Chk1 Double Nickase Plasmid (h): sc-400223-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Chk1 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
- Chk1 Double Nickase Plasmid (h) and Chk1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CHEK1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Chk1 Antibody (G-4): sc-8408
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Chk1 Double Nickase Plasmid (h) | sc-400223-NIC | 20 µg | $410.00 | |||
Chk1 Double Nickase Plasmid (h2) | sc-400223-NIC-2 | 20 µg | $410.00 |
CHEK1 encodes checkpoint kinase 1 (Chk1), a serine/threonine kinase that coordinates the DNA damage response and replication stress signaling to preserve genome stability. Activated primarily downstream of ATR, Chk1 phosphorylates substrates such as CDC25 phosphatases to restrain CDK activity, enforce S and G2/M checkpoints, and stabilize stalled replication forks. Through these functions, CHEK1 integrates cell-cycle progression with DNA repair pathways including homologous recombination and fork protection mechanisms. Dysregulated Chk1 signaling is frequently linked to replication stress tolerance and chromosomal instability observed across multiple cancer types, making it a widely studied node in oncogenic stress biology.
Chk1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CHEK1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CHEK1. 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 CHEK1 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 CHEK1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.