MTDH Double Nickase Plasmid (h): sc-413927-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MTDH 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
- MTDH Double Nickase Plasmid (h) and MTDH Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MTDH. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MTDH Antibody (2F11C3D4): sc-517220
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MTDH Double Nickase Plasmid (h) | sc-413927-NIC | 20 µg | $410.00 |
MTDH (metadherin/AEG-1) encodes a multifunctional scaffold protein that coordinates transcriptional and post-transcriptional programs linked to cellular stress responses, survival, and inflammatory signaling. It has been implicated in activation of pathways such as NF-κB and PI3K–AKT, modulation of MAPK signaling, and regulation of mRNA translation and RNA-binding complexes that shape proteostasis. MTDH also interfaces with cell adhesion and vesicular trafficking processes, influencing cytoskeletal dynamics and cellular plasticity. Dysregulated MTDH expression is frequently associated with oncogenic signaling networks and phenotypes relevant to tumor progression, metastasis, and treatment response, making it a common target for mechanistic studies in cancer biology.
MTDH Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MTDH locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MTDH. 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 MTDH 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 MTDH-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.