MYCBP Double Nickase Plasmid (h): sc-404476-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MYCBP 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
- MYCBP Double Nickase Plasmid (h) and MYCBP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MYCBP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MYCBP Antibody (2E9): sc-517020
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYCBP Double Nickase Plasmid (h) | sc-404476-NIC | 20 µg | $410.00 | |||
MYCBP Double Nickase Plasmid (h2) | sc-404476-NIC-2 | 20 µg | $410.00 |
MYCBP (MYC binding protein) encodes a small nuclear cofactor that associates with MYC and modulates MYC-dependent transcriptional programs controlling cell growth, metabolism, and proliferation. By influencing MYC/MAX-driven gene expression, MYCBP can affect RNA polymerase II transcriptional regulation, cell-cycle progression, and cellular stress responses. Altered MYC pathway activity is a common feature of many cancers, making MYCBP a useful node for dissecting MYC-centered regulatory circuits. Research on MYCBP also supports investigation of transcriptional co-regulator balance and context-dependent control of oncogenic signaling networks.
MYCBP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MYCBP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MYCBP. 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 MYCBP 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 MYCBP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.