TRIM72 Double Nickase Plasmid (h): sc-403554-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIM72 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
- TRIM72 Double Nickase Plasmid (h) and TRIM72 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIM72. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRIM72 Antibody (A-10): sc-514706
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRIM72 Double Nickase Plasmid (h) | sc-403554-NIC | 20 µg | $410.00 | |||
TRIM72 Double Nickase Plasmid (h2) | sc-403554-NIC-2 | 20 µg | $410.00 |
TRIM72 (also known as MG53) encodes a muscle-enriched tripartite motif E3 ubiquitin ligase that coordinates plasma membrane repair and proteostasis in response to mechanical or oxidative injury. TRIM72 participates in vesicle trafficking and injury-induced signaling by scaffolding repair complexes and modulating ubiquitin-dependent turnover of key components, integrating with stress-response and membrane remodeling processes. In striated muscle and cardiomyocytes, TRIM72 activity influences cellular resilience by regulating repair efficiency and downstream inflammatory and metabolic cues. Dysregulated TRIM72 expression or function has been associated with muscle damage phenotypes and cardiometabolic stress states, making it relevant for mechanistic studies of membrane integrity and stress signaling in human cells.
TRIM72 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIM72 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIM72. 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 TRIM72 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 TRIM72-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.