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.
MuRF1 Double Nickase Plasmid (m): sc-436648-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MuRF1 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
- MuRF1 Double Nickase Plasmid (m) and MuRF1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Trim63. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MuRF1 Antibody (C-11): sc-398608
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MuRF1 Double Nickase Plasmid (m) | sc-436648-NIC | 20 µg | $410.00 | |||
MuRF1 Double Nickase Plasmid (m2) | sc-436648-NIC-2 | 20 µg | $410.00 |
Mouse Trim63 encodes MuRF1, a muscle-specific RING finger E3 ubiquitin ligase that regulates proteostasis by targeting myofibrillar and sarcomeric proteins for ubiquitin-dependent degradation. MuRF1 functions within the ubiquitin–proteasome system and interfaces with pathways controlling muscle remodeling, autophagy–proteasome crosstalk, and stress-responsive signaling that shapes fiber size and contractile composition. Altered Trim63/MuRF1 activity is commonly studied in contexts of skeletal and cardiac muscle atrophy, disuse or denervation responses, cachexia-associated wasting, and cardiomyopathy-related remodeling. As a nodal regulator of muscle catabolism, MuRF1 provides a genetically tractable entry point for dissecting transcriptional and post-translational programs that govern muscle mass maintenance.
MuRF1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Trim63 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Trim63. 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 Trim63 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 Trim63-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.