PHF5A Double Nickase Plasmid (h): sc-407986-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PHF5A 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
- PHF5A Double Nickase Plasmid (h) and PHF5A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PHF5A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PHF5A Double Nickase Plasmid (h) | sc-407986-NIC | 20 µg | $410.00 | |||
PHF5A Double Nickase Plasmid (h2) | sc-407986-NIC-2 | 20 µg | $410.00 |
PHF5A (PHD finger protein 5A) is an evolutionarily conserved component of the SF3b subcomplex of the U2 snRNP, functioning as a critical adaptor in pre-mRNA splicing and splice-site recognition during early spliceosome assembly. By stabilizing interactions within the branch point region, PHF5A supports accurate intron removal and influences alternative splicing programs that shape cell-cycle progression, DNA damage responses, and differentiation states. Dysregulated spliceosome function and splicing-factor dependencies are recurrent features of proliferative and stress-adapted cell systems, making PHF5A a useful node for interrogating RNA processing control. Perturbation of PHF5A has been linked to altered transcript isoform balance and downstream pathway remodeling, relevant to models of genomic instability and oncogenic signaling.
PHF5A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PHF5A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PHF5A. 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 PHF5A 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 PHF5A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.