Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
BTLA CRISPR Activation Plasmid (h): sc-417186-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTLA CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- BTLA CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by BTLA CRISPR Activation Plasmid (h) and BTLA CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the BTLA transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BTLA Antibody (4B8): sc-517004
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BTLA CRISPR Activation Plasmid (h) | sc-417186-ACT | 20 µg | $397.00 | |||
BTLA CRISPR Activation Plasmid (h2) | sc-417186-ACT-2 | 20 µg | $397.00 |
B and T lymphocyte associated (BTLA) is an immunoregulatory receptor of the CD28 superfamily expressed on multiple lymphocyte subsets, where it functions as an inhibitory checkpoint to restrain antigen receptor signaling and maintain peripheral tolerance. Upon engagement with its ligand HVEM (TNFRSF14), BTLA recruits phosphatases through cytoplasmic ITIM/ITSM motifs to attenuate proximal kinase cascades, shaping T cell activation, cytokine production, and immune homeostasis. This pathway intersects with broader coinhibitory networks that calibrate adaptive immune responses during inflammation and chronic antigen exposure. Altered BTLA expression or signaling has been associated with immune dysregulation and has been studied in the context of autoimmunity, infection, and tumor immunology.
BTLA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BTLA expression without altering the underlying DNA sequence.
BTLA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BTLA 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 BTLA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BTLA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BTLA locus and enabling the study of BTLA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BTLA pathway restoration in tumor cells with silenced or reduced BTLA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.