HEL308 Lentiviral Activation Particles (h): sc-404447-LAC

Human HELQ encodes the HEL308 DNA helicase, an ATP-dependent 3′→5′ helicase that promotes genome stability by processing stalled replication forks and recombination intermediates. HEL308/HELQ functions in DNA damage tolerance, replication stress responses, and interstrand crosslink repair, interfacing with homologous recombination and S-phase checkpoint signaling to limit chromosomal aberrations. Disruption or dysregulation of HELQ-associated pathways has been linked to impaired replication fork recovery and elevated mutational burden, making it relevant to studies of cancer susceptibility and DNA repair deficiency phenotypes. As a replication-coupled helicase, HEL308 is frequently examined in contexts where fork protection, lesion bypass, and recombination control determine cell fate under genotoxic stress.

HEL308 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 HELQ upregulation across a broader range of human cell types.

HEL308 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 HELQ transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous HEL308 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native HELQ 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.