karyopherin α7 CRISPR Activation Plasmid (h2): sc-418827-ACT-2

Human KPNA7 encodes karyopherin alpha 7, an importin-α family adaptor that recognizes classical nuclear localization signals and partners with importin-β to mediate selective nucleocytoplasmic transport through the nuclear pore complex. KPNA7 supports nuclear import of regulatory proteins involved in transcriptional control, cell-cycle progression, and early developmental programs, linking it to broader nuclear transport and chromatin-associated pathways. Dysregulated importin-α signaling and altered KPNA7 expression have been reported in contexts of aberrant proliferation and tumor biology, suggesting relevance to mechanisms of oncogenic transcription factor localization and genome regulation. KPNA7 reagents are useful for dissecting cargo specificity, mapping nuclear import networks, and evaluating how perturbations in nuclear trafficking influence gene expression and cellular phenotypes in human model systems.

karyopherin α7 CRISPR Activation Plasmid (h2) provides a targeted, non-destructive approach to upregulating endogenous KPNA7 expression without altering the underlying DNA sequence.

karyopherin α7 CRISPR Activation Plasmid (h2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KPNA7 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the KPNA7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous karyopherin α7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KPNA7 locus and enabling the study of karyopherin α7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of karyopherin α7 pathway restoration in tumor cells with silenced or reduced KPNA7 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.