
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C20orf54 CRISPR Activation Plasmid (h) | sc-405094-ACT | 20 µg | $397.00 |
SLC52A3 encodes C20orf54, a high-affinity riboflavin (vitamin B2) transporter that mediates cellular uptake of riboflavin to support FAD and FMN biosynthesis. Through regulation of flavin cofactor availability, C20orf54 influences mitochondrial oxidative metabolism, redox homeostasis, and flavoprotein-dependent pathways, including electron transport and fatty acid oxidation. Altered SLC52A3 activity has been linked to riboflavin transport deficiencies and downstream metabolic and neurophysiological dysfunction, making it relevant for studying nutrient transport, mitochondrial bioenergetics, and stress-response signaling.
C20orf54 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC52A3 expression without altering the underlying DNA sequence.
C20orf54 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC52A3 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 SLC52A3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C20orf54 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC52A3 locus and enabling the study of C20orf54-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C20orf54 pathway restoration in tumor cells with silenced or reduced SLC52A3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.