CDK5RAP3 Lentiviral Activation Particles (h): sc-408965-LAC

CDK5RAP3 (also known as C53) is a multifunctional cytoplasmic and perinuclear protein implicated in regulating cell-cycle progression, stress-adaptive signaling, and protein homeostasis. It has been linked to modulation of kinase-driven pathways, ubiquitin-dependent processes, and endoplasmic reticulum–associated quality control, connecting it to cellular responses to proteotoxic and metabolic stress. Through these roles, CDK5RAP3 is studied in contexts where proliferation, apoptosis, and adaptive stress programs are remodeled, including oncogenic signaling and inflammation-associated phenotypes. Altered CDK5RAP3 expression has been reported in multiple tumor types, motivating mechanistic research on how it influences growth control and pathway crosstalk in human cells.

CDK5RAP3 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 CDK5RAP3 upregulation across a broader range of human cell types.

CDK5RAP3 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 CDK5RAP3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CDK5RAP3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CDK5RAP3 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.