Date published: 2026-7-6

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ALG2 CRISPR/Cas9 KO Plasmid (h): sc-410220

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ALG2 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 ALG2 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

    ALG2 CRISPR/Cas9 KO Plasmid (h)

    sc-410220
    20 µg
    $397.00

    Overview

    ALG2 encodes alpha-1,3/1,6-mannosyltransferase 2, a key enzyme in the endoplasmic reticulum N-linked glycosylation pathway that extends lipid-linked oligosaccharide intermediates during early glycan assembly. By supporting proper protein folding, quality control, and trafficking through the secretory pathway, ALG2 influences ER homeostasis and proteostasis networks. Disruption of N-glycosylation steps can perturb membrane and secreted protein maturation, eliciting ER stress and altered cell signaling. Variants affecting ALG2 function have been associated with congenital disorders of glycosylation, linking this enzyme to systems-level impacts on development and cellular physiology.

    ALG2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ALG2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ALG2 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 ALG2 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 ALG2 protein expression.

    This CRISPR knockout system enables efficient generation of ALG2-deficient cell models for investigation of ALG2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting ALG2 exon(s) critical for ALG2 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 ALG2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by ALG2 CRISPR/Cas9 KO Plasmid (h) and ALG2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ALG2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by ALG2 HDR Plasmid (h) and ALG2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ALG2 homology arms to support homology-directed repair at defined ALG2 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.