
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
apoL1 CRISPR Activation Plasmid (h) | sc-403137-ACT | 20 µg | $397.00 | |||
apoL1 CRISPR Activation Plasmid (h2) | sc-403137-ACT-2 | 20 µg | $397.00 |
APOL1 encodes apolipoprotein L1 (apoL1), a lipid-binding protein implicated in innate immune defense and cellular stress responses. apoL1 is associated with endosomal and autophagic membranes and has been linked to regulation of vesicular trafficking, programmed cell death pathways, and interferon-inducible signaling networks. In kidney-relevant cell types, APOL1 expression and variant-dependent activity have been studied in the context of podocyte homeostasis, mitochondrial dysfunction, and inflammatory signaling. Dysregulated APOL1 biology is widely investigated for its contribution to mechanisms underlying proteinuric kidney phenotypes and immune-mediated injury models.
apoL1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous APOL1 expression without altering the underlying DNA sequence.
apoL1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the APOL1 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 APOL1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous apoL1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native APOL1 locus and enabling the study of apoL1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of apoL1 pathway restoration in tumor cells with silenced or reduced APOL1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.