MARCH1 Double Nickase Plasmid (m): sc-428465-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MARCH1 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
- MARCH1 Double Nickase Plasmid (m) and MARCH1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting March1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MARCH1 Double Nickase Plasmid (m) | sc-428465-NIC | 20 µg | $410.00 |
Mouse MARCH1 (membrane associated ring-CH-type finger 1) encodes an E3 ubiquitin ligase that localizes to endosomal and plasma membrane compartments and regulates immune signaling by controlling the ubiquitination and trafficking of key surface proteins. MARCH1 promotes internalization and degradation of antigen presentation molecules such as MHC class II and the co-stimulatory molecule CD86, shaping dendritic cell and B cell activation, peripheral tolerance, and inflammatory responses. Through ubiquitin-dependent sorting and lysosomal turnover, MARCH1 connects membrane protein homeostasis with pathways governing endocytosis, vesicular transport, and adaptive immunity. Dysregulated MARCH1 activity has been implicated in altered antigen presentation and immune homeostasis, supporting its study in models of autoimmunity, infection, and tumor-immune interactions.
MARCH1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the March1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within March1. 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 March1 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 March1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.