PLC γ1 Double Nickase Plasmid (h): sc-400472-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PLC γ1 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
- PLC γ1 Double Nickase Plasmid (h) and PLC γ1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PLCG1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PLC γ1 Antibody (E-12): sc-7290
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PLC γ1 Double Nickase Plasmid (h) | sc-400472-NIC | 20 µg | $410.00 | |||
PLC γ1 Double Nickase Plasmid (h2) | sc-400472-NIC-2 | 20 µg | $410.00 |
PLCG1 encodes phospholipase Cγ1 (PLCγ1), a receptor-proximal signaling enzyme that hydrolyzes PIP2 to generate IP3 and diacylglycerol, driving intracellular Ca2+ mobilization and protein kinase C activation. PLCγ1 is activated downstream of receptor tyrosine kinases and immune receptors, integrating signals that regulate proliferation, differentiation, cytoskeletal remodeling, and cell migration. This axis interfaces with PI3K–AKT and MAPK/ERK signaling and shapes transcriptional outputs through Ca2+-dependent effectors. Dysregulated PLCG1 activity has been implicated in oncogenic signaling contexts and aberrant immune cell activation, supporting its relevance in mechanistic studies of signal transduction.
PLC γ1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PLCG1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PLCG1. 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 PLCG1 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 PLCG1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.