TBX2 Double Nickase Plasmid (m): sc-423279-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TBX2 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
- TBX2 Double Nickase Plasmid (m) and TBX2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tbx2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TBX2 Antibody (D-3): sc-514291
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TBX2 Double Nickase Plasmid (m) | sc-423279-NIC | 20 µg | $410.00 |
Mouse Tbx2 encodes the T-box transcription factor TBX2, a sequence-specific DNA-binding regulator that shapes embryonic patterning and organogenesis, including limb and cardiac development. TBX2 functions predominantly as a transcriptional repressor and interfaces with cell-cycle and differentiation programs through modulation of CDK inhibitors and developmental signaling networks such as BMP and Wnt pathways. Altered TBX2 activity has been linked to dysregulated proliferation and lineage specification, making it a useful node for studying developmental gene regulatory circuits. In disease-relevant research contexts, TBX2 is frequently examined for its roles in oncogenic transcriptional programs, bypass of senescence, and tumor cell plasticity in model systems.
TBX2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tbx2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tbx2. 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 Tbx2 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 Tbx2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.