HBO1 CRISPR Activation Plasmid (h): sc-416462-ACT

Human KAT7 encodes the histone acetyltransferase HBO1, a MYST family enzyme that acetylates histone H4 and H3 to promote chromatin accessibility and transcriptional competence. HBO1 functions in multiprotein complexes that couple epigenetic regulation to DNA replication licensing, supporting pre-replication complex assembly and S-phase progression. Through its roles in chromatin remodeling, gene expression control, and genome maintenance, KAT7/HBO1 is frequently studied in pathways governing cell proliferation, differentiation, and DNA damage responses. Dysregulated histone acetylation and replication-associated chromatin states involving HBO1 have been implicated in oncogenic transcriptional programs and other diseases linked to epigenetic instability.

HBO1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KAT7 expression without altering the underlying DNA sequence.

HBO1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KAT7 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 KAT7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HBO1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KAT7 locus and enabling the study of HBO1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HBO1 pathway restoration in tumor cells with silenced or reduced KAT7 expression.

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