CHD7 Double Nickase Plasmid (m): sc-435822-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CHD7 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
- CHD7 Double Nickase Plasmid (m) and CHD7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Chd7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CHD7 Antibody (F-11): sc-390742
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CHD7 Double Nickase Plasmid (m) | sc-435822-NIC | 20 µg | $410.00 | |||
CHD7 Double Nickase Plasmid (m2) | sc-435822-NIC-2 | 20 µg | $410.00 |
Chd7 encodes CHD7, an ATP-dependent chromatin remodeler of the CHD family that regulates enhancer accessibility and transcriptional programs during embryonic development and tissue patterning. In mouse cells, CHD7 influences lineage specification and cell fate decisions by coordinating nucleosome positioning with transcription factor binding in pathways that govern neural crest, neurogenesis, and sensory organ development. Altered CHD7 function disrupts chromatin organization and gene expression networks, making it a widely used model for studying developmental syndromes and congenital phenotype mechanisms. CHD7 also interfaces with broader epigenetic regulation processes, including promoter–enhancer communication and transcriptional elongation control.
CHD7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Chd7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Chd7. 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 Chd7 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 Chd7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.