Adipsin CRISPR/Cas9 KO Plasmid (h): sc-401782
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Adipsin CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the Adipsin genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- 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 CRISPR/Cas9 KO Plasmid (h) | sc-401782 | 20 µg | $397.00 |
Overview
Complement factor D (CFD), also known as adipsin, is a serine protease that regulates the alternative pathway of complement by cleaving factor B when bound to C3b, promoting assembly of the C3 convertase and amplifying complement activation. In humans, CFD is highly expressed in adipose tissue and links innate immune surveillance with metabolic homeostasis, influencing inflammatory tone and adipokine signaling. Altered CFD activity has been associated with dysregulated complement-driven inflammation and has been studied in the context of adipose tissue remodeling, cardiometabolic traits, and immune-mediated tissue injury. As a secreted enzyme, adipsin provides a tractable node for dissecting crosstalk between complement proteolysis, cytokine networks, and cellular stress responses.
Adipsin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CFD gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CFD together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the CFD open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish Adipsin protein expression.
This CRISPR knockout system enables efficient generation of CFD-deficient cell models for investigation of Adipsin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CFD exon(s) critical for Adipsin function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple CFD genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Adipsin CRISPR/Cas9 KO Plasmid (h) and Adipsin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CFD locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Adipsin HDR Plasmid (h) and Adipsin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CFD homology arms to support homology-directed repair at defined CFD target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.