BIGM103 CRISPR/Cas9 KO Plasmid (m): sc-426620
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BIGM103 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 BIGM103 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 | |
BIGM103 CRISPR/Cas9 KO Plasmid (m) | sc-426620 | 20 µg | $397.00 |
Overview
Slc39a8 encodes a ZIP family metal ion transporter (BIGM103) that primarily mediates cellular uptake of divalent cations, with a strong emphasis on manganese homeostasis. By controlling intracellular Mn availability, SLC39A8 influences Mn-dependent enzyme activity and supports processes such as glycosylation, mitochondrial metabolism, and redox balance. Altered SLC39A8 function has been linked to dysregulated metal handling and downstream effects on inflammatory signaling and metabolic pathways, making it relevant for studying nutrient–gene interactions and stress-responsive cellular phenotypes. In mouse systems, Slc39a8 is frequently investigated in the context of transporter biology, innate immune responses, and metabolism-related traits.
BIGM103 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Slc39a8 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Slc39a8 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 Slc39a8 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 BIGM103 protein expression.
This CRISPR knockout system enables efficient generation of Slc39a8-deficient cell models for investigation of BIGM103 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Slc39a8 exon(s) critical for BIGM103 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 Slc39a8 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BIGM103 CRISPR/Cas9 KO Plasmid (m) and BIGM103 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Slc39a8 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BIGM103 HDR Plasmid (m) and BIGM103 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Slc39a8 homology arms to support homology-directed repair at defined Slc39a8 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.