CtBP2 Lentiviral Activation Particles (h2): sc-401865-LAC-2

Human CTBP2 encodes C-terminal binding protein 2 (CtBP2), a NADH-sensitive transcriptional coregulator that functions predominantly as a corepressor by partnering with sequence-specific transcription factors and chromatin-modifying enzymes to regulate gene expression programs. CtBP2 integrates metabolic state with epigenetic control through recruitment of histone deacetylases and other remodeling complexes, influencing processes such as epithelial–mesenchymal transition, cell cycle progression, DNA damage responses, and neuronal synapse-associated transcription (including roles linked to the CtBP2/RIBEYE isoform). Dysregulation of CTBP2-dependent transcriptional networks has been associated with tumor progression and metastasis biology as well as neurodevelopmental and sensory-system phenotypes, making it a relevant target for mechanistic studies. Gene editing of CTBP2 supports functional interrogation of transcriptional repression circuits, mapping protein–protein interaction dependencies, and dissecting pathway-specific gene regulatory effects in human cellular models.

CtBP2 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient CTBP2 upregulation across a broader range of human cell types.

CtBP2 Lentiviral Activation Particles (h2) 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 CTBP2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CtBP2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CTBP2 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.