Date published: 2026-7-8

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Gβ 5 CRISPR/Cas9 KO Plasmid (m): sc-420611

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Gβ 5 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 Gβ 5 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: Gβ 5 Antibody (C-6): sc-515379
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Gβ 5 CRISPR/Cas9 KO Plasmid (m)

    sc-420611
    20 µg
    $397.00

    Overview

    Gnb5 encodes the Gβ5 subunit, an atypical G protein beta component that forms obligate complexes with R7 family RGS proteins to accelerate Gα GTP hydrolysis and sharpen GPCR signal termination. In mouse cells, Gβ5–RGS assemblies regulate the kinetics and amplitude of cAMP and Ca²⁺-linked signaling downstream of neurotransmitter and sensory receptors, shaping neuronal excitability and synaptic transmission. Through control of GPCR-driven pathways, Gβ5 influences network-level signaling processes including neuromodulation and stimulus adaptation. Dysregulation of GNB5-associated signaling has been linked to neurodevelopmental and sensory phenotypes, supporting its relevance in mechanistic studies of GPCR timing and neuronal circuit function.

    Gβ 5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Gnb5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Gnb5 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 Gnb5 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 Gβ 5 protein expression.

    This CRISPR knockout system enables efficient generation of Gnb5-deficient cell models for investigation of Gβ 5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Gnb5 exon(s) critical for Gβ 5 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 Gnb5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Gβ 5 CRISPR/Cas9 KO Plasmid (m) and Gβ 5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Gnb5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Gβ 5 HDR Plasmid (m) and Gβ 5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Gnb5 homology arms to support homology-directed repair at defined Gnb5 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.