Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
MerTK Double Nickase Plasmid (m): sc-421631-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MerTK Double Nickase Plasmid (m) 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
- MerTK Double Nickase Plasmid (m) and MerTK Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mertk. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MerTK Antibody (B-1): sc-365499
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MerTK Double Nickase Plasmid (m) | sc-421631-NIC | 20 µg | $410.00 | |||
MerTK Double Nickase Plasmid (m2) | sc-421631-NIC-2 | 20 µg | $410.00 |
Mouse Mertk encodes MerTK, a TAM family receptor tyrosine kinase that recognizes phosphatidylserine on apoptotic cells via bridging ligands such as GAS6 and PROS1, promoting efferocytosis and immune homeostasis. MerTK signaling engages PI3K–AKT, MAPK/ERK, and STAT pathways to coordinate cytoskeletal remodeling, phagosome maturation, and anti-inflammatory transcriptional programs in macrophages, microglia, dendritic cells, and retinal pigment epithelium. Disrupted Mertk function has been linked to defective clearance of dying cells, altered innate immune regulation, and tissue degeneration, making it relevant to studies of neuroinflammation, retinal homeostasis, and autoimmune-like phenotypes in mouse models. As a node integrating phagocytic uptake with cytokine tuning, MerTK is frequently interrogated in myeloid signaling and clearance pathway research.
MerTK Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mertk locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mertk. 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 Mertk 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 Mertk-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.