MOZ CRISPR Activation Plasmid (h): sc-403564-ACT

Human KAT6A encodes the lysine acetyltransferase MOZ, a MYST family histone acetyltransferase that acetylates H3/H4 and functions as a transcriptional co-regulator at enhancers and promoters. MOZ integrates with chromatin remodeling and RNA polymerase II–dependent transcription to control cell-fate programs, including hematopoietic differentiation and stem/progenitor maintenance. Through its roles in epigenetic regulation, KAT6A influences pathways governing proliferation, DNA damage responses, and lineage-specific gene expression. Dysregulation of KAT6A/MOZ activity, including oncogenic fusion events and altered expression, has been implicated in hematologic malignancies and broader transcriptional/epigenomic instability relevant to cancer biology research.

MOZ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KAT6A expression without altering the underlying DNA sequence.

MOZ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KAT6A 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 KAT6A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MOZ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KAT6A locus and enabling the study of MOZ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MOZ pathway restoration in tumor cells with silenced or reduced KAT6A expression.

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