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.
Histamine H1 Receptor CRISPR Activation Plasmid (h): sc-401393-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Histamine H1 Receptor CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Histamine H1 Receptor 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 Histamine H1 Receptor CRISPR Activation Plasmid (h) and Histamine H1 Receptor CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the HRH1 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: Histamine H1 Receptor Antibody (G-11): sc-374621
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Histamine H1 Receptor CRISPR Activation Plasmid (h) | sc-401393-ACT | 20 µg | $397.00 | |||
Histamine H1 Receptor CRISPR Activation Plasmid (h2) | sc-401393-ACT-2 | 20 µg | $397.00 |
HRH1 encodes the human histamine H1 receptor, a G protein–coupled receptor that primarily couples to Gq/11 to activate phospholipase Cβ, elevate intracellular Ca2+, and stimulate PKC-dependent signaling. Downstream pathways include MAPK/ERK cascades and transcriptional programs that regulate vascular permeability, smooth muscle tone, and neuroimmune communication. HRH1 activity modulates inflammatory cell trafficking and cytokine production and has been linked to allergic inflammation, pruritus, airway hyperresponsiveness, and neurotransmission-related phenotypes relevant to sleep–wake regulation. In cellular models, HRH1 provides a tractable node for interrogating GPCR signaling dynamics, second-messenger coupling, and stimulus-dependent gene expression.
Histamine H1 Receptor CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HRH1 expression without altering the underlying DNA sequence.
Histamine H1 Receptor CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HRH1 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 HRH1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Histamine H1 Receptor expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HRH1 locus and enabling the study of Histamine H1 Receptor-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Histamine H1 Receptor pathway restoration in tumor cells with silenced or reduced HRH1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.