Per1 CRISPR Activation Plasmid (h): sc-401260-ACT

Human PER1 encodes the Period circadian regulator 1 (Per1), a core component of the molecular clock that generates near-24-hour rhythms through transcriptional–translational feedback loops. Per1 participates in circadian regulation of gene expression in pathways controlling cell cycle progression, DNA damage responses, metabolism, and endocrine signaling, interfacing with CLOCK/ARNTL-driven transcription and CRY-mediated repression. Altered PER1 expression or rhythmicity has been associated with circadian rhythm disorders and has been reported in studies of tumor biology, mood-related phenotypes, and metabolic dysregulation, reflecting broad effects on cellular timing mechanisms. Because PER1 links environmental cues to downstream transcriptional programs, it is frequently used to interrogate clock-controlled networks and time-of-day–dependent cellular phenotypes.

Per1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PER1 expression without altering the underlying DNA sequence.

Per1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PER1 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 PER1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Per1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PER1 locus and enabling the study of Per1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Per1 pathway restoration in tumor cells with silenced or reduced PER1 expression.

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