PI 3-kinase p110 δ CRISPR Activation Plasmid (h): sc-400426-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PI 3-kinase p110 δ CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- PI 3-kinase p110 δ CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by PI 3-kinase p110 δ CRISPR Activation Plasmid (h) and PI 3-kinase p110 δ CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PIK3CD transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PI 3-kinase p110δ Antibody (A-8): sc-55589
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PI 3-kinase p110 δ CRISPR Activation Plasmid (h) | sc-400426-ACT | 20 µg | $397.00 |
PIK3CD encodes the catalytic p110δ subunit of class I phosphoinositide 3-kinase (PI3K), a key regulator of signal transduction downstream of antigen receptors, cytokine receptors, and select receptor tyrosine kinases. PI3K p110δ catalyzes generation of PIP3 to activate AKT-mTOR signaling, shaping lymphocyte development, activation, survival, and metabolic reprogramming, and influencing chemotaxis and vesicular trafficking through downstream effectors. Dysregulated PIK3CD activity perturbs immune homeostasis and inflammatory signaling and is widely studied in contexts such as immunodeficiency, autoimmunity, and hematologic malignancy biology. As a node in PI3K/AKT, mTOR, and NF-κB-linked networks, p110δ provides a tractable handle for dissecting pathway cross-talk in immune and cancer-relevant cellular models.
PI 3-kinase p110 δ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PIK3CD expression without altering the underlying DNA sequence.
PI 3-kinase p110 δ CRISPR Activation Plasmid (h) 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 p110 δ 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 p110 δ-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 p110 δ pathway restoration in tumor cells with silenced or reduced PIK3CD expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.