BBS1 Double Nickase Plasmid (h): sc-410535-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BBS1 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
- BBS1 Double Nickase Plasmid (h) and BBS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BBS1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BBS1 Antibody (F-1): sc-365138
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BBS1 Double Nickase Plasmid (h) | sc-410535-NIC | 20 µg | $410.00 | |||
BBS1 Double Nickase Plasmid (h2) | sc-410535-NIC-2 | 20 µg | $410.00 |
BBS1 encodes a core subunit of the BBSome, a multiprotein complex that cooperates with the IFT machinery to regulate ciliary membrane protein trafficking and signaling competence of primary cilia. Through control of receptor localization and turnover, BBS1 influences cilia-dependent pathways including Hedgehog and GPCR-mediated signaling, with downstream effects on cellular homeostasis, neuroendocrine regulation, and development. Disruption of BBS1 impairs ciliogenesis and cargo sorting, leading to altered signal transduction and defects in ciliary composition. Variants in human BBS1 are strongly associated with Bardet–Biedl syndrome and related ciliopathies, supporting its broad relevance in studying cilia-linked disease mechanisms.
BBS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BBS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BBS1. 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 BBS1 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 BBS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.