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.
Rad23B Double Nickase Plasmid (h): sc-402106-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rad23B 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
- Rad23B Double Nickase Plasmid (h) and Rad23B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RAD23B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Rad23B Antibody (H-8): sc-137088
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rad23B Double Nickase Plasmid (h) | sc-402106-NIC | 20 µg | $410.00 | |||
Rad23B Double Nickase Plasmid (h2) | sc-402106-NIC-2 | 20 µg | $410.00 |
Human RAD23B encodes Rad23B, a ubiquitin receptor and DNA repair factor that couples nucleotide excision repair (NER) with proteostasis through interactions with the 26S proteasome. Rad23B participates in recognition and processing of helix-distorting DNA lesions and contributes to genome maintenance following UV and chemical damage, while also modulating ubiquitin-dependent degradation by binding ubiquitinated substrates. Through these roles, RAD23B supports cellular responses to replication stress and DNA damage signaling pathways that influence cell-cycle control. Dysregulation of NER and ubiquitin–proteasome pathways involving RAD23B has been associated with altered genomic stability and cancer-relevant phenotypes in experimental models.
Rad23B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RAD23B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RAD23B. 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 RAD23B 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 RAD23B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.