Dnmt3b Double Nickase Plasmid (h): sc-400332-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Dnmt3b 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
- Dnmt3b Double Nickase Plasmid (h) and Dnmt3b Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DNMT3B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Dnmt3b Antibody (G-9): sc-376043
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Dnmt3b Double Nickase Plasmid (h) | sc-400332-NIC | 20 µg | $410.00 | |||
Dnmt3b Double Nickase Plasmid (h2) | sc-400332-NIC-2 | 20 µg | $410.00 |
DNMT3B encodes Dnmt3b, a de novo DNA methyltransferase that establishes CpG methylation patterns during development and contributes to long-term epigenetic gene regulation. Dnmt3b functions within chromatin-associated complexes to shape transcriptional programs, influence genomic imprinting, and help maintain genome stability by modulating repetitive element methylation. Its activity intersects with DNA replication–coupled methylation maintenance and broader epigenetic pathways controlling lineage specification and cell identity. Dysregulated DNMT3B-dependent methylation is associated with aberrant promoter methylation and epigenomic instability observed across multiple disease-relevant cellular states.
Dnmt3b Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DNMT3B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DNMT3B. 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 DNMT3B 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 DNMT3B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.