TMEM2 Double Nickase Plasmid (h): sc-407487-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM2 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
- TMEM2 Double Nickase Plasmid (h) and TMEM2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TMEM2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM2 Double Nickase Plasmid (h) | sc-407487-NIC | 20 µg | $410.00 | |||
TMEM2 Double Nickase Plasmid (h2) | sc-407487-NIC-2 | 20 µg | $410.00 |
TMEM2 encodes a single-pass transmembrane protein with hyaluronidase activity that contributes to extracellular matrix remodeling by depolymerizing high–molecular weight hyaluronan at the cell surface. Through modulation of hyaluronan turnover and pericellular matrix composition, TMEM2 influences cell adhesion, migration, and tissue morphogenesis, processes that intersect with integrin signaling and mechanotransduction pathways. Altered hyaluronan dynamics and TMEM2 dysregulation have been linked to changes in tumor microenvironment biology, invasive behavior, and stromal interactions across multiple cancer contexts. TMEM2 is therefore a useful target for dissecting how extracellular matrix catabolism shapes cell-state transitions and microenvironment-dependent phenotypes.
TMEM2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TMEM2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TMEM2. 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 TMEM2 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 TMEM2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.