RBM7 Double Nickase Plasmid (h): sc-408808-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RBM7 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
- RBM7 Double Nickase Plasmid (h) and RBM7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RBM7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RBM7 Double Nickase Plasmid (h) | sc-408808-NIC | 20 µg | $410.00 | |||
RBM7 Double Nickase Plasmid (h2) | sc-408808-NIC-2 | 20 µg | $410.00 |
RBM7 encodes an RNA-binding protein that functions as a core component of the nuclear exosome targeting (NEXT) complex, coupling RNA recognition to recruitment of the RNA exosome for degradation of short-lived and aberrant nuclear transcripts. Through regulation of pervasive transcription products, promoter-upstream transcripts, and noncoding RNAs, RBM7 contributes to RNA quality control, transcriptional homeostasis, and genome integrity. RBM7-dependent RNA surveillance intersects with processes such as RNA polymerase II transcription, RNA processing, and cellular stress responses. Dysregulated RNA metabolism and impaired nuclear RNA decay pathways in which RBM7 participates are relevant to mechanistic studies of cancer and neurodegeneration where transcriptome instability is a common feature.
RBM7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RBM7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RBM7. 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 RBM7 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 RBM7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.