Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Vitamin D Receptor/VDR Double Nickase Plasmid (m): sc-423664-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Vitamin D Receptor/VDR 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
- Vitamin D Receptor/VDR Double Nickase Plasmid (m) and Vitamin D Receptor/VDR Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Vdr. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Vitamin D Receptor/VDR Antibody (D-6): sc-13133
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Vitamin D Receptor/VDR Double Nickase Plasmid (m) | sc-423664-NIC | 20 µg | $410.00 |
Vdr encodes the vitamin D receptor (VDR), a ligand-activated nuclear receptor that heterodimerizes with RXR to regulate transcription at vitamin D response elements and reshape chromatin states across diverse target loci. In mouse cells, VDR signaling integrates calcium and phosphate homeostasis with cellular programs controlling differentiation, barrier integrity, and immune modulation, and it can intersect with Wnt/β-catenin, NF-κB, and MAPK-linked transcriptional networks. Vdr activity influences osteoblast and osteoclast gene expression, epithelial tight-junction and antimicrobial responses, and metabolic pathways responsive to endocrine cues. Perturbation of Vdr-dependent transcription is widely studied in models of bone and mineral disorders, inflammatory phenotypes, and altered epithelial or metabolic homeostasis.
Vitamin D Receptor/VDR Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Vdr locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Vdr. 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 Vdr 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 Vdr-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.