The BABAM1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the HAP1 near-haploid human cell line. This product provides a loss-of-function model for BABAM1 (NBA1), a core subunit of the BRCA1-A complex essential for DNA double-strand break repair. The polyclonal format results from CRISPR/Cas9-mediated disruption of the BABAM1 gene, producing a heterogeneous pool of edited cells that collectively abolish BABAM1 protein expression. Researchers can utilize this knockout model to investigate DNA damage signaling and homologous recombination without the need for single-cell cloning.
The HAP1 cell line is a fibroblast-like near-haploid model derived from the KBM-7 chronic myeloid leukemia line. Its haploid karyotype permits efficient CRISPR/Cas9 gene editing and unambiguous loss-of-function phenotypes, making it a preferred system for genetic screens. HAP1 cells retain functional DNA damage response and cell cycle checkpoint pathways, enabling direct assessment of genomic stability maintenance factors such as BABAM1.
BABAM1 is a critical component of the BRCA1-A complex, recruited to DNA double-strand breaks via the RAP80-ABRAXAS1 interaction. It facilitates BRCA1-dependent homologous recombination repair and G2/M checkpoint activation. Upstream, ATM and ATR kinases trigger complex assembly upon genotoxic stress. BABAM1 also engages in the BRISC deubiquitinase complex, regulating K63-linked deubiquitination and immune signaling. Key interacting partners include MERIT40, BRCC36, BRE, and BRCA1, with downstream effectors CtIP and RAD51 executing repair. Thus, BABAM1 coordinates DNA repair with cell cycle arrest and other cellular responses to maintain genome stability.
In the HAP1 background, the BABAM1 polyclonal knockout provides a clean loss-of-function system, eliminating diploid compensation. Loss of BABAM1 disrupts BRCA1-A complex assembly, impairing homologous recombination repair and abrogating the G2/M checkpoint. These cells exhibit hypersensitivity to ionizing radiation and PARP inhibitors, mirroring BRCAness phenotypes. The polyclonal nature captures diverse gene disruptions, yielding a robust model for studying DDR pathways and synthetic lethal interactions.
This knockout model is suited for western blotting, immunofluorescence, and co-immunoprecipitation to assess BRCA1-A complex integrity. Functional assays include homologous recombination reporter systems, colony formation under genotoxic stress, and cell cycle flow cytometry. Drug sensitivity profiling with PARP inhibitors and RNA-seq-based transcriptomics are additional applications. For breast and ovarian cancer research and functional genomics, these cells offer a versatile platform. For further information, please contact Ascent Research.
