TMEM98 Double Nickase Plasmid (h): sc-409870-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM98 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
- TMEM98 Double Nickase Plasmid (h) and TMEM98 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TMEM98. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM98 Double Nickase Plasmid (h) | sc-409870-NIC | 20 µg | $410.00 | |||
TMEM98 Double Nickase Plasmid (h2) | sc-409870-NIC-2 | 20 µg | $410.00 |
TMEM98 encodes a small transmembrane protein enriched in ocular tissues and implicated in the regulation of extracellular matrix organization and cell–cell signaling at epithelial and glial interfaces. Human genetic studies associate TMEM98 with inherited eye phenotypes including nanophthalmos and related anterior segment abnormalities, highlighting its relevance to pathways governing ocular growth and tissue homeostasis. At the cellular level, TMEM98 is linked to membrane-localized processes that influence signaling crosstalk and structural maintenance, making it a useful target for dissecting how membrane proteins modulate developmental and stress-responsive programs. Experimental perturbation of TMEM98 supports investigations into genotype–phenotype relationships in eye development and disease-relevant cellular models.
TMEM98 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TMEM98 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TMEM98. 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 TMEM98 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 TMEM98-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.