
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Slfn12 CRISPR Activation Plasmid (h) | sc-404339-ACT | 20 µg | $397.00 |
Human SLFN12 (Schlafen family member 12) encodes Slfn12, a cytoplasmic protein within the Schlafen family implicated in regulation of cell differentiation, proliferation control, and context-dependent modulation of immune-associated gene expression. Schlafen proteins are commonly linked to interferon-stimulated signaling and RNA metabolic processes, shaping translational programs and stress responses that influence epithelial and hematopoietic cell states. Altered SLFN12 expression has been reported across multiple disease-relevant contexts, including inflammatory signaling and cancer-associated phenotypes, where shifts in differentiation and growth pathways are frequently observed. As a result, SLFN12 is of interest for dissecting transcriptional and post-transcriptional networks that couple innate signaling to lineage commitment and cellular homeostasis.
Slfn12 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLFN12 expression without altering the underlying DNA sequence.
Slfn12 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLFN12 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 SLFN12 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Slfn12 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLFN12 locus and enabling the study of Slfn12-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Slfn12 pathway restoration in tumor cells with silenced or reduced SLFN12 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.