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.
AVP Receptor V1a CRISPR Activation Plasmid (h): sc-401691-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AVP Receptor V1a CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- AVP Receptor V1a 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 AVP Receptor V1a CRISPR Activation Plasmid (h) and AVP Receptor V1a CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the AVPR1A 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: AVP Receptor V1a Antibody (721CT25.2.1): sc-517313
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AVP Receptor V1a CRISPR Activation Plasmid (h) | sc-401691-ACT | 20 µg | $397.00 |
AVPR1A encodes the human arginine vasopressin receptor 1A (V1a), a seven-transmembrane GPCR that couples predominantly to Gq/11 to activate phospholipase C, inositol phosphate signaling, intracellular Ca²⁺ mobilization, and PKC-dependent transcriptional programs. V1a signaling influences vascular smooth muscle tone, platelet and endothelial responses, and neuroendocrine circuits regulating stress reactivity and social behavior, integrating with MAPK/ERK and other downstream pathways. Altered AVPR1A expression or signaling has been investigated in cardiovascular and neuropsychiatric research contexts, including blood pressure regulation, vasoconstrictive phenotypes, and behavioral trait association studies. These links make AVPR1A a useful target for dissecting GPCR signal transduction and vasopressin axis biology in cell-based models.
AVP Receptor V1a CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous AVPR1A expression without altering the underlying DNA sequence.
AVP Receptor V1a CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the AVPR1A 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 AVPR1A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous AVP Receptor V1a expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native AVPR1A locus and enabling the study of AVP Receptor V1a-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of AVP Receptor V1a pathway restoration in tumor cells with silenced or reduced AVPR1A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.