VRK1 Double Nickase Plasmid (h): sc-404617-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VRK1 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
- VRK1 Double Nickase Plasmid (h) and VRK1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting VRK1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: VRK1 Antibody (A-11): sc-271061
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VRK1 Double Nickase Plasmid (h) | sc-404617-NIC | 20 µg | $410.00 | |||
VRK1 Double Nickase Plasmid (h2) | sc-404617-NIC-2 | 20 µg | $410.00 |
Vaccinia-related kinase 1 (VRK1) is a serine/threonine kinase that localizes primarily to the nucleus and regulates chromatin dynamics, cell-cycle progression, and DNA damage responses. VRK1 phosphorylates substrates such as histone H3 and p53, linking it to mitotic entry, transcriptional control, and checkpoint signaling pathways that safeguard genome integrity. Through modulation of nuclear envelope and chromatin-associated processes, VRK1 helps coordinate proliferation with replication stress and repair. Altered VRK1 activity or expression has been associated with neurodevelopmental and neuromuscular phenotypes and is frequently studied in the context of aberrant cell growth and genome stability.
VRK1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the VRK1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within VRK1. 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 VRK1 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 VRK1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.