BimEL Double Nickase Plasmid (h): sc-400515-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BimEL 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
- BimEL Double Nickase Plasmid (h) and BimEL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BCL2L11. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BimEL Double Nickase Plasmid (h) | sc-400515-NIC | 20 µg | $410.00 | |||
BimEL Double Nickase Plasmid (h2) | sc-400515-NIC-2 | 20 µg | $410.00 |
BCL2L11 encodes the BH3-only pro-apoptotic protein Bim, and the Bim_EL isoform is a widely expressed splice variant that integrates cellular stress signals to initiate mitochondrial outer membrane permeabilization. Bim_EL promotes intrinsic apoptosis by neutralizing anti-apoptotic BCL-2 family members and facilitating BAX/BAK activation, linking growth factor withdrawal, ER stress, and cytoskeletal cues to caspase activation. Its activity is regulated by transcriptional control (e.g., FOXO), post-translational phosphorylation (e.g., MAPK/ERK-dependent turnover), and sequestration to the microtubule network, positioning Bim_EL at the interface of survival and death pathways. Dysregulation of BCL2L11-mediated apoptotic priming has been implicated in oncogenic survival, immune homeostasis defects, and altered responses to cellular stress, making it a key node in apoptosis and cell fate research.
BimEL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BCL2L11 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BCL2L11. 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 BCL2L11 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 BCL2L11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.