Hus1 Double Nickase Plasmid (h): sc-403287-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Hus1 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
- Hus1 Double Nickase Plasmid (h) and Hus1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HUS1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Hus1 Antibody (G-3): sc-166440
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Hus1 Double Nickase Plasmid (h) | sc-403287-NIC | 20 µg | $410.00 | |||
Hus1 Double Nickase Plasmid (h2) | sc-403287-NIC-2 | 20 µg | $410.00 |
HUS1 encodes Hus1, a core component of the RAD9A–RAD1–HUS1 (9-1-1) sliding clamp that is loaded onto damaged DNA to coordinate the ATR-dependent DNA damage response. Through interactions with checkpoint and repair factors, Hus1 helps promote replication fork stability, S-phase checkpoint signaling, and resolution of diverse lesions including those arising from replication stress. Disruption of this pathway can increase genomic instability and alter cell-cycle progression, making HUS1 function relevant to studies of mutational processes and DNA repair proficiency in human cells. HUS1 is therefore widely used as a mechanistic entry point for interrogating checkpoint control, genome maintenance, and stress-response networks.
Hus1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HUS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HUS1. 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 HUS1 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 HUS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.