C1orf115 Lentiviral Activation Particles (h2): sc-413237-LAC-2

Human C1orf115 encodes a poorly characterized protein with limited functional annotation, reported primarily through transcriptomic and proteomic surveys rather than defined biochemical activity. Current evidence suggests C1orf115 may participate in cell-state–dependent regulatory programs, with expression patterns implicating roles in fundamental processes such as cellular differentiation, stress responses, and broader transcriptional or post-transcriptional control networks. Altered C1orf115 expression has been observed in disease-associated datasets, supporting its use as a candidate gene for mechanistic studies of dysregulated gene expression in complex disorders, including cancer-relevant signatures. Gene editing of C1orf115 enables targeted loss- or gain-of-function interrogation to map pathway connectivity, identify interaction partners, and validate genotype–phenotype relationships in human cell models.

C1orf115 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 C1orf115 upregulation across a broader range of human cell types.

C1orf115 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 C1orf115 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous C1orf115 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native C1orf115 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.