MDM2 Double Nickase Plasmid (h): sc-400045-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MDM2 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
- MDM2 Double Nickase Plasmid (h) and MDM2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MDM2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MDM2 Antibody (SMP14): sc-965
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MDM2 Double Nickase Plasmid (h) | sc-400045-NIC | 20 µg | $410.00 | |||
MDM2 Double Nickase Plasmid (h2) | sc-400045-NIC-2 | 20 µg | $410.00 |
MDM2 encodes an E3 ubiquitin ligase that serves as a central negative regulator of TP53 by ubiquitinating p53 and promoting its nuclear export and proteasomal degradation. Through this feedback loop, MDM2 shapes cellular responses to DNA damage and oncogenic stress, influencing cell-cycle checkpoints, apoptosis, and senescence via the p53 transcriptional program. MDM2 also interfaces with RB/E2F signaling and stress-activated kinase pathways, integrating growth factor cues with genome surveillance. Dysregulated MDM2 expression or activity is frequently linked to impaired p53 pathway control and is widely studied in the context of tumor biology, genome instability, and therapy-response mechanisms.
MDM2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MDM2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MDM2. 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 MDM2 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 MDM2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.