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.
TXA2R CRISPR Activation Plasmid (h): sc-402468-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TXA2R CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TXA2R 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 TXA2R CRISPR Activation Plasmid (h) and TXA2R CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TBXA2R 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: TXA2R Antibody (G-2): sc-515033
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TXA2R CRISPR Activation Plasmid (h) | sc-402468-ACT | 20 µg | $397.00 | |||
TXA2R CRISPR Activation Plasmid (h2) | sc-402468-ACT-2 | 20 µg | $397.00 |
TBXA2R encodes the human thromboxane A2 receptor (TXA2R), a G protein-coupled receptor that binds thromboxane A2 to regulate platelet activation, vascular smooth muscle contraction, and inflammatory signaling. Upon ligand engagement, TXA2R primarily couples to Gq/11 and G12/13 pathways, promoting phospholipase C activation, intracellular calcium mobilization, RhoA signaling, and downstream MAPK responses that influence cell shape change, secretion, and adhesion. This receptor integrates eicosanoid metabolism with hemostatic and vascular homeostasis and is frequently studied in contexts of thrombosis biology, vasoreactivity, and inflammatory microenvironments. Altered TXA2R signaling has been linked to dysregulated platelet function and vascular pathology mechanisms, supporting its relevance in cardiometabolic and immune-associated disease research models.
TXA2R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TBXA2R expression without altering the underlying DNA sequence.
TXA2R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TBXA2R 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 TBXA2R transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TXA2R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TBXA2R locus and enabling the study of TXA2R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TXA2R pathway restoration in tumor cells with silenced or reduced TBXA2R expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.