PHF10 Double Nickase Plasmid (h): sc-410593-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PHF10 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
- PHF10 Double Nickase Plasmid (h) and PHF10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PHF10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PHF10 Double Nickase Plasmid (h) | sc-410593-NIC | 20 µg | $410.00 |
PHF10 (PHD finger protein 10) is a chromatin-associated factor implicated in ATP-dependent chromatin remodeling and transcriptional control. It is linked to the PBAF (Polybromo-associated BRG1-associated factor) form of the SWI/SNF complex, contributing to regulation of gene expression programs that influence cell proliferation, differentiation, and lineage specification. Through its roles in chromatin accessibility and promoter/enhancer function, PHF10 helps coordinate developmental and stress-responsive transcriptional networks. Dysregulation of SWI/SNF-associated components, including PHF10-containing assemblies, is relevant to studies of cancer biology and neurodevelopmental processes where altered chromatin remodeling and transcriptional fidelity are common features.
PHF10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PHF10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PHF10. 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 PHF10 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 PHF10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.