C1orf173 CRISPR Activation Plasmid (h): sc-409362-ACT

ERICH3 (also referred to as C1orf173) encodes a glutamate-rich protein with limited functional annotation, making it a useful target for mechanistic studies of poorly characterized human genes. Available evidence from expression profiling and genetic association studies suggests ERICH3 may influence cellular regulatory programs linked to neuronal biology and stress-responsive transcription, potentially intersecting with pathways that control gene expression homeostasis and proteostasis. As a largely uncharacterized open reading frame, ERICH3 is frequently investigated to connect genotype to phenotype in systems-level analyses. Dysregulated expression patterns have been reported in disease-relevant datasets, supporting its use in exploratory research on molecular correlates of complex traits.

C1orf173 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ERICH3 expression without altering the underlying DNA sequence.

C1orf173 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ERICH3 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 ERICH3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C1orf173 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ERICH3 locus and enabling the study of C1orf173-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C1orf173 pathway restoration in tumor cells with silenced or reduced ERICH3 expression.

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