RCC1 Lentiviral Activation Particles (h): sc-402078-LAC

Human RCC1 encodes Regulator of Chromosome Condensation 1, a chromatin-bound guanine nucleotide exchange factor (GEF) for Ran that establishes the RanGTP gradient required for nucleocytoplasmic transport. By coupling to chromatin during mitosis, RCC1 supports spindle assembly, nuclear envelope reformation, and faithful chromosome segregation, linking it to core processes in cell cycle progression and genome stability. RCC1 activity intersects with pathways governing mitotic checkpoint control and DNA damage responses through its effects on nuclear trafficking and mitotic dynamics. Dysregulated RCC1 expression or function has been associated with proliferative phenotypes and chromosomal instability observed across multiple cancer contexts, making it a relevant node for mechanistic studies of cell division and nuclear transport.

RCC1 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 RCC1 upregulation across a broader range of human cell types.

RCC1 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 RCC1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous RCC1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native RCC1 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.