FMR2 CRISPR/Cas9 KO Plasmid (m): sc-420393
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FMR2 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 FMR2 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 | |
FMR2 CRISPR/Cas9 KO Plasmid (m) | sc-420393 | 20 µg | $397.00 |
Overview
Aff2 encodes FMR2 (also known as AF4/FMR2 family member 2), a nuclear protein implicated in transcriptional regulation and RNA metabolism in the nervous system. FMR2 contains functional domains associated with chromatin-linked gene control and has been connected to activity-dependent gene expression programs that shape neuronal differentiation and synaptic plasticity. Disruption of AFF2/FMR2 function is linked to X‑linked intellectual disability and neurodevelopmental phenotypes, making it a relevant target for studying gene regulatory mechanisms underlying cognition and behavior. In mouse models, Aff2 perturbation supports investigation of how transcriptional control interfaces with neuronal maturation, circuit function, and downstream pathways influencing learning and memory.
FMR2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Aff2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Aff2 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 Aff2 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 FMR2 protein expression.
This CRISPR knockout system enables efficient generation of Aff2-deficient cell models for investigation of FMR2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Aff2 exon(s) critical for FMR2 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 Aff2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FMR2 CRISPR/Cas9 KO Plasmid (m) and FMR2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Aff2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FMR2 HDR Plasmid (m) and FMR2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Aff2 homology arms to support homology-directed repair at defined Aff2 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.