LMP7 Double Nickase Plasmid (m): sc-421450-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LMP7 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
- LMP7 Double Nickase Plasmid (m) and LMP7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Psmb8. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LMP7 Antibody (D-2): sc-374089
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LMP7 Double Nickase Plasmid (m) | sc-421450-NIC | 20 µg | $410.00 | |||
LMP7 Double Nickase Plasmid (m2) | sc-421450-NIC-2 | 20 µg | $410.00 |
Psmb8 encodes the immunoproteasome catalytic subunit LMP7 (β5i), a specialized protease that replaces constitutive proteasome components in response to inflammatory cues such as interferon signaling. LMP7 modulates ubiquitin–proteasome pathway proteolysis and shapes the repertoire of peptides generated for MHC class I antigen presentation, influencing adaptive immune surveillance. In mouse immune cells, immunoproteasome activity contributes to proteostasis under oxidative or inflammatory stress and impacts NF-κB-associated inflammatory programs. Altered PSMB8/LMP7 function has been linked to dysregulated antigen processing and inflammatory phenotypes, supporting its relevance for mechanistic studies of immune regulation and immunopathology.
LMP7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Psmb8 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Psmb8. 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 Psmb8 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 Psmb8-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.