RBM35B Double Nickase Plasmid (h): sc-408008-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RBM35B 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
- RBM35B Double Nickase Plasmid (h) and RBM35B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ESRP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RBM35B Double Nickase Plasmid (h) | sc-408008-NIC | 20 µg | $410.00 | |||
RBM35B Double Nickase Plasmid (h2) | sc-408008-NIC-2 | 20 µg | $410.00 |
ESRP2 (RBM35B) is an epithelial-specific RNA-binding protein that regulates alternative pre-mRNA splicing programs involved in cell polarity, adhesion, and differentiation. By modulating exon inclusion across networks linked to epithelial–mesenchymal transition (EMT), ESRP2 helps maintain epithelial identity and influences signaling outputs from pathways such as receptor tyrosine kinase and TGF-β-associated transcriptional responses. Dysregulated ESRP2 expression or splicing activity has been associated with altered isoform usage in cancer-related progression models and with perturbations in epithelial development and barrier function. As a splicing regulator, ESRP2 provides a mechanistic entry point to study isoform-dependent phenotypes, transcriptome remodeling, and RNA processing defects in human cell systems.
RBM35B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ESRP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ESRP2. 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 ESRP2 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 ESRP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.