SAMHD1 Double Nickase Plasmid (m): sc-424985-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SAMHD1 Double Nickase Plasmid (m) 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
- SAMHD1 Double Nickase Plasmid (m) and SAMHD1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Samhd1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SAMHD1 Double Nickase Plasmid (m) | sc-424985-NIC | 20 µg | $410.00 | |||
SAMHD1 Double Nickase Plasmid (m2) | sc-424985-NIC-2 | 20 µg | $410.00 |
Mouse SAMHD1 (Samhd1) encodes a dNTP triphosphohydrolase that regulates intracellular deoxynucleotide pools and supports genome stability during DNA replication and repair. By modulating nucleotide availability, SAMHD1 influences cell-cycle progression, replication stress responses, and DNA damage signaling, and it can affect the permissiveness of cells to retroelements and viral reverse transcription. SAMHD1 activity is linked to innate immune homeostasis through impacts on cytosolic nucleic acid sensing pathways and interferon-stimulated gene programs. Dysregulation of SAMHD1-dependent nucleotide metabolism and nucleic acid surveillance has been associated with inflammatory phenotypes and tumor biology in experimental models, making Samhd1 a useful locus for mechanistic studies of genome maintenance and immune signaling.
SAMHD1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Samhd1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Samhd1. 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 Samhd1 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 Samhd1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.