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.
Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h): sc-403321-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Nicotinic Acetylcholine Receptor gamma/CHRNG 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 Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h) and Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CHRNG 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: Nicotinic Acetylcholine Receptor gamma/CHRNG Antibody (66): sc-58597
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h) | sc-403321-ACT | 20 µg | $397.00 |
CHRNG encodes the gamma subunit of the nicotinic acetylcholine receptor (nAChR), a ligand-gated ion channel that mediates acetylcholine-dependent cation flux and membrane depolarization in developing skeletal muscle. The gamma-containing receptor is a hallmark of fetal/denervated muscle and is replaced by the epsilon subunit in mature neuromuscular junctions, linking CHRNG to developmental synaptogenesis and receptor subunit switching. Through participation in cholinergic signaling and activity-dependent muscle differentiation programs, CHRNG influences neuromuscular transmission and excitability. Pathogenic variation in CHRNG has been associated with congenital myasthenic phenotypes and fetal akinesia-related syndromes, making it relevant for studies of neuromuscular development and disease mechanisms.
Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CHRNG expression without altering the underlying DNA sequence.
Nicotinic Acetylcholine Receptor gamma/CHRNG CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CHRNG 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 CHRNG transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Nicotinic Acetylcholine Receptor gamma/CHRNG expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CHRNG locus and enabling the study of Nicotinic Acetylcholine Receptor gamma/CHRNG-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Nicotinic Acetylcholine Receptor gamma/CHRNG pathway restoration in tumor cells with silenced or reduced CHRNG expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.