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.
Btk Double Nickase Plasmid (h): sc-400603-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Btk 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
- Btk Double Nickase Plasmid (h) and Btk Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BTK. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Btk Antibody (E-9): sc-28387
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Btk Double Nickase Plasmid (h) | sc-400603-NIC | 20 µg | $410.00 | |||
Btk Double Nickase Plasmid (h2) | sc-400603-NIC-2 | 20 µg | $410.00 |
Bruton's tyrosine kinase (BTK; Btk) is a non-receptor Tec family kinase that transduces signals downstream of the B cell receptor and multiple immunoreceptors, coupling activation inputs to phospholipase Cγ2, calcium flux, MAPK, PI3K–AKT, and NF-κB signaling. In human hematopoietic cells, BTK helps coordinate B-cell development, antigen-driven activation, cytokine production, and innate immune receptor responses in myeloid lineages. Dysregulated BTK signaling is implicated in immune dysfunction and contributes to pathogenic survival and activation programs in several B-cell malignancies, making it a widely used node for mechanistic studies of lymphocyte signaling. BTK also interfaces with pathways controlling cell adhesion and migration, supporting research on immune cell trafficking and microenvironmental interactions.
Btk Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BTK locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BTK. 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 BTK 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 BTK-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.