SETD2 Double Nickase Plasmid (m): sc-433485-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SETD2 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
- SETD2 Double Nickase Plasmid (m) and SETD2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Setd2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SETD2 Double Nickase Plasmid (m) | sc-433485-NIC | 20 µg | $410.00 | |||
SETD2 Double Nickase Plasmid (m2) | sc-433485-NIC-2 | 20 µg | $410.00 |
Mouse Setd2 encodes SETD2, the sole methyltransferase responsible for H3K36 trimethylation (H3K36me3) on actively transcribed chromatin, linking transcriptional elongation to epigenetic regulation. This mark coordinates co-transcriptional RNA processing, DNA mismatch repair, and genome stability, and also supports crosstalk with DNA damage response pathways during replication stress. SETD2-dependent chromatin states influence alternative splicing and recruitment of repair factors at sites of double-strand breaks. Dysregulation of SETD2 activity and H3K36me3 patterning is associated with tumor biology and altered differentiation programs, making Setd2 a key target for mechanistic studies in epigenetics and genome maintenance.
SETD2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Setd2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Setd2. 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 Setd2 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 Setd2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.