Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Bim Double Nickase Plasmid (m2): sc-419332-NIC-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Bim Double Nickase Plasmid (m2) 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
- Bim Double Nickase Plasmid (m2) and Bim Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Bcl2l11. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Bim Antibody (H-5): sc-374358
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Bim Double Nickase Plasmid (m2) | sc-419332-NIC-2 | 20 µg | $410.00 |
Mouse Bcl2l11 encodes the BH3-only Bcl-2 family protein Bim, a potent pro-apoptotic regulator that promotes mitochondrial outer membrane permeabilization by antagonizing anti-apoptotic Bcl-2 proteins and activating Bax/Bak. Bim integrates signals from cytokine withdrawal, oxidative and ER stress, and growth-factor pathways including PI3K–AKT and MAPK/ERK, thereby shaping intrinsic apoptosis, immune cell homeostasis, and tolerance through deletion of autoreactive lymphocytes. Dysregulated Bcl2l11/Bim activity has been linked to altered lymphocyte survival, autoimmunity, and tumor cell persistence in preclinical models, making it a key node in stress-response and cell-fate decision networks. Gene editing of mouse Bcl2l11 supports mechanistic studies of apoptosis signaling, hematopoietic and immune phenotypes, and context-specific dependencies in cancer and inflammatory disease research models.
Bim Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Bcl2l11 locus in mouse 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.