CDYL Lentiviral Activation Particles (h): sc-406624-LAC

Human CDYL (chromodomain Y-like) is a chromatin-associated transcriptional coregulator that links epigenetic recognition to transcriptional repression through interactions with histone modifications and chromatin remodeling factors. CDYL contributes to heterochromatin formation and regulation of gene expression programs involved in neuronal development, cell-cycle control, and differentiation by modulating histone acetylation and methylation states. Through its role in chromatin compaction and transcriptional silencing, CDYL influences pathways governing genome stability and cellular identity. Dysregulated CDYL activity and altered chromatin states have been associated with aberrant transcriptional networks relevant to cancer biology and neurodevelopmental phenotypes.

CDYL 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 CDYL upregulation across a broader range of human cell types.

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