
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF13A CRISPR Activation Plasmid (h) | sc-403751-ACT | 20 µg | $397.00 |
KIF13A encodes a kinesin-3 family microtubule motor that supports plus-end–directed transport of vesicles and protein complexes, contributing to polarized trafficking and cytoskeletal organization. KIF13A activity is linked to endosomal and membrane transport processes that influence cell polarity, signaling dynamics, and spatial control of cargo delivery. Through its role in intracellular transport, KIF13A can impact pathways governing membrane receptor distribution and junctional integrity. Altered regulation of these processes has been associated with phenotypes relevant to inflammation, epithelial barrier function, and other contexts where trafficking-dependent signaling is critical.
KIF13A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KIF13A expression without altering the underlying DNA sequence.
KIF13A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KIF13A 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 KIF13A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KIF13A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KIF13A locus and enabling the study of KIF13A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KIF13A pathway restoration in tumor cells with silenced or reduced KIF13A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.