Herc5 Double Nickase Plasmid (h): sc-404993-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Herc5 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
- Herc5 Double Nickase Plasmid (h) and Herc5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HERC5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Herc5 Double Nickase Plasmid (h) | sc-404993-NIC | 20 µg | $410.00 | |||
Herc5 Double Nickase Plasmid (h2) | sc-404993-NIC-2 | 20 µg | $410.00 |
HERC5 encodes an interferon-inducible E3 ligase that functions as a principal E3 for ISG15 conjugation (ISGylation), modifying newly synthesized proteins and shaping innate antiviral defenses. Herc5 localizes to ribosomes and coordinates with the E1 (UBE1L) and E2 (UBE2L6) enzymes to regulate protein stability, trafficking, and immune signaling outputs in response to type I interferon. Through control of ISGylation dynamics, HERC5 influences pathways linked to pathogen restriction, stress responses, and proteostasis, and its dysregulation is studied in contexts of altered interferon signaling and inflammatory states. This gene is frequently examined as a node connecting ubiquitin-like modification to host–virus interactions and immune-mediated cellular phenotypes.
Herc5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HERC5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HERC5. 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 HERC5 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 HERC5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.