TMEM173 Double Nickase Plasmid (m): sc-428364-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM173 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
- TMEM173 Double Nickase Plasmid (m) and TMEM173 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tmem173. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TMEM173 Antibody (C-10): sc-518172
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM173 Double Nickase Plasmid (m) | sc-428364-NIC | 20 µg | $410.00 | |||
TMEM173 Double Nickase Plasmid (m2) | sc-428364-NIC-2 | 20 µg | $410.00 |
Tmem173 encodes TMEM173 (also known as STING), an endoplasmic reticulum–resident adaptor that coordinates innate immune sensing of cytosolic DNA. Upon binding cyclic dinucleotides produced by cGAS, TMEM173 drives TBK1–IRF3 signaling and NF-κB activation, promoting type I interferon and inflammatory gene programs. This pathway intersects with autophagy and cell stress responses and shapes antiviral defense, responses to intracellular bacteria, and tumor–immune microenvironment signaling in mouse models. Dysregulated TMEM173 signaling has been linked to aberrant inflammation and autoimmune-like phenotypes, making it a frequent target in studies of immunopathology and host–pathogen interactions.
TMEM173 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tmem173 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tmem173. 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 Tmem173 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 Tmem173-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.