TFIIH p62 Double Nickase Plasmid (h): sc-402239-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TFIIH p62 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
- TFIIH p62 Double Nickase Plasmid (h) and TFIIH p62 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GTF2H1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TFIIH p62 Antibody (H-10): sc-25329
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TFIIH p62 Double Nickase Plasmid (h) | sc-402239-NIC | 20 µg | $410.00 | |||
TFIIH p62 Double Nickase Plasmid (h2) | sc-402239-NIC-2 | 20 µg | $410.00 |
GTF2H1 encodes TFIIH p62, an essential subunit of the TFIIH complex that couples RNA polymerase II transcription initiation with nucleotide excision repair. Through interactions with other TFIIH components, p62 contributes to promoter opening and supports DNA damage verification and repair during global genome and transcription-coupled NER. These functions integrate with core transcriptional control, DNA damage response signaling, and maintenance of genome stability. Disruption of TFIIH activity is implicated in disorders characterized by defective DNA repair and transcriptional dysregulation, including syndromes within the xeroderma pigmentosum–Cockayne spectrum and trichothiodystrophy.
TFIIH p62 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GTF2H1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GTF2H1. 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 GTF2H1 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 GTF2H1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.