Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
MAD2B Double Nickase Plasmid (m): sc-428124-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MAD2B 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
- MAD2B Double Nickase Plasmid (m) and MAD2B Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mad2l2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MAD2B Antibody (14): sc-135977
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAD2B Double Nickase Plasmid (m) | sc-428124-NIC | 20 µg | $410.00 | |||
MAD2B Double Nickase Plasmid (m2) | sc-428124-NIC-2 | 20 µg | $410.00 |
Mad2l2 (MAD2B/REV7) encodes a HORMA domain protein that functions in genome maintenance by coordinating DNA damage tolerance and repair pathway choice. In mammalian cells, MAD2B is a key subunit of DNA polymerase ζ, supporting translesion DNA synthesis, and it also participates in double-strand break repair regulation through interactions with factors that influence end resection and pathway selection. Beyond repair, MAD2B has been linked to cell-cycle control and mitotic checkpoint-associated processes via interactions with APC/C regulators, connecting replication stress responses to proliferative signaling. Dysregulation of MAD2B-dependent repair and checkpoint networks is relevant to mechanisms underlying genomic instability, a hallmark feature studied across cancer biology and other genome integrity disorders.
MAD2B Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mad2l2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mad2l2. 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 Mad2l2 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 Mad2l2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.