JAZF1 CRISPR Activation Plasmid (h): sc-404839-ACT

JAZF1 (juxtaposed with another zinc finger protein 1) encodes a zinc finger transcriptional regulator that modulates gene expression programs linked to cellular metabolism, differentiation, and stress-adaptive responses. In human cells, JAZF1 has been connected to nuclear transcriptional control networks that influence lipid and glucose homeostasis and broader endocrine signaling contexts. Genetic studies have associated JAZF1 loci with metabolic trait variation, including type 2 diabetes susceptibility, and altered JAZF1 activity has been explored in endocrine-related pathophysiology. These features make JAZF1 a useful node for dissecting transcriptional circuitry and metabolic pathway regulation in biomedical research models.

JAZF1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous JAZF1 expression without altering the underlying DNA sequence.

JAZF1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the JAZF1 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 JAZF1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous JAZF1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native JAZF1 locus and enabling the study of JAZF1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of JAZF1 pathway restoration in tumor cells with silenced or reduced JAZF1 expression.

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