C6orf141 CRISPR Activation Plasmid (h): sc-418416-ACT

C6orf141 (human) encodes a poorly characterized protein with limited functional annotation, and current evidence suggests it may contribute to cell-type–specific regulatory programs rather than a core metabolic pathway. Transcriptomic datasets indicate variable expression across tissues and developmental contexts, supporting investigation of roles in transcriptional control, cellular differentiation, or stress-adaptive processes. Because mechanistic data remain sparse, C6orf141 is frequently studied as an uncharacterized open reading frame to map protein interaction networks, subcellular localization, and downstream gene signatures. Altered expression patterns observed in selected disease-omics studies motivate research into potential associations with dysregulated gene expression states, while avoiding assumptions about causality.

C6orf141 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous C6orf141 expression without altering the underlying DNA sequence.

C6orf141 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the C6orf141 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 C6orf141 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C6orf141 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native C6orf141 locus and enabling the study of C6orf141-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C6orf141 pathway restoration in tumor cells with silenced or reduced C6orf141 expression.

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