient generation of Cd79b-deficient cell models for investigation of CD79B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Cd79b exon(s) critical for CD79B 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 Cd79b genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CD79B CRISPR/Cas9 KO Plasmid (m) and CD79B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cd79b locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CD79B HDR Plasmid (m) and CD79B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cd79b homology arms to support homology-directed repair at defined Cd79b 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.