The FIRRM Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the FIRRM gene in the near-haploid HAP1 cell line. This product provides a genetically disrupted model for investigating FIRRM function in genome maintenance. The polyclonal population carries heterogeneous loss-of-function alleles introduced by CRISPR/Cas9-mediated gene disruption, enabling pooled functional studies without clonal isolation. Users can employ this model to dissect FIRRM-dependent DNA repair mechanisms and cellular responses to genotoxic stress in a physiologically relevant human cell context.
The parental HAP1 cell line is a near-haploid, chronic myeloid leukemia (CML)-derived model widely utilized for genetic screening and loss-of-function analyses. Its haploid karyotype simplifies genotype?Cphenotype correlations by eliminating confounding wild-type alleles, making it an ideal background for knockout studies. HAP1 cells retain functional DNA damage response pathways and are susceptible to perturbation of genome stability networks, providing a sensitive system to evaluate the consequences of FIRRM depletion on homologous recombination repair and cellular survival.
FIRRM is an essential regulator of homologous recombination, functioning as a scaffold that interacts with FIGNL1 to promote the timely disassembly of RAD51 nucleoprotein filaments. This activity is critical for efficient repair of DNA double-strand breaks and interstrand crosslinks, and it is activated by the ATM/ATR kinases in response to DNA damage. FIRRM complexes with FIGNL1, RAD51, and BRCA2, and operates within the Fanconi anemia pathway alongside factors such as FANCD2. Loss of FIRRM disrupts RAD51 filament dynamics, leading to persistent DNA damage and chromosomal instability.
In HAP1 cells, knockout of FIRRM provides a clean loss-of-function model to study genome instability and repair pathway defects. The near-haploid background amplifies phenotypic consequences, facilitating robust detection of impaired homologous recombination, increased sensitivity to crosslinking agents like mitomycin C, and accumulation of DNA damage markers. This model is particularly suited for dissecting FIRRM??s role in the context of cancer-associated mutations and for screening modulators of the FIGNL1?CFIRRM?CRAD51 axis.
Researchers can employ FIRRM knockout HAP1 polyclonal cells in a variety of assays, including mitomycin C sensitivity tests, colony formation assays, and immunofluorescence-based quantification of RAD51 foci to assess homologous recombination proficiency. The model also supports transcriptomic profiling via RNA-seq and synthetic lethality screens with PARP inhibitors or other DNA-damaging therapeutics. These applications make it valuable for cancer biology, Fanconi anemia research, and drug discovery targeting genome instability. For detailed product specifications and ordering, please contact Ascent Research.
