PPP2R3A Double Nickase Plasmid (h): sc-402433-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PPP2R3A Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- PPP2R3A Double Nickase Plasmid (h) and PPP2R3A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PPP2R3A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PPP2R3A Double Nickase Plasmid (h) | sc-402433-NIC | 20 µg | $410.00 | |||
PPP2R3A Double Nickase Plasmid (h2) | sc-402433-NIC-2 | 20 µg | $410.00 |
PPP2R3A encodes PR130, a regulatory B″ subunit of protein phosphatase 2A (PP2A) that helps direct PP2A holoenzyme assembly, subcellular localization, and substrate selection. Through PP2A-mediated dephosphorylation, PPP2R3A influences phosphorylation-dependent control of cell cycle progression, cytoskeletal organization, and signal transduction cascades that integrate kinase-driven inputs. Altered PP2A regulation is broadly linked to disrupted growth and stress-response signaling, and changes in PPP2R3A expression or function have been investigated in the context of oncogenic pathway rewiring and other phosphorylation-centric disease mechanisms. As a result, PPP2R3A is frequently studied to dissect how PP2A specificity shapes downstream pathway outputs and cellular phenotypes.
PPP2R3A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PPP2R3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PPP2R3A. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt PPP2R3A function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of PPP2R3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.