
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APOBEC3B CRISPR Activation Plasmid (h) | sc-401700-ACT | 20 µg | $397.00 | |||
APOBEC3B CRISPR Activation Plasmid (h2) | sc-401700-ACT-2 | 20 µg | $397.00 |
APOBEC3B encodes a cytidine deaminase that edits single-stranded DNA by converting cytosine to uracil, functioning in intrinsic antiviral defense and restriction of retroelements. Its activity interfaces with DNA replication and repair processes, including replication stress responses and mutagenic lesion processing, thereby shaping genome-wide mutation patterns. Dysregulated APOBEC3B expression is associated with elevated somatic mutational burden and characteristic APOBEC mutation signatures across multiple tumor types. As a result, APOBEC3B is widely studied in pathways controlling genome stability, innate immune signaling, and mutation-driven adaptation.
APOBEC3B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous APOBEC3B expression without altering the underlying DNA sequence.
APOBEC3B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the APOBEC3B 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 APOBEC3B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous APOBEC3B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native APOBEC3B locus and enabling the study of APOBEC3B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of APOBEC3B pathway restoration in tumor cells with silenced or reduced APOBEC3B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.