SMCR7L Double Nickase Plasmid (h): sc-407077-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SMCR7L 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
- SMCR7L Double Nickase Plasmid (h) and SMCR7L Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MIEF1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SMCR7L Antibody (A-6): sc-514135
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SMCR7L Double Nickase Plasmid (h) | sc-407077-NIC | 20 µg | $410.00 | |||
SMCR7L Double Nickase Plasmid (h2) | sc-407077-NIC-2 | 20 µg | $410.00 |
MIEF1 encodes SMCR7L (also known as MID51), an outer mitochondrial membrane protein that functions as a receptor for the dynamin-related GTPase DRP1 and helps coordinate mitochondrial fission with organelle distribution. By modulating fission–fusion balance, SMCR7L influences oxidative phosphorylation efficiency, mitochondrial quality control, and susceptibility to stress pathways such as mitophagy and apoptosis. Dysregulation of mitochondrial dynamics is broadly implicated in neurodegeneration, cardiometabolic disorders, and cancer-associated metabolic remodeling, making MIEF1 a relevant target for mechanistic studies of mitochondrial homeostasis.
SMCR7L Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MIEF1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MIEF1. 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 MIEF1 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 MIEF1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.