
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HIRA CRISPR Activation Plasmid (h) | sc-404262-ACT | 20 µg | $397.00 |
Human HIRA encodes a histone chaperone that partners with ASF1A/ASF1B to deposit the histone variant H3.3 in a DNA replication–independent manner, shaping chromatin accessibility and long-term transcriptional states. HIRA-dependent H3.3 incorporation supports genome stability, replication stress responses, senescence-associated chromatin remodeling, and proper regulation of developmental and cell cycle gene programs. By influencing nucleosome assembly at promoters, enhancers, and sites of DNA damage, HIRA links epigenetic maintenance to pathways controlling differentiation, proliferation, and cellular aging. Dysregulated HIRA function or expression has been connected to aberrant chromatin organization and transcriptional programs observed in cancer biology and neurodevelopmental contexts, making it a useful node for mechanistic epigenetics studies.
HIRA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HIRA expression without altering the underlying DNA sequence.
HIRA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HIRA 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 HIRA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HIRA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HIRA locus and enabling the study of HIRA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HIRA pathway restoration in tumor cells with silenced or reduced HIRA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.