ALR CRISPR/Cas9 KO Plasmid (h): sc-403367
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ALR 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 ALR 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: ALR Antibody (E-7): sc-365885
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALR CRISPR/Cas9 KO Plasmid (h) | sc-403367 | 20 µg | $397.00 |
Overview
Human GFER encodes augmenter of liver regeneration (ALR), a FAD-dependent sulfhydryl oxidase localized primarily to the mitochondrial intermembrane space that supports oxidative protein folding and mitochondrial biogenesis. ALR functions within the MIA40/ERV1 (CHCHD4/GFER) disulfide relay to import and mature cysteine-rich proteins, thereby influencing respiratory chain integrity, redox homeostasis, and cellular survival programs. Through these roles, ALR impacts processes including energy metabolism, reactive oxygen species handling, and stress responses that are frequently altered in metabolic dysfunction and tumor-associated mitochondrial remodeling. Dysregulation of GFER/ALR has been associated with mitochondrial disease phenotypes and broader pathology linked to impaired protein import and oxidative folding capacity.
ALR CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GFER gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GFER 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 GFER 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 ALR protein expression.
This CRISPR knockout system enables efficient generation of GFER-deficient cell models for investigation of ALR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GFER exon(s) critical for ALR 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 GFER genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ALR CRISPR/Cas9 KO Plasmid (h) and ALR CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GFER locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ALR HDR Plasmid (h) and ALR HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GFER homology arms to support homology-directed repair at defined GFER 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.