DDB1 Lentiviral Activation Particles (m): sc-419966-LAC

Mouse DDB1 (damage specific DNA binding protein 1) is a core component of the CUL4–DDB1 E3 ubiquitin ligase complex that coordinates substrate ubiquitination to regulate protein turnover across the cell cycle. It participates in nucleotide excision repair and replication-associated DNA damage responses, linking chromatin-associated lesions to ubiquitin-dependent signaling and proteostasis. Through interactions with DCAF substrate receptors, DDB1 helps govern chromatin remodeling, replication licensing, and checkpoint control. Dysregulated DDB1-dependent ubiquitination and genome maintenance pathways are relevant to studies of oncogenic stress, developmental phenotypes, and neurodegeneration-associated DNA repair defects in mouse models.

DDB1 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Ddb1 upregulation across a broader range of human cell types.

DDB1 Lentiviral Activation Particles (m) 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 Ddb1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous DDB1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ddb1 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.