C1orf115 CRISPR Activation Plasmid (h): sc-413237-ACT

C1orf115 (human) encodes a poorly characterized protein with limited functional annotation, suggesting roles that may be context-dependent and best resolved through perturbation studies. Available transcript and proteomic datasets indicate cell type–specific expression patterns, supporting investigation in lineage differentiation, stress-adaptive programs, or other regulated cellular states. Because mechanistic links to canonical signaling pathways remain incompletely defined, modulation of C1orf115 expression is useful for mapping downstream transcriptional responses and protein-interaction networks. Altered expression signatures of uncharacterized open reading frames such as C1orf115 are frequently surveyed in cancer and neurobiology datasets, making it relevant for exploratory disease-associated pathway studies without presupposing causality.

C1orf115 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous C1orf115 expression without altering the underlying DNA sequence.

C1orf115 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the C1orf115 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 C1orf115 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C1orf115 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native C1orf115 locus and enabling the study of C1orf115-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C1orf115 pathway restoration in tumor cells with silenced or reduced C1orf115 expression.

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