TET2 Double Nickase Plasmid (m): sc-431916-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TET2 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
- TET2 Double Nickase Plasmid (m) and TET2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tet2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TET2 Double Nickase Plasmid (m) | sc-431916-NIC | 20 µg | $410.00 | |||
TET2 Double Nickase Plasmid (m2) | sc-431916-NIC-2 | 20 µg | $410.00 |
Mouse Tet2 encodes the dioxygenase TET2, a key regulator of epigenetic reprogramming that catalyzes oxidation of 5-methylcytosine to 5-hydroxymethylcytosine and downstream derivatives, thereby shaping DNA demethylation dynamics. TET2 activity influences chromatin accessibility and transcriptional programs that govern hematopoietic stem and progenitor cell self-renewal, lineage commitment, and immune cell differentiation. Through integration with DNA methylation maintenance and chromatin-modifying pathways, TET2 helps coordinate enhancer function and cytokine-responsive gene expression. Altered Tet2 function is widely used to model dysregulated epigenetic control relevant to hematologic and inflammatory disease mechanisms in vivo and in cell-based systems.
TET2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tet2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tet2. 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 Tet2 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 Tet2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.