Bcl-9L Double Nickase Plasmid (h2): sc-415290-NIC-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Bcl-9L Double Nickase Plasmid (h2) 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
- Bcl-9L Double Nickase Plasmid (h2) and Bcl-9L Double Nickase Plasmid (h22) encode distinct paired gRNA designs targeting BCL9L. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Bcl-9L Double Nickase Plasmid (h2) | sc-415290-NIC-2 | 20 µg | $410.00 |
Human BCL9L encodes Bcl-9L, a transcriptional co-activator that binds β-catenin and cooperates with TCF/LEF factors to potentiate canonical Wnt signaling and downstream gene expression programs controlling proliferation, differentiation, and epithelial homeostasis. Through its interactions with nuclear transcriptional complexes and chromatin-associated regulators, Bcl-9L helps shape context-specific Wnt target selection and influences processes such as cell fate specification, migration, and stem-like properties. Dysregulation of BCL9L-dependent β-catenin transcriptional activity has been linked to aberrant Wnt pathway output observed in multiple cancers and developmental disorders. Gene editing of BCL9L supports mechanistic studies of Wnt/β-catenin transcription, mapping protein–protein interaction dependencies, and functional genomics screens to dissect pathway crosstalk and oncogenic transcriptional networks in human cells.
Bcl-9L Double Nickase Plasmid (h2) consists of a matched pair of plasmids engineered for high-specificity editing of the BCL9L locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BCL9L. 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 BCL9L 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 BCL9L-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.