Bcr Double Nickase Plasmid (h): sc-401514-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Bcr 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
- Bcr Double Nickase Plasmid (h) and Bcr Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BCR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Bcr Antibody (B-12): sc-28375
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Bcr Double Nickase Plasmid (h) | sc-401514-NIC | 20 µg | $410.00 | |||
Bcr Double Nickase Plasmid (h2) | sc-401514-NIC-2 | 20 µg | $410.00 |
BCR encodes Bcr, a multidomain protein with serine/threonine kinase and Rho-family GTPase regulatory activities that coordinates cytoskeletal remodeling and intracellular signaling. Bcr functions as a GTPase-activating protein for RAC1 and related small GTPases, linking upstream cues to actin dynamics, adhesion, and cell motility programs. It also contributes to signaling networks that modulate proliferation and stress responses through interactions with phosphorylation-dependent pathways. Altered BCR function is biologically relevant in hematologic disease contexts, most notably through oncogenic fusion events that dysregulate tyrosine kinase signaling and downstream transcriptional programs.
Bcr Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BCR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BCR. 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 BCR 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 BCR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.