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.
MCR CRISPR Activation Plasmid (h): sc-400672-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCR CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- MCR 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 MCR CRISPR Activation Plasmid (h) and MCR CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the NR3C2 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: MCR Antibody (H10E4C9F): sc-53000
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCR CRISPR Activation Plasmid (h) | sc-400672-ACT | 20 µg | $397.00 |
NR3C2 encodes the mineralocorticoid receptor (MCR), a ligand-activated nuclear receptor transcription factor that responds primarily to aldosterone and participates in glucocorticoid signaling in a tissue-dependent manner. Upon activation, MCR translocates to the nucleus and binds hormone response elements to regulate genes controlling epithelial sodium transport, potassium homeostasis, fluid balance, and blood pressure regulation, including pathways converging on ENaC and Na⁺/K⁺-ATPase activity. NR3C2 signaling also intersects with inflammatory and fibrotic gene programs in cardiovascular, renal, and neural tissues through context-specific crosstalk with MAPK and other transcriptional regulators. Dysregulation or mutation of NR3C2 is implicated in disorders of salt handling and blood pressure control and is studied in kidney and heart disease mechanisms, stress-responsive neurobiology, and endocrine regulation.
MCR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NR3C2 expression without altering the underlying DNA sequence.
MCR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NR3C2 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 NR3C2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MCR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NR3C2 locus and enabling the study of MCR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MCR pathway restoration in tumor cells with silenced or reduced NR3C2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.