Blk Double Nickase Plasmid (h): sc-402737-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Blk 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
- Blk Double Nickase Plasmid (h) and Blk Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BLK. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Blk Antibody (9D10D1): sc-65980
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Blk Double Nickase Plasmid (h) | sc-402737-NIC | 20 µg | $410.00 | |||
Blk Double Nickase Plasmid (h2) | sc-402737-NIC-2 | 20 µg | $410.00 |
BLK encodes B lymphoid tyrosine kinase (Blk), a Src family non-receptor tyrosine kinase enriched in B cells that couples B-cell receptor engagement to downstream phosphorylation cascades. Blk participates in proximal immunoreceptor signaling and modulates pathways controlling calcium flux, MAPK activation, and PI3K-dependent survival and differentiation programs. Altered BLK expression or activity has been linked to dysregulated B-cell development and aberrant immune signaling, and genetic associations implicate BLK in autoimmune disease susceptibility. These properties make BLK a useful target for probing mechanisms of B-cell activation, tolerance, and signaling network rewiring in human immune models.
Blk Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BLK locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BLK. 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 BLK 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 BLK-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.