SLC48A1 CRISPR/Cas9 KO Plasmid (m): sc-426721
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC48A1 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 (m) | sc-426721 | 20 µg | $397.00 |
Overview
Slc48a1 encodes SLC48A1 (also known as heme-responsive gene 1, HRG1), a lysosomal membrane transporter that exports heme from the lysosomal lumen to the cytosol following erythrophagocytosis and endosomal/lysosomal turnover of heme-containing cargo. By mobilizing lysosomal heme for catabolism and recycling, SLC48A1 supports iron homeostasis, heme detoxification, and macrophage-mediated handling of erythrocyte-derived heme. This activity interfaces with pathways controlling heme degradation, oxidative stress responses, and reticuloendothelial iron recycling. Dysregulation of lysosomal heme transport is relevant to inflammatory and hematologic research contexts where aberrant heme/iron balance contributes to tissue stress and altered innate immune function.
SLC48A1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Slc48a1 gene in mouse 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 (m) and SLC48A1 CRISPR/Cas9 KO Plasmid (m2) 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 (m) and SLC48A1 HDR Plasmid (m2) 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.