
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
hSNF2H CRISPR Activation Plasmid (h) | sc-403825-ACT | 20 µg | $397.00 |
SMARCA5 encodes the human ISWI ATP-dependent chromatin remodeler hSNF2H, a catalytic subunit that repositions nucleosomes to regulate chromatin accessibility. hSNF2H supports DNA replication and repair, transcriptional control, and higher-order chromatin organization through remodeling complexes such as ACF, CHRAC, WICH, and RSF. By coordinating nucleosome spacing and facilitating replication-coupled chromatin assembly, SMARCA5 influences cell cycle progression and genome stability pathways. Dysregulated chromatin remodeling and altered SMARCA5 activity have been implicated in proliferative and neurodevelopmental phenotypes, making it a useful target for studying epigenetic mechanisms underlying disease-relevant gene expression programs.
hSNF2H CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SMARCA5 expression without altering the underlying DNA sequence.
hSNF2H CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SMARCA5 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 SMARCA5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous hSNF2H expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SMARCA5 locus and enabling the study of hSNF2H-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of hSNF2H pathway restoration in tumor cells with silenced or reduced SMARCA5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.