
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SUR-1 CRISPR Activation Plasmid (h) | sc-401540-ACT | 20 µg | $397.00 |
ABCC8 encodes the sulfonylurea receptor 1 (SUR-1), an ATP-binding cassette subfamily C regulatory subunit of ATP-sensitive potassium (KATP) channels that couple cellular energy status to membrane excitability. In pancreatic β cells, SUR-1 partners with KCNJ11 to control KATP channel gating, shaping glucose-stimulated depolarization, Ca2+ influx, and insulin granule exocytosis. Beyond endocrine signaling, SUR-1–containing KATP channels contribute to electrophysiological regulation in excitable tissues through metabolic sensing and ion homeostasis. Genetic variation or dysregulation of ABCC8 is linked to disorders of insulin secretion and glucose homeostasis, making it a frequent target for mechanistic studies in metabolic disease models.
SUR-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ABCC8 expression without altering the underlying DNA sequence.
SUR-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ABCC8 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 ABCC8 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SUR-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ABCC8 locus and enabling the study of SUR-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SUR-1 pathway restoration in tumor cells with silenced or reduced ABCC8 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.