Nup37 Lentiviral Activation Particles (h): sc-409458-LAC

NUP37 encodes Nup37, a core component of the Nup107–160 subcomplex of the nuclear pore complex that supports nuclear envelope assembly and nucleocytoplasmic transport of proteins and RNAs. By contributing to NPC architecture, Nup37 helps coordinate cell-cycle progression, mitotic events, and genome regulation through controlled trafficking of transcription factors and signaling mediators. Perturbation of nuclear pore composition is frequently linked to altered chromatin organization and stress-response signaling, making NUP37 a useful entry point for studying transport-dependent regulation of proliferation and differentiation. Dysregulated expression or dependency on nucleoporin function has been reported across multiple tumor contexts, supporting research into nuclear transport vulnerabilities and pathway rewiring without implying therapeutic use.

Nup37 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 NUP37 upregulation across a broader range of human cell types.

Nup37 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 NUP37 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Nup37 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NUP37 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.