IGSF10 Double Nickase Plasmid (h): sc-415415-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IGSF10 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
- IGSF10 Double Nickase Plasmid (h) and IGSF10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IGSF10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IGSF10 Double Nickase Plasmid (h) | sc-415415-NIC | 20 µg | $410.00 | |||
IGSF10 Double Nickase Plasmid (h2) | sc-415415-NIC-2 | 20 µg | $410.00 |
IGSF10 encodes an immunoglobulin superfamily transmembrane protein implicated in cell–cell communication and extracellular matrix-associated adhesion processes that influence tissue organization and developmental patterning. Expression and genetic studies have linked IGSF10 to modulation of migratory behaviors and signaling contexts that intersect with cell adhesion, cytoskeletal remodeling, and differentiation programs. In human biology, IGSF10 has been investigated in relation to neurodevelopmental timing and reproductive axis regulation, including associations reported for delayed puberty phenotypes, and it is also explored as a context-dependent factor in tumor biology. These features make IGSF10 a useful target for dissecting adhesion-related regulatory networks and phenotypic outcomes in relevant cell models.
IGSF10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IGSF10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IGSF10. 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 IGSF10 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 IGSF10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.