
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HLA-DQB1 CRISPR Activation Plasmid (h) | sc-403051-ACT | 20 µg | $397.00 |
HLA-DQB1 encodes the β chain of the HLA-DQ class II major histocompatibility complex, which pairs with HLA-DQA to present extracellularly derived peptides to CD4+ T cells. This antigen presentation axis is central to adaptive immune activation, thymic selection, and peripheral tolerance, shaping T cell help and downstream B cell responses. Variation in HLA-DQB1 influences peptide-binding specificity and is strongly linked to autoimmune predisposition and immune-mediated inflammation, including type 1 diabetes and celiac disease. Dysregulated HLA-DQ expression and altered antigen presentation can also affect tumor immune surveillance and responses to inflammatory cues.
HLA-DQB1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HLA-DQB1 expression without altering the underlying DNA sequence.
HLA-DQB1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HLA-DQB1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the HLA-DQB1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HLA-DQB1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HLA-DQB1 locus and enabling the study of HLA-DQB1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HLA-DQB1 pathway restoration in tumor cells with silenced or reduced HLA-DQB1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.