MORF Double Nickase Plasmid (h): sc-418605-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MORF 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
- MORF Double Nickase Plasmid (h) and MORF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KAT6B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MORF Double Nickase Plasmid (h) | sc-418605-NIC | 20 µg | $410.00 | |||
MORF Double Nickase Plasmid (h2) | sc-418605-NIC-2 | 20 µg | $410.00 |
KAT6B encodes the human lysine acetyltransferase MORF (also known as MYST4), a nuclear histone acetyltransferase that modifies chromatin to regulate transcriptional programs controlling cell fate decisions, proliferation, and differentiation. MORF functions within multiprotein chromatin-modifying complexes and contributes to acetylation of histones such as H3, shaping promoter and enhancer accessibility across developmental gene networks. KAT6B activity intersects with epigenetic regulation of lineage specification and DNA-templated processes including transcriptional initiation and elongation. Dysregulated KAT6B/MORF function and dosage are linked to developmental syndromes and cancer-associated transcriptional reprogramming, making it a key target for studying chromatin-driven mechanisms of disease biology.
MORF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KAT6B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KAT6B. 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 KAT6B 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 KAT6B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.