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.
CD79B Double Nickase Plasmid (h): sc-401760-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD79B 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
- CD79B Double Nickase Plasmid (h) and CD79B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CD79B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD79B Antibody (B29/123): sc-53210
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD79B Double Nickase Plasmid (h) | sc-401760-NIC | 20 µg | $410.00 | |||
CD79B Double Nickase Plasmid (h2) | sc-401760-NIC-2 | 20 µg | $410.00 |
CD79B encodes the Ig-β (CD79B) signaling subunit of the B cell antigen receptor (BCR) complex, forming a heterodimer with CD79A to couple antigen recognition to intracellular signaling. Its cytoplasmic ITAM motifs are phosphorylated upon BCR engagement, recruiting SYK and propagating signaling through BTK, PI3K–AKT, and NF-κB pathways that regulate B cell activation, survival, and differentiation. CD79B function influences receptor trafficking and signal amplitude, integrating with processes such as antigen-dependent selection and immune tolerance. Alterations in BCR pathway components, including CD79B, are widely studied in the context of B cell dysregulation and lymphoid malignancy biology, supporting its relevance as a mechanistic node in immunology and hematologic disease research.
CD79B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CD79B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CD79B. 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 CD79B 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 CD79B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.