
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IP3KC CRISPR Activation Plasmid (h) | sc-408964-ACT | 20 µg | $397.00 |
ITPKC encodes inositol-trisphosphate 3-kinase C (IP3KC), an enzyme that phosphorylates inositol 1,4,5-trisphosphate (IP3) to generate IP4, thereby modulating IP3-dependent Ca2+ mobilization from intracellular stores. By shaping cytosolic Ca2+ dynamics, IP3KC influences downstream signaling cascades that couple second-messenger flux to transcriptional programs, including pathways linked to lymphocyte activation and broader immune signaling. Altered ITPKC activity has been associated with dysregulated Ca2+-dependent responses and inflammatory phenotypes, making it relevant for mechanistic studies of signal integration and immune cell function. As a node in phosphoinositide metabolism and Ca2+ signaling, IP3KC is frequently investigated in contexts where stimulus-dependent transcription and cellular activation thresholds are under study.
IP3KC CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ITPKC expression without altering the underlying DNA sequence.
IP3KC CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ITPKC 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 ITPKC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IP3KC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ITPKC locus and enabling the study of IP3KC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IP3KC pathway restoration in tumor cells with silenced or reduced ITPKC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.