C15orf39 CRISPR Activation Plasmid (h): sc-412724-ACT

C15orf39 encodes a poorly characterized human protein with limited functional annotation, but available evidence supports a role in fundamental cellular homeostasis processes such as regulation of gene expression and protein turnover. Transcriptomic and proteomic observations suggest C15orf39 may participate in pathways that influence cell-cycle progression, stress responses, and mitochondrial or metabolic adaptation, depending on cellular context. Altered C15orf39 expression has been reported in select disease-associated datasets, indicating potential relevance to dysregulated proliferation and genome maintenance programs. As a result, controlled upregulation of C15orf39 is useful for probing downstream transcriptional networks and pathway dependencies in human cell models.

C15orf39 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous C15orf39 expression without altering the underlying DNA sequence.

C15orf39 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the C15orf39 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 C15orf39 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C15orf39 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native C15orf39 locus and enabling the study of C15orf39-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C15orf39 pathway restoration in tumor cells with silenced or reduced C15orf39 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.