Per1 Lentiviral Activation Particles (h): sc-401260-LAC

Human PER1 (Period Circadian Regulator 1) encodes Per1, a core component of the molecular circadian clock that helps generate ~24-hour rhythms through transcriptional–translational feedback loops with CLOCK/ARNTL (BMAL1), CRY proteins, and other PER family members. Per1 modulates circadian control of cell cycle progression, DNA damage responses, metabolic gene expression, and endocrine signaling by shaping rhythmic transcriptional programs across tissues. Dysregulated PER1 activity and circadian misalignment have been associated with altered sleep–wake regulation and broader links to metabolic and neuropsychiatric phenotypes, as well as oncogenic processes in which clock-controlled checkpoints and stress pathways are perturbed. PER1 research is therefore relevant to studies of chronobiology, transcriptional regulation, and timing-dependent cellular stress responses in human model systems.

Per1 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient PER1 upregulation across a broader range of human cell types.

Per1 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the PER1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Per1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PER1 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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