FAM122A CRISPR/Cas9 KO Plasmid (m): sc-426886
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAM122A 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 FAM122A 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 | |
FAM122A CRISPR/Cas9 KO Plasmid (m) | sc-426886 | 20 µg | $397.00 |
Overview
Fam122a encodes FAM122A, a conserved regulatory protein implicated in controlling serine/threonine phosphatase activity, most notably through modulation of PP2A complexes. By influencing PP2A-dependent dephosphorylation, FAM122A can affect phosphorylation-driven signaling programs linked to cell-cycle progression, DNA damage responses, and broader proteostasis networks. Disruption of PP2A regulation is widely connected to altered growth control and stress signaling, making Fam122a a useful target for mechanistic studies of phosphatase-centric pathways. In mouse systems, Fam122a perturbation supports investigation of how phosphorylation homeostasis shapes cellular phenotypes relevant to disease-associated signaling dysregulation.
FAM122A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fam122a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fam122a 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 Fam122a 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 FAM122A protein expression.
This CRISPR knockout system enables efficient generation of Fam122a-deficient cell models for investigation of FAM122A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fam122a exon(s) critical for FAM122A 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 Fam122a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FAM122A CRISPR/Cas9 KO Plasmid (m) and FAM122A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fam122a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FAM122A HDR Plasmid (m) and FAM122A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fam122a homology arms to support homology-directed repair at defined Fam122a 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.