
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ANP32D CRISPR Activation Plasmid (h) | sc-410569-ACT | 20 µg | $397.00 |
ANP32D (acidic nuclear phosphoprotein 32 family member D) is a human nuclear protein in the ANP32 family implicated in chromatin-associated regulation of gene expression and RNA-related processes. ANP32 proteins are characterized by leucine-rich repeats and an acidic C-terminal region that can influence protein–protein interactions involved in transcriptional control, nucleocytoplasmic dynamics, and cellular stress responses. Through these functions, ANP32D is relevant to pathways governing proliferation and apoptosis, and its altered expression has been explored in contexts where epigenetic and transcriptional programs are disrupted. Studying ANP32D helps clarify how nuclear phosphoprotein networks shape cell-state transitions and disease-associated gene regulatory circuitry.
ANP32D CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ANP32D expression without altering the underlying DNA sequence.
ANP32D CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ANP32D 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 ANP32D transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ANP32D expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ANP32D locus and enabling the study of ANP32D-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ANP32D pathway restoration in tumor cells with silenced or reduced ANP32D expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.