MLL3 Double Nickase Plasmid (h): sc-402052-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MLL3 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
- MLL3 Double Nickase Plasmid (h) and MLL3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KMT2C. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MLL3 Double Nickase Plasmid (h) | sc-402052-NIC | 20 µg | $410.00 |
KMT2C (MLL3) encodes a SET domain–containing histone methyltransferase that predominantly catalyzes H3K4 mono-methylation at enhancers, shaping chromatin accessibility and context-specific transcriptional programs. As a core component of COMPASS-like regulatory complexes, MLL3 coordinates enhancer–promoter communication and integrates signals from lineage-determining transcription factors during development and differentiation. Disruption of KMT2C perturbs enhancer architecture and transcriptional homeostasis, impacting pathways linked to DNA damage response, cell cycle control, and cell fate decisions. KMT2C alterations are recurrent in multiple cancer types and neurodevelopmental disorders, making MLL3 a key node for studying epigenetic dysregulation.
MLL3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KMT2C locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KMT2C. 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 KMT2C 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 KMT2C-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.