GFRαL CRISPR/Cas9 KO Plasmid (m): sc-436523
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GFRαL 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 GFRαL 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 | |
GFRαL CRISPR/Cas9 KO Plasmid (m) | sc-436523 | 20 µg | $397.00 |
Overview
Mouse Gfral encodes GFRαL (GFRAL), a glycosylphosphatidylinositol-anchored co-receptor that selectively binds GDF15 and signals through the RET receptor tyrosine kinase. This pathway activates downstream MAPK/ERK and PI3K/AKT signaling to regulate neuronal circuitry controlling energy balance, feeding behavior, and systemic metabolic homeostasis. GFRAL expression is enriched in hindbrain regions involved in appetite control, linking GDF15–GFRAL–RET signaling to body weight regulation and stress-associated anorexia-like responses in preclinical models. Consequently, Gfral is widely studied in neuro-metabolic signaling, cachexia-related biology, and mechanisms connecting inflammatory cues to central regulation of metabolism.
GFRαL CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Gfral gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Gfral 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 Gfral 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 GFRαL protein expression.
This CRISPR knockout system enables efficient generation of Gfral-deficient cell models for investigation of GFRαL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Gfral exon(s) critical for GFRαL 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 Gfral genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GFRαL CRISPR/Cas9 KO Plasmid (m) and GFRαL CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Gfral locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GFRαL HDR Plasmid (m) and GFRαL HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Gfral homology arms to support homology-directed repair at defined Gfral 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.