MLL2 Double Nickase Plasmid (h): sc-401659-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MLL2 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
- MLL2 Double Nickase Plasmid (h) and MLL2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KMT2D. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MLL2 Antibody (2E1): sc-293217
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MLL2 Double Nickase Plasmid (h) | sc-401659-NIC | 20 µg | $410.00 |
KMT2D (MLL2) encodes a SET domain–containing histone lysine methyltransferase that primarily catalyzes H3K4 mono- and di-methylation at enhancers to support transcriptional initiation and cell type–specific gene expression programs. As a core regulator of chromatin accessibility, MLL2 integrates with COMPASS-like complexes to coordinate enhancer priming, lineage commitment, and signal-responsive transcription across developmental and immune pathways. Disruption of KMT2D perturbs epigenetic control of differentiation and DNA damage–responsive transcriptional networks, contributing to altered cellular identity and genome regulation. Genetic and epigenomic studies have linked KMT2D dysregulation to developmental syndromes and diverse cancer-associated chromatin remodeling phenotypes, making it a key target in functional genomics.
MLL2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KMT2D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KMT2D. 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 KMT2D 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 KMT2D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.