
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CTL2 CRISPR Activation Plasmid (h) | sc-402652-ACT | 20 µg | $397.00 |
SLC44A2 encodes choline transporter-like protein 2 (CTL2), a multi-pass membrane transporter implicated in cellular choline uptake and phospholipid metabolism that supports membrane biogenesis and signaling. CTL2 activity links to pathways governing lipid homeostasis, mitochondrial function, and stress responses through regulation of choline availability for phosphatidylcholine synthesis. Expression of SLC44A2 has been associated with myeloid and endothelial cell biology, including processes relevant to inflammation and thrombosis. Genetic and immunologic studies have connected CTL2 to hematologic and vascular phenotypes, making it a useful target for mechanistic investigation in disease-relevant cell models.
CTL2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC44A2 expression without altering the underlying DNA sequence.
CTL2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC44A2 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 SLC44A2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CTL2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC44A2 locus and enabling the study of CTL2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CTL2 pathway restoration in tumor cells with silenced or reduced SLC44A2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.