FAM72A CRISPR/Cas9 KO Plasmid (h): sc-409422
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAM72A 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 FAM72A 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 | |
FAM72A CRISPR/Cas9 KO Plasmid (h) | sc-409422 | 20 µg | $397.00 |
Overview
FAM72A encodes a vertebrate-restricted protein linked to cell-cycle–associated programs and proliferative states, with enriched expression in dividing cells and developing neural tissues. Although its molecular mechanism is still being defined, FAM72A has been associated with regulation of genome stability and DNA damage–related processes that interface with replication stress responses. Transcriptomic and genomic studies frequently report altered FAM72A expression in multiple tumor types, consistent with a role in oncogenic proliferation and lineage plasticity. These observations make FAM72A a useful target for investigating cell-cycle control, DNA repair pathway dependencies, and biomarkers of highly proliferative cell populations.
FAM72A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FAM72A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FAM72A 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 FAM72A 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 FAM72A protein expression.
This CRISPR knockout system enables efficient generation of FAM72A-deficient cell models for investigation of FAM72A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FAM72A exon(s) critical for FAM72A 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 FAM72A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FAM72A CRISPR/Cas9 KO Plasmid (h) and FAM72A CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FAM72A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FAM72A HDR Plasmid (h) and FAM72A HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FAM72A homology arms to support homology-directed repair at defined FAM72A 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.