
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TAPBPL CRISPR Activation Plasmid (h) | sc-409990-ACT | 20 µg | $397.00 |
TAPBPL (TAP binding protein-like) is an endoplasmic reticulum–resident immunoregulatory protein that modulates peptide loading and quality control of MHC class I complexes. By interacting with components of the antigen presentation machinery, TAPBPL helps shape the repertoire and stability of peptide–MHC I at the cell surface, influencing CD8+ T cell recognition. Its activity links ER proteostasis, peptide editing, and immune surveillance pathways that are frequently altered in contexts of immune evasion. Dysregulated antigen presentation associated with TAPBPL function is therefore relevant to studies of tumor immunology, infection biology, and inflammatory signaling.
TAPBPL CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TAPBPL expression without altering the underlying DNA sequence.
TAPBPL CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TAPBPL 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 TAPBPL transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TAPBPL expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TAPBPL locus and enabling the study of TAPBPL-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TAPBPL pathway restoration in tumor cells with silenced or reduced TAPBPL expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.