HLA-DRβ1 Double Nickase Plasmid (h): sc-406727-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HLA-DRβ1 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-DRβ1 Double Nickase Plasmid (h) and HLA-DRβ1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HLA-DRB1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HLA-DRβ1 Double Nickase Plasmid (h) | sc-406727-NIC | 20 µg | $410.00 | |||
HLA-DRβ1 Double Nickase Plasmid (h2) | sc-406727-NIC-2 | 20 µg | $410.00 |
HLA-DRB1 encodes the beta chain of the HLA-DR MHC class II heterodimer, a central mediator of adaptive immunity that presents extracellular peptide antigens to CD4+ T cells. HLA-DRβ1 expression and peptide loading depend on the endosomal antigen-processing pathway, including invariant chain (CD74) trafficking and HLA-DM–mediated peptide exchange, shaping T-cell repertoire and activation thresholds. Variation or altered regulation of HLA-DRB1 is strongly associated with immune-mediated disease susceptibility and transplant-related alloreactivity, reflecting its role in antigen specificity and immune tolerance. As a highly polymorphic locus, it is widely studied for mechanisms of autoimmunity, host–pathogen interactions, and antigen presentation dynamics in human cells.
HLA-DRβ1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HLA-DRB1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HLA-DRB1. 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-DRB1 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-DRB1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.