ENL Double Nickase Plasmid (h): sc-408751-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ENL 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
- ENL Double Nickase Plasmid (h) and ENL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MLLT1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ENL Antibody (D-6): sc-393196
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ENL Double Nickase Plasmid (h) | sc-408751-NIC | 20 µg | $410.00 |
MLLT1 encodes the transcriptional coactivator ENL, a YEATS domain protein that binds acetylated histones and helps couple chromatin state to RNA polymerase II–dependent transcriptional elongation. ENL functions within Super Elongation Complex–related assemblies and cooperates with epigenetic regulators to control enhancer and promoter activity during hematopoietic and developmental gene programs. Dysregulated ENL-dependent transcription is implicated in oncogenic gene expression signatures, including contexts where MLLT1 participates in chromosomal rearrangements and aberrant chromatin recruitment. These properties make MLLT1/ENL a useful target for dissecting chromatin-reader mechanisms, transcriptional pause release, and lineage-specific regulatory networks in human cells.
ENL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MLLT1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MLLT1. 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 MLLT1 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 MLLT1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.