CD37 Double Nickase Plasmid (h): sc-404423-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD37 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
- CD37 Double Nickase Plasmid (h) and CD37 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CD37. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD37 Antibody (M-B372): sc-23924
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD37 Double Nickase Plasmid (h) | sc-404423-NIC | 20 µg | $410.00 | |||
CD37 Double Nickase Plasmid (h2) | sc-404423-NIC-2 | 20 µg | $410.00 |
CD37 is a tetraspanin family surface glycoprotein highly enriched on mature B cells and other leukocyte subsets, where it organizes membrane microdomains that coordinate receptor signaling, adhesion, and trafficking. By scaffolding partner proteins and regulating B cell receptor–proximal signaling, CD37 influences downstream pathways controlling activation thresholds, proliferation, and survival. It contributes to immune synapse formation and endocytic processes that shape antigen handling and intercellular communication. Altered CD37 expression or function has been implicated in immune dysregulation and B cell malignancy biology, supporting its use as a mechanistic marker in lymphoid signaling studies.
CD37 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CD37 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CD37. 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 CD37 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 CD37-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.