U11/U12 snRNP 20K Double Nickase Plasmid (h): sc-409456-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- U11/U12 snRNP 20K 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
- U11/U12 snRNP 20K Double Nickase Plasmid (h) and U11/U12 snRNP 20K Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZMAT5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
U11/U12 snRNP 20K Double Nickase Plasmid (h) | sc-409456-NIC | 20 µg | $410.00 |
ZMAT5 encodes U11/U12 snRNP 20K, a core component of the minor (U12-dependent) spliceosome that participates in recognition and processing of U12-type introns. Through its role in pre-mRNA splicing and spliceosome assembly, U11/U12 snRNP 20K helps maintain transcript fidelity for genes enriched in signaling, DNA repair, and cell-cycle regulation. Disruption of minor spliceosome function can alter isoform balance and trigger widespread changes in gene expression programs linked to differentiation and stress responses. Consequently, ZMAT5 is relevant to studies of splicing dysregulation observed in genetic disorders and cancer-associated RNA processing phenotypes.
U11/U12 snRNP 20K Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZMAT5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZMAT5. 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 ZMAT5 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 ZMAT5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.