MagT1 Double Nickase Plasmid (h): sc-404484-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MagT1 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
- MagT1 Double Nickase Plasmid (h) and MagT1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MAGT1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MagT1 Double Nickase Plasmid (h) | sc-404484-NIC | 20 µg | $410.00 |
MAGT1 encodes MagT1, an endoplasmic reticulum membrane protein with roles in magnesium homeostasis and N-linked glycosylation as a subunit of the oligosaccharyltransferase complex. By supporting co-translational protein glycosylation and quality control, MagT1 influences secretory pathway proteostasis and surface expression of select immune receptors. MAGT1 dysfunction has been linked to immunodeficiency phenotypes with altered lymphocyte signaling and susceptibility to dysregulated cellular stress responses, making it relevant to studies of immune cell biology and ER-associated pathways. In human systems, MAGT1 perturbation is therefore used to interrogate glycoprotein maturation, ion-dependent signaling, and downstream effects on receptor trafficking.
MagT1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MAGT1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MAGT1. 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 MAGT1 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 MAGT1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.