
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF2C Lentiviral Activation Particles (h) | sc-404645-LAC | 200 µl | $455.00 |
KIF2C (also known as MCAK) encodes a kinesin-13 family microtubule depolymerase that regulates microtubule plus-end dynamics during mitosis. By controlling kinetochore–microtubule attachments, spindle assembly, and chromosome congression, KIF2C helps ensure accurate chromosome segregation and mitotic fidelity. Its activity interfaces with cell-cycle and spindle checkpoint processes and is functionally linked to pathways governing genome stability. Dysregulated KIF2C expression or function is frequently studied in the context of chromosomal instability and proliferative disease biology, where altered microtubule dynamics can contribute to aneuploidy-associated phenotypes.
KIF2C 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 KIF2C upregulation across a broader range of human cell types.
KIF2C 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 KIF2C transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous KIF2C expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native KIF2C 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.