ODR4 Lentiviral Activation Particles (h2): sc-417633-LAC-2

Human C1orf27 encodes ODR4, an endoplasmic reticulum–associated transmembrane protein implicated in the biosynthesis, folding, and trafficking of G protein–coupled receptors and other secretory pathway clients. ODR4 contributes to ER quality control and proteostasis by influencing receptor maturation and surface delivery, linking it to cellular processes such as GPCR signaling competency and stress-responsive pathways including the unfolded protein response. Dysregulated ODR4 function or expression has been associated in the literature with altered receptor homeostasis and has been explored in contexts where GPCR and ER stress networks are perturbed, including cancer- and neurobiology-relevant models. Gene editing of C1orf27 provides a tractable approach to dissect ER trafficking mechanisms, map receptor interactomes, and build isogenic cell systems for functional genomics studies of secretory pathway regulation.

ODR4 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient C1orf27 upregulation across a broader range of human cell types.

ODR4 Lentiviral Activation Particles (h2) 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 C1orf27 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ODR4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native C1orf27 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.