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.
Adipsin Double Nickase Plasmid (h): sc-401782-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Adipsin 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
- Adipsin Double Nickase Plasmid (h) and Adipsin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CFD. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Adipsin Antibody (D10/4): sc-47683
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Adipsin Double Nickase Plasmid (h) | sc-401782-NIC | 20 µg | $410.00 | |||
Adipsin Double Nickase Plasmid (h2) | sc-401782-NIC-2 | 20 µg | $410.00 |
Complement factor D (CFD), also known as adipsin, is a serine protease that functions as the rate-limiting enzyme of the alternative complement pathway by cleaving factor B in the presence of C3b to generate the C3 convertase. Through this role it modulates complement amplification, opsonization, and inflammatory signaling, linking innate immunity with tissue homeostasis. CFD is highly expressed in adipose tissue and has been implicated in crosstalk between metabolic regulation and immune activation. Dysregulated complement activity involving CFD is associated with inflammatory and metabolic phenotypes and is frequently studied in the context of adipose biology, complement-driven tissue injury, and immune-mediated disease mechanisms.
Adipsin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CFD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CFD. 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 CFD 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 CFD-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.