Date published: 2026-7-9

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SH2-B CRISPR/Cas9 KO Plasmid (m): sc-422909

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SH2-B 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 SH2-B 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: SH2-B α/β/γ/δ Antibody (C-11): sc-514142
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SH2-B CRISPR/Cas9 KO Plasmid (m)

    sc-422909
    20 µg
    $397.00

    Overview

    Mouse Sh2b1 encodes the adaptor protein SH2-B, a cytoplasmic signaling scaffold that couples activated receptor tyrosine kinases and cytokine receptors to downstream pathways such as JAK/STAT, PI3K–AKT, and MAPK. Through its SH2 domain and protein–protein interaction motifs, SH2-B modulates signal amplitude and duration to influence cellular proliferation, differentiation, and metabolic regulation. Sh2b1-dependent signaling is widely studied in the context of energy homeostasis and insulin/leptin-responsive networks, and altered SH2B1 function has been linked to phenotypes involving metabolic dysregulation and neuroendocrine control. In immune and neuronal systems, SH2-B also contributes to receptor-mediated signaling events that shape inflammatory responses and synaptic/neurite-associated processes.

    SH2-B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sh2b1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sh2b1 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 Sh2b1 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 SH2-B protein expression.

    This CRISPR knockout system enables efficient generation of Sh2b1-deficient cell models for investigation of SH2-B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Sh2b1 exon(s) critical for SH2-B 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 Sh2b1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SH2-B CRISPR/Cas9 KO Plasmid (m) and SH2-B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sh2b1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SH2-B HDR Plasmid (m) and SH2-B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sh2b1 homology arms to support homology-directed repair at defined Sh2b1 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.