B-Myb Double Nickase Plasmid (h): sc-401318-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- B-Myb 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
- B-Myb Double Nickase Plasmid (h) and B-Myb Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MYBL2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: B-Myb Antibody (C-5): sc-390198
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
B-Myb Double Nickase Plasmid (h) | sc-401318-NIC | 20 µg | $410.00 | |||
B-Myb Double Nickase Plasmid (h2) | sc-401318-NIC-2 | 20 µg | $410.00 |
MYBL2 encodes the B-Myb transcription factor, a core regulator of cell cycle progression that coordinates expression of genes required for S phase entry and G2/M transition. B-Myb participates in proliferation-associated transcriptional programs, including networks controlled by E2F family factors and the MMB/FOXM1 axis that supports mitotic gene expression. Through these pathways, MYBL2 influences DNA replication, checkpoint control, and genome stability. Dysregulated MYBL2 expression has been linked to altered proliferative capacity and has been studied as a biomarker-associated driver of tumor biology in multiple cancer types.
B-Myb Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MYBL2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MYBL2. 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 MYBL2 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 MYBL2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.