SH2D1A Double Nickase Plasmid (h): sc-404747-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SH2D1A 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
- SH2D1A Double Nickase Plasmid (h) and SH2D1A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SH2D1A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SH2D1A Antibody (A-8): sc-398118
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SH2D1A Double Nickase Plasmid (h) | sc-404747-NIC | 20 µg | $410.00 | |||
SH2D1A Double Nickase Plasmid (h2) | sc-404747-NIC-2 | 20 µg | $410.00 |
SH2D1A encodes an SH2 domain–containing adaptor protein (SAP) that couples SLAM family receptors to downstream signaling in T cells and NK cells, shaping cytotoxic function, cytokine production, and lymphocyte cooperation. By modulating interactions with kinases and inhibitory phosphatases, SH2D1A influences immune synapse formation and signaling thresholds that govern antiviral and humoral immune responses. Perturbation of SH2D1A disrupts SLAM-mediated pathways controlling cytotoxic lymphocyte activity and B cell help, leading to immune dysregulation. Loss-of-function variants are linked to X-linked lymphoproliferative disease type 1, with susceptibility to severe EBV-associated immunopathology and broader defects in immune homeostasis.
SH2D1A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SH2D1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SH2D1A. 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 SH2D1A 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 SH2D1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.