Mxi1 Double Nickase Plasmid (h): sc-403155-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mxi1 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
- Mxi1 Double Nickase Plasmid (h) and Mxi1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MXI1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Mxi1 Antibody (MXI1C2a): sc-130627
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mxi1 Double Nickase Plasmid (h) | sc-403155-NIC | 20 µg | $410.00 | |||
Mxi1 Double Nickase Plasmid (h2) | sc-403155-NIC-2 | 20 µg | $410.00 |
Human MXI1 encodes Mxi1, a basic helix–loop–helix leucine zipper transcriptional repressor in the MYC/MAX/MAD network that counterbalances MYC-driven transcription. Mxi1 heterodimerizes with MAX and recruits SIN3/HDAC corepressor complexes to E-box–containing promoters, shaping chromatin state and regulating programs controlling cell-cycle progression, differentiation, and apoptosis. Through this antagonism of MYC activity, MXI1 influences oncogenic signaling nodes and cellular proliferation checkpoints. Altered MXI1 function or expression has been implicated in tumor biology and is frequently studied in the context of MYC dependency, lineage specification, and stress-response transcriptional programs.
Mxi1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MXI1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MXI1. 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 MXI1 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 MXI1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.