Tyro3 Double Nickase Plasmid (m): sc-423567-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tyro3 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
- Tyro3 Double Nickase Plasmid (m) and Tyro3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tyro3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Tyro3 Antibody (B-4): sc-166360
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tyro3 Double Nickase Plasmid (m) | sc-423567-NIC | 20 µg | $410.00 |
Tyro3 encodes a receptor tyrosine kinase in the TAM family that binds the ligands GAS6 and Protein S to regulate cell survival, proliferation, and phagocytic clearance of apoptotic cells. In mouse tissues, TYRO3 signaling engages PI3K–AKT and MAPK/ERK pathways and intersects with immune homeostasis programs that constrain inflammatory signaling and support tissue remodeling. The receptor is implicated in neuronal maintenance and synaptic function as well as in myeloid cell regulation within the innate immune system. Dysregulated TAM receptor activity, including TYRO3, has been associated with altered immune tolerance and has been studied in contexts of chronic inflammation, autoimmunity, and cancer-related signaling networks.
Tyro3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tyro3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tyro3. 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 Tyro3 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 Tyro3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.