CHD7 Lentiviral Activation Particles (h): sc-404017-LAC

CHD7 encodes chromodomain helicase DNA-binding protein 7, an ATP-dependent chromatin remodeler that reads histone marks and regulates nucleosome positioning to control transcriptional programs during development and lineage specification. It integrates epigenetic signaling with enhancer and promoter accessibility, influencing processes such as neural crest development, neurogenesis, and organ morphogenesis through broad modulation of gene expression networks. CHD7 activity intersects with pathways governing chromatin organization, RNA polymerase II transcription, and cell fate decisions. Dysregulated CHD7 function is linked to developmental disorders, including CHARGE syndrome, and is studied in the context of neurodevelopmental and congenital phenotypes.

CHD7 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 CHD7 upregulation across a broader range of human cell types.

CHD7 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 CHD7 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CHD7 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CHD7 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.