
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAM208A CRISPR/Cas9 KO Plasmid (h) | sc-405884 | 20 µg | $397.00 |
FAM208A encodes a nuclear protein that participates in chromatin-associated processes influencing transcriptional regulation and genome maintenance. It has been linked to DNA damage response pathways and epigenetic control through interactions with multiprotein nuclear complexes, supporting proper cell-cycle progression and stress adaptation. Altered regulation of chromatin organization and repair fidelity involving FAM208A may contribute to genomic instability phenotypes observed in cancer and other proliferative disorders. Its predominantly nuclear localization makes it a useful target for dissecting mechanisms that couple chromatin state to gene expression and DNA repair outcomes in human cells.
FAM208A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FAM208A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FAM208A 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 FAM208A 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 FAM208A protein expression.
This CRISPR knockout system enables efficient generation of FAM208A-deficient cell models for investigation of FAM208A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.