Date published: 2026-7-4

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Sar1a CRISPR/Cas9 KO Plasmid (m): sc-422799

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Sar1a 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 Sar1a 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: Sar1a Antibody (K-44): sc-130463
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Sar1a CRISPR/Cas9 KO Plasmid (m)

    sc-422799
    20 µg
    $397.00

    Overview

    Sar1a encodes the small GTPase SAR1A, an essential initiator of COPII-coated vesicle formation at endoplasmic reticulum exit sites that drives ER-to-Golgi trafficking. By cycling between GDP- and GTP-bound states, SAR1A promotes membrane curvature and recruits SEC23/SEC24 and SEC13/SEC31 complexes, supporting secretory pathway flux and proteostasis. Sar1a-dependent trafficking influences lipid and lipoprotein handling, extracellular matrix secretion, and cell-surface receptor delivery, linking it to broad regulation of signaling and differentiation programs. Disruption of COPII-mediated transport and ER homeostasis is implicated in stress responses and pathology relevant to developmental and metabolic phenotypes, making Sar1a a useful node for mechanistic studies of secretion-dependent biology.

    Sar1a CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sar1a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sar1a 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 Sar1a 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 Sar1a protein expression.

    This CRISPR knockout system enables efficient generation of Sar1a-deficient cell models for investigation of Sar1a signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Sar1a exon(s) critical for Sar1a 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 Sar1a genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Sar1a CRISPR/Cas9 KO Plasmid (m) and Sar1a CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sar1a locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Sar1a HDR Plasmid (m) and Sar1a HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sar1a homology arms to support homology-directed repair at defined Sar1a 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.