SLC48A1 CRISPR/Cas9 KO Plasmid (h): sc-405746
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC48A1 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 SLC48A1 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLC48A1 CRISPR/Cas9 KO Plasmid (h) | sc-405746 | 20 µg | $397.00 |
Overview
SLC48A1 encodes a lysosomal heme transporter (also known as HRG1) that mediates heme translocation from the phagolysosomal lumen to the cytosol during erythrophagocytosis and heme catabolism. By controlling intracellular heme availability, SLC48A1 influences heme–iron recycling, redox homeostasis, and heme-dependent signaling pathways in macrophages and other phagocytic cells. Disruption of heme trafficking can alter oxidative stress responses and iron handling, linking SLC48A1 function to cellular programs involved in inflammation and tissue homeostasis. SLC48A1 is therefore relevant to research on heme metabolism, lysosome biology, and mechanisms underlying iron-related dysregulation in human disease contexts.
SLC48A1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SLC48A1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SLC48A1 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 SLC48A1 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 SLC48A1 protein expression.
This CRISPR knockout system enables efficient generation of SLC48A1-deficient cell models for investigation of SLC48A1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SLC48A1 exon(s) critical for SLC48A1 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 SLC48A1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SLC48A1 CRISPR/Cas9 KO Plasmid (h) and SLC48A1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SLC48A1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SLC48A1 HDR Plasmid (h) and SLC48A1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SLC48A1 homology arms to support homology-directed repair at defined SLC48A1 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.