APOBEC3B Lentiviral Activation Particles (h): sc-401700-LAC

APOBEC3B (apolipoprotein B mRNA editing enzyme catalytic subunit 3B) is a cytidine deaminase that converts cytosine to uracil in single-stranded DNA, contributing to innate antiviral restriction and endogenous retroelement control. Its activity interfaces with DNA replication and repair processes by generating lesions that can be processed into mutations, thereby influencing genomic stability. Dysregulated APOBEC3B expression has been linked to characteristic mutational signatures observed across multiple cancer types and is studied in the context of tumor evolution, DNA damage responses, and replication stress. As a nuclear APOBEC family member, APOBEC3B is widely used to investigate mechanisms of mutagenesis, host–virus interactions, and determinants of mutation-driven phenotypes in human cells.

APOBEC3B Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient APOBEC3B upregulation across a broader range of human cell types.

APOBEC3B Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the APOBEC3B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous APOBEC3B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native APOBEC3B genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.