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.
CHT1 CRISPR Activation Plasmid (h): sc-404869-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CHT1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- CHT1 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 CHT1 CRISPR Activation Plasmid (h) and CHT1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SLC5A7 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: CHT1 Antibody (62-2ES): sc-33713
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CHT1 CRISPR Activation Plasmid (h) | sc-404869-ACT | 20 µg | $397.00 |
SLC5A7 encodes the high-affinity choline transporter 1 (CHT1), a plasma membrane solute carrier that mediates sodium-dependent choline uptake as the rate-limiting step for acetylcholine synthesis in cholinergic neurons. By controlling intracellular choline availability for choline acetyltransferase, CHT1 links membrane transport to synaptic vesicle cycling and sustained cholinergic neurotransmission. Altered SLC5A7 activity has been associated with impaired neuromuscular and central cholinergic signaling, connecting this transporter to pathways relevant to motor function, cognitive processes, and autonomic regulation. As a determinant of presynaptic acetylcholine production, CHT1 is frequently studied in neuronal differentiation models and in systems interrogating synaptic transmission and metabolic coupling to neurotransmitter synthesis.
CHT1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC5A7 expression without altering the underlying DNA sequence.
CHT1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC5A7 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 SLC5A7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CHT1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC5A7 locus and enabling the study of CHT1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CHT1 pathway restoration in tumor cells with silenced or reduced SLC5A7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.