G530011O06Rik Lentiviral Activation Particles (m): sc-437289-LAC

Mouse G530011O06Rik encodes a largely uncharacterized protein with limited functional annotation, frequently studied as part of transcriptomic and systems biology efforts to resolve novel regulators of cellular state. Available expression data suggest context-dependent regulation that may reflect roles in basic processes such as transcriptional control, RNA metabolism, or signaling-associated gene networks. Because the gene’s pathway placement remains incompletely defined, perturbation-based studies are often used to map downstream transcriptional programs and interacting pathways. Altered expression patterns of poorly characterized RIKEN genes like G530011O06Rik are commonly investigated as biomarkers or modulators in disease-relevant models, including inflammation, metabolic stress, and neurobiological phenotypes, without implying causality.

G530011O06Rik Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient G530011O06Rik upregulation across a broader range of human cell types.

G530011O06Rik Lentiviral Activation Particles (m) 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 G530011O06Rik transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous G530011O06Rik expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native G530011O06Rik 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.