
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APOBEC3A CRISPR Activation Plasmid (h) | sc-418267-ACT | 20 µg | $397.00 |
Human APOBEC3A encodes a zinc-dependent cytidine deaminase of the APOBEC family that catalyzes C-to-U editing on single-stranded DNA and can influence genome stability during replication stress. It participates in innate antiviral defense and intersects with DNA damage response and repair processes, including pathways linked to replication fork processing and mutagenesis. Dysregulated APOBEC3A activity has been associated with characteristic cytidine deamination mutational signatures observed across multiple cancer types and with inflammatory contexts that elevate ssDNA substrates. As a result, APOBEC3A is widely studied for its roles in host–pathogen interactions, endogenous retroelement restriction, and mechanisms that shape somatic mutation landscapes.
APOBEC3A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous APOBEC3A expression without altering the underlying DNA sequence.
APOBEC3A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the APOBEC3A 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 APOBEC3A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous APOBEC3A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native APOBEC3A locus and enabling the study of APOBEC3A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of APOBEC3A pathway restoration in tumor cells with silenced or reduced APOBEC3A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.