Nicotinic Acetylcholine Receptor delta/CHRND CRISPR Activation Plasmid (h): sc-404001-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Nicotinic Acetylcholine Receptor delta/CHRND CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Nicotinic Acetylcholine Receptor delta/CHRND 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 delta/CHRND CRISPR Activation Plasmid (h) and Nicotinic Acetylcholine Receptor delta/CHRND CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CHRND 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 delta/CHRND Antibody (C-4): sc-390896
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nicotinic Acetylcholine Receptor delta/CHRND CRISPR Activation Plasmid (h) | sc-404001-ACT | 20 µg | $397.00 |
CHRND encodes the delta subunit of the muscle-type nicotinic acetylcholine receptor (nAChR), a ligand-gated ion channel that assembles at the neuromuscular junction to mediate rapid synaptic transmission. Upon acetylcholine binding, the receptor opens to permit cation influx, coupling neurotransmission to membrane depolarization and excitation–contraction processes. CHRND contributes to receptor assembly, channel gating, and postsynaptic stability within cholinergic signaling pathways. Altered nAChR subunit composition or function is relevant to disorders of neuromuscular transmission, supporting its use in studies of synapse biology and receptor biogenesis.
Nicotinic Acetylcholine Receptor delta/CHRND CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CHRND expression without altering the underlying DNA sequence.
Nicotinic Acetylcholine Receptor delta/CHRND CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CHRND 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 CHRND transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Nicotinic Acetylcholine Receptor delta/CHRND expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CHRND locus and enabling the study of Nicotinic Acetylcholine Receptor delta/CHRND-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 delta/CHRND pathway restoration in tumor cells with silenced or reduced CHRND expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.