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.
bradykinin B1 R CRISPR Activation Plasmid (h): sc-401169-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- bradykinin B1 R CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- bradykinin B1 R 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 bradykinin B1 R CRISPR Activation Plasmid (h) and bradykinin B1 R CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the BDKRB1 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: bradykinin B1 R Antibody (F-11): sc-518136
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
bradykinin B1 R CRISPR Activation Plasmid (h) | sc-401169-ACT | 20 µg | $397.00 |
BDKRB1 encodes the bradykinin B1 receptor (bradykinin B1 R), an inducible G protein–coupled receptor that is upregulated by inflammatory cytokines and tissue injury. Upon binding des-Arg bradykinin peptides, bradykinin B1 R signals through Gαq/PLCβ to increase intracellular Ca²⁺ and activate PKC, and can also engage MAPK and NF-κB pathways to modulate chemokine production, vascular permeability, and leukocyte trafficking. Expression is typically low in homeostatic tissues but rises in activated endothelium, smooth muscle, and immune cells, linking BDKRB1 to inflammatory and nociceptive programs. Dysregulated BDKRB1 signaling has been associated with chronic inflammation, neuropathic pain biology, vascular dysfunction, and tissue remodeling contexts relevant to cardiometabolic and neuroinflammatory research.
bradykinin B1 R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BDKRB1 expression without altering the underlying DNA sequence.
bradykinin B1 R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BDKRB1 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 BDKRB1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous bradykinin B1 R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BDKRB1 locus and enabling the study of bradykinin B1 R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of bradykinin B1 R pathway restoration in tumor cells with silenced or reduced BDKRB1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.