SMEK1 Double Nickase Plasmid (h): sc-412572-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SMEK1 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
- SMEK1 Double Nickase Plasmid (h) and SMEK1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PPP4R3A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SMEK1 Double Nickase Plasmid (h) | sc-412572-NIC | 20 µg | $410.00 | |||
SMEK1 Double Nickase Plasmid (h2) | sc-412572-NIC-2 | 20 µg | $410.00 |
PPP4R3A encodes SMEK1, a regulatory subunit of protein phosphatase 4 that helps direct PP4 catalytic activity to specific substrates and subcellular compartments. SMEK1 participates in phosphorylation-dependent control of cell-cycle progression, DNA damage responses, and stress-adaptive signaling by modulating dephosphorylation events that shape chromatin and checkpoint outputs. Through these functions, PPP4R3A is relevant to mechanisms that influence genome stability and proliferation programs commonly perturbed in cancer biology. Altered SMEK1-linked phosphatase regulation has also been investigated in contexts of differentiation and tissue homeostasis, where signaling fidelity impacts disease-associated cellular phenotypes.
SMEK1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PPP4R3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PPP4R3A. 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 PPP4R3A 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 PPP4R3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.