TM4SF1 Double Nickase Plasmid (h): sc-404779-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TM4SF1 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
- TM4SF1 Double Nickase Plasmid (h) and TM4SF1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TM4SF1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TM4SF1 Double Nickase Plasmid (h) | sc-404779-NIC | 20 µg | $410.00 | |||
TM4SF1 Double Nickase Plasmid (h2) | sc-404779-NIC-2 | 20 µg | $410.00 |
TM4SF1 (transmembrane 4 L six family member 1) encodes a tetraspanin-like cell surface glycoprotein that organizes membrane microdomains and modulates cell–cell and cell–matrix interactions. It participates in processes linked to cytoskeletal remodeling, cell adhesion, migration, and signaling cross-talk with integrins and growth factor pathways. TM4SF1 expression is frequently used as a marker of activated endothelial and epithelial states and has been associated with angiogenic programs, invasive phenotypes, and remodeling of the tumor microenvironment. As a result, TM4SF1 is widely studied in mechanisms underlying vascular biology, metastatic progression, and stress-adaptive signaling in cancer models.
TM4SF1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TM4SF1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TM4SF1. 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 TM4SF1 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 TM4SF1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.