
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARID2 CRISPR Activation Plasmid (h) | sc-401863-ACT | 20 µg | $397.00 |
ARID2 encodes an AT-rich interaction domain–containing subunit of the PBAF (SWI/SNF) ATP-dependent chromatin remodeling complex that regulates nucleosome positioning and transcriptional programs. Through coordination of enhancer and promoter accessibility, ARID2 influences lineage specification, DNA damage responses, and cellular differentiation states. Altered ARID2 activity has been associated with dysregulated epigenetic control and transcriptional networks implicated in tumorigenesis and other diseases characterized by aberrant chromatin regulation. As a chromatin remodeler component, ARID2 is commonly studied in pathways governing genome stability, interferon-stimulated gene regulation, and context-dependent control of cell cycle and apoptosis.
ARID2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ARID2 expression without altering the underlying DNA sequence.
ARID2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ARID2 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 ARID2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ARID2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ARID2 locus and enabling the study of ARID2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ARID2 pathway restoration in tumor cells with silenced or reduced ARID2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.