
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
INPP5E CRISPR Activation Plasmid (h) | sc-405923-ACT | 20 µg | $397.00 |
INPP5E encodes inositol polyphosphate-5-phosphatase E, a phosphoinositide 5-phosphatase that hydrolyzes PI(4,5)P2 and PI(3,4,5)P3 to shape membrane lipid signaling. The protein is enriched at the primary cilium where it regulates ciliary phosphoinositide composition, trafficking of signaling receptors, and downstream pathways including Hedgehog and other cilia-dependent signaling modules. Through these roles, INPP5E contributes to ciliogenesis, neuronal development, and maintenance of cellular polarity. Disruption or dysregulation of INPP5E has been linked to human ciliopathies, supporting its relevance for studying cilium-centered mechanisms of disease.
INPP5E CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous INPP5E expression without altering the underlying DNA sequence.
INPP5E CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the INPP5E 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 INPP5E transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous INPP5E expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native INPP5E locus and enabling the study of INPP5E-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of INPP5E pathway restoration in tumor cells with silenced or reduced INPP5E expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.