TM9SF4 Double Nickase Plasmid (h): sc-406168-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TM9SF4 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
- TM9SF4 Double Nickase Plasmid (h) and TM9SF4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TM9SF4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TM9SF4 Antibody (A-3): sc-374473
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TM9SF4 Double Nickase Plasmid (h) | sc-406168-NIC | 20 µg | $410.00 | |||
TM9SF4 Double Nickase Plasmid (h2) | sc-406168-NIC-2 | 20 µg | $410.00 |
TM9SF4 (transmembrane 9 superfamily member 4) encodes a multi-pass membrane protein enriched in endomembrane compartments, where it has been linked to regulation of vesicular trafficking and organelle homeostasis. TM9SF4 has been implicated in control of endosomal–lysosomal maturation and Golgi-associated processes that influence protein sorting and membrane composition. Through these roles, TM9SF4 can affect receptor turnover, cell-surface proteostasis, and stress-adaptive trafficking programs. Altered TM9SF4 expression or activity has been associated with oncogenic phenotypes in some contexts, making it relevant for mechanistic studies of tumor cell fitness, invasion, and microenvironmental adaptation.
TM9SF4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TM9SF4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TM9SF4. 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 TM9SF4 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 TM9SF4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.