
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SRCAP Lentiviral Activation Particles (h) | sc-403049-LAC | 200 µl | $455.00 |
SRCAP (Snf2-related CREBBP activator protein) encodes an ATP-dependent chromatin remodeler that serves as the catalytic subunit of the SRCAP complex, which mediates histone variant exchange by depositing H2A.Z into nucleosomes. Through regulation of nucleosome positioning and chromatin accessibility, SRCAP influences transcriptional control programs, DNA repair responses, and cell-cycle–linked chromatin dynamics. SRCAP-dependent H2A.Z incorporation contributes to promoter and enhancer function and intersects with pathways governing genome stability and differentiation. Genetic disruption or dysregulation of SRCAP has been associated with neurodevelopmental phenotypes and altered transcriptional regulation, supporting its relevance for mechanistic studies of chromatin remodeling in human cells.
SRCAP 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 SRCAP upregulation across a broader range of human cell types.
SRCAP 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 SRCAP transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SRCAP expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SRCAP 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.