hepcidin CRISPR/Cas9 KO Plasmid (h): sc-403222
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- hepcidin 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 hepcidin 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: hepcidin Antibody (56-Z): sc-100277
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
hepcidin CRISPR/Cas9 KO Plasmid (h) | sc-403222 | 20 µg | $397.00 |
Overview
HAMP encodes hepcidin, a liver-derived peptide hormone that is the central regulator of systemic iron homeostasis. Hepcidin binds and promotes internalization of the iron exporter ferroportin (SLC40A1), thereby limiting dietary iron absorption in the intestine and iron release from macrophages and hepatocytes. Its transcription integrates signals from the BMP/SMAD pathway, inflammatory cytokine signaling (notably IL-6/STAT3), hypoxia/erythropoietic demand, and circulating transferrin saturation to maintain iron balance. Dysregulated HAMP expression is linked to iron-loading phenotypes and anemia-associated iron restriction, making it a key node for studying iron metabolism and inflammatory iron sequestration mechanisms.
hepcidin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the HAMP gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the HAMP 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 HAMP 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 hepcidin protein expression.
This CRISPR knockout system enables efficient generation of HAMP-deficient cell models for investigation of hepcidin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting HAMP exon(s) critical for hepcidin 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 HAMP genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by hepcidin CRISPR/Cas9 KO Plasmid (h) and hepcidin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the HAMP locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by hepcidin HDR Plasmid (h) and hepcidin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by HAMP homology arms to support homology-directed repair at defined HAMP 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.