Date published: 2026-7-5

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HLA-DQA1 Double Nickase Plasmid (h): sc-403480-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • HLA-DQA1 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • HLA-DQA1 Double Nickase Plasmid (h) and HLA-DQA1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HLA-DQA1. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    HLA-DQA1 Double Nickase Plasmid (h)

    sc-403480-NIC
    20 µg
    $410.00

    HLA-DQA1 Double Nickase Plasmid (h2)

    sc-403480-NIC-2
    20 µg
    $410.00

    HLA-DQA1 encodes the alpha chain of the HLA-DQ heterodimer, a major histocompatibility complex (MHC) class II molecule expressed primarily on antigen-presenting cells. In the endosomal antigen-processing pathway, HLA-DQ presents extracellularly derived peptides to CD4+ T cells, shaping thymic selection, peripheral immune tolerance, and adaptive immune activation. Allelic variation and altered expression of HLA-DQA1 influence peptide-binding repertoires and are associated with immune-mediated disease susceptibility, including autoimmunity and transplant-related alloreactivity. As part of the HLA class II locus, HLA-DQA1 is commonly studied in contexts of antigen presentation, T cell polarization, and inflammatory signaling networks.

    HLA-DQA1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HLA-DQA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HLA-DQA1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt HLA-DQA1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of HLA-DQA1-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.