Date published: 2026-7-10

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GIT2 CRISPR/Cas9 KO Plasmid (m): sc-424063

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • GIT2 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 GIT2 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

    GIT2 CRISPR/Cas9 KO Plasmid (m)

    sc-424063
    20 µg
    $397.00

    Overview

    GIT2 (G protein-coupled receptor kinase-interacting ArfGAP 2) is an ARF GTPase-activating scaffold that coordinates membrane trafficking and cytoskeletal remodeling by integrating signals from GPCR-associated kinases and small GTPases. In mouse cells, GIT2 functions within paxillin/PIX/PAK signaling complexes to regulate focal adhesion turnover, cell spreading, and directed migration, coupling these processes to actin dynamics and endocytosis. It also contributes to stress-responsive signaling and receptor internalization, linking adhesion and signaling networks that shape cellular responses to environmental cues. Dysregulated GIT2-associated pathways have been examined in contexts involving altered motility and inflammatory signaling, supporting its relevance in mechanistic studies of tissue remodeling and disease-associated cell behavior.

    GIT2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Git2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Git2 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 Git2 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 GIT2 protein expression.

    This CRISPR knockout system enables efficient generation of Git2-deficient cell models for investigation of GIT2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Git2 exon(s) critical for GIT2 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 Git2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by GIT2 CRISPR/Cas9 KO Plasmid (m) and GIT2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Git2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by GIT2 HDR Plasmid (m) and GIT2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Git2 homology arms to support homology-directed repair at defined Git2 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.