SUV420H1 Double Nickase Plasmid (h): sc-404615-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SUV420H1 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
- SUV420H1 Double Nickase Plasmid (h) and SUV420H1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KMT5B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SUV420H1 Double Nickase Plasmid (h) | sc-404615-NIC | 20 µg | $410.00 | |||
SUV420H1 Double Nickase Plasmid (h2) | sc-404615-NIC-2 | 20 µg | $410.00 |
KMT5B encodes the human histone lysine methyltransferase SUV420H1, an enzyme that catalyzes H4K20 di- and trimethylation and helps establish repressive chromatin states. Through shaping higher-order chromatin architecture and epigenetic memory, SUV420H1 influences DNA replication timing, genome stability, and DNA damage repair, intersecting with cell-cycle control and chromatin remodeling pathways. Altered H4K20 methylation patterns and dysregulated SUV420H1 activity have been linked to aberrant transcriptional programs and genomic instability observed across multiple disease contexts, including cancer and neurodevelopmental disorders. These properties make KMT5B a useful target for studying chromatin-dependent regulation of gene expression and maintenance of epigenome integrity in human cells.
SUV420H1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KMT5B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KMT5B. 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 KMT5B 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 KMT5B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.