
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLX4IP CRISPR Activation Plasmid (h) | sc-407109-ACT | 20 µg | $397.00 |
Human SLX4IP (SLX4 interacting protein) is a nuclear factor implicated in the maintenance of genome integrity through interactions with structure-specific endonuclease networks and DNA repair scaffolds. It has been linked to pathways governing replication-associated DNA damage responses, telomere homeostasis, and resolution of complex DNA structures that can arise during replication stress. Altered SLX4IP expression has been associated with telomere length regulation mechanisms that influence cellular proliferative capacity and genome stability phenotypes. These functions make SLX4IP a useful target for investigating DNA repair pathway wiring, chromosomal stability, and stress-adaptive programs relevant to cancer and other genome-instability–associated conditions.
SLX4IP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLX4IP expression without altering the underlying DNA sequence.
SLX4IP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLX4IP 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 SLX4IP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLX4IP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLX4IP locus and enabling the study of SLX4IP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLX4IP pathway restoration in tumor cells with silenced or reduced SLX4IP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.