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.
SLC26A3 CRISPR Activation Plasmid (h): sc-403891-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC26A3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SLC26A3 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 SLC26A3 CRISPR Activation Plasmid (h) and SLC26A3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SLC26A3 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: SLC26A3 Antibody (H-8): sc-376187
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLC26A3 CRISPR Activation Plasmid (h) | sc-403891-ACT | 20 µg | $397.00 |
SLC26A3 encodes a chloride/bicarbonate exchanger (DRA) predominantly expressed in intestinal epithelial cells, where it supports electroneutral NaCl absorption and regulates luminal pH through coordinated anion transport. By coupling Cl⁻ uptake to HCO₃⁻ secretion, SLC26A3 contributes to epithelial ion homeostasis and fluid balance, interacting functionally with transport networks that include CFTR and other SLC26 family members. Disruption or reduced expression of SLC26A3 is linked to congenital chloride diarrhea and broader perturbations of gastrointestinal electrolyte handling, making it a relevant target for studying epithelial transport physiology. Altered SLC26A3 activity also intersects with pathways controlling mucosal barrier function and inflammatory responses via changes in ionic microenvironment.
SLC26A3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC26A3 expression without altering the underlying DNA sequence.
SLC26A3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC26A3 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 SLC26A3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLC26A3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC26A3 locus and enabling the study of SLC26A3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLC26A3 pathway restoration in tumor cells with silenced or reduced SLC26A3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.