
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CAS CRISPR Activation Plasmid (m) | sc-431044-ACT | 20 µg | $397.00 |
Mouse Cse1l encodes CAS, a karyopherin family protein that functions as an exportin for importin-α, regulating nucleocytoplasmic transport and the recycling of nuclear import machinery. By controlling nuclear trafficking, CAS contributes to cell-cycle progression, proliferation, and stress-responsive transcriptional programs, linking transport dynamics to chromatin regulation and mitotic fidelity. Altered CAS activity has been associated with changes in apoptosis, cell migration, and genome stability, processes frequently investigated in oncogenesis and developmental phenotypes. Cse1l is therefore relevant for studying how nuclear transport interfaces with signaling pathways and transcriptional control in disease-relevant cellular states.
CAS CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cse1l expression without altering the underlying DNA sequence.
CAS CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Cse1l 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 Cse1l transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CAS expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Cse1l locus and enabling the study of CAS-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CAS pathway restoration in tumor cells with silenced or reduced Cse1l expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.