GATA-2 Double Nickase Plasmid (m): sc-420494-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GATA-2 Double Nickase Plasmid (m) 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
- GATA-2 Double Nickase Plasmid (m) and GATA-2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Gata2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GATA-2 Antibody (H-6): sc-515178
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GATA-2 Double Nickase Plasmid (m) | sc-420494-NIC | 20 µg | $410.00 | |||
GATA-2 Double Nickase Plasmid (m2) | sc-420494-NIC-2 | 20 µg | $410.00 |
Mouse Gata2 encodes the zinc-finger transcription factor GATA-2, a master regulator of hematopoietic stem and progenitor cell maintenance, endothelial specification, and early lympho-myeloid differentiation. GATA-2 binds WGATAR motifs to coordinate transcriptional programs that intersect with cytokine and growth factor signaling, including stem cell factor/c-KIT, Notch, and BMP/TGF-β-associated pathways, thereby shaping self-renewal and lineage commitment. Dysregulated GATA-2 activity perturbs hematopoietic homeostasis and vascular development, making Gata2 a key locus for studying mechanisms underlying bone marrow failure phenotypes, leukemogenesis-related transcriptional rewiring, and inflammatory stress responses in murine models.
GATA-2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Gata2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Gata2. 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 Gata2 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 Gata2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.