
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PI 3-kinase p110δ CRISPR Activation Plasmid (m) | sc-422232-ACT | 20 µg | $397.00 |
Pik3cd encodes the catalytic p110δ subunit of class I phosphoinositide 3-kinase (PI3K), a key enzyme that converts PIP2 to PIP3 to initiate downstream AKT/mTOR signaling. PI3K p110δ is enriched in hematopoietic lineages and supports antigen receptor signaling, chemokine-driven migration, and cytokine-mediated survival programs that shape immune cell activation and differentiation. Altered Pik3cd activity can perturb immune homeostasis and inflammatory signaling, making it a widely used node for dissecting signal transduction in leukocytes. In mouse models, modulation of p110δ provides a tractable entry point to study pathway crosstalk with MAPK, NF-κB, and metabolic control of immune function.
PI 3-kinase p110δ CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Pik3cd expression without altering the underlying DNA sequence.
PI 3-kinase p110δ CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Pik3cd 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 Pik3cd transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PI 3-kinase p110δ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Pik3cd locus and enabling the study of PI 3-kinase p110δ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PI 3-kinase p110δ pathway restoration in tumor cells with silenced or reduced Pik3cd expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.