MBD6 Double Nickase Plasmid (h): sc-414039-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MBD6 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
- MBD6 Double Nickase Plasmid (h) and MBD6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MBD6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MBD6 Double Nickase Plasmid (h) | sc-414039-NIC | 20 µg | $410.00 |
Methyl-CpG binding domain protein 6 (MBD6) is a chromatin-associated factor that recognizes DNA methylation features and helps interpret epigenetic marks to shape transcriptional programs. In human cells, MBD6 is linked to regulation of gene expression through chromatin remodeling and maintenance of repressive chromatin states, influencing processes such as cell identity and differentiation. Because methylation-dependent chromatin control is frequently altered in cancer and neurodevelopmental phenotypes, perturbing MBD6 provides a route to interrogate how epigenetic readers modulate transcriptional networks under normal and disease-relevant contexts. Functional studies of MBD6 can clarify crosstalk between DNA methylation, histone modifications, and genome stability pathways.
MBD6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MBD6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MBD6. 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 MBD6 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 MBD6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.