The ASCC2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for the targeted disruption of the ASCC2 gene in the near-haploid HAP1 cell line. This polyclonal pool provides a genetically heterogeneous loss-of-function model, enabling robust investigation of ASCC2-dependent cellular processes without clonal selection artifacts. The knockout population is generated using CRISPR/Cas9-mediated gene disruption, and the polyclonal format facilitates functional studies where batch-to-batch consistency and representation of diverse editing outcomes are desirable.
The HAP1 cell line is a male chronic myeloid leukemia-derived adherent cell line with a near-haploid karyotype and fibroblast-like morphology. Its haploid nature makes it an ideal platform for functional genomics and genetic screens, as the presence of a single copy of most genes simplifies knockout generation and phenotypic analysis. This cell line is widely employed in haploid genetic screening platforms to investigate gene function in DNA repair, signaling, and cellular stress responses.
ASCC2 encodes a subunit of the ASC-1 complex essential for transcription-coupled DNA alkylation repair and RNA quality control. Activated by ATM/ATR kinases and stress-induced transcription factors, the complex (ASCC1, ASCC2, TRIP4) is recruited to alkylation damage sites, where ASCC2 facilitates repair through interaction with ALKBH3 demethylase, removing alkylation lesions and preserving genomic integrity. Additionally, ASCC2 acts as a transcriptional coactivator by interacting with RNA polymerase II and processing factors, linking transcription to RNA surveillance. This dual role positions ASCC2 at the nexus of DNA damage response and gene expression regulation.
In the HAP1 background, ablation of ASCC2 provides a powerful system to dissect the molecular mechanisms underlying DNA alkylation repair and RNA surveillance. The knockout model is particularly relevant for researching neurodevelopmental disorders, amyotrophic lateral sclerosis, and spinal muscular atrophy, conditions associated with defects in DNA repair and RNA metabolism. By eliminating ASCC2 function, researchers can investigate the contribution of the ASC-1 complex to cellular responses to alkylating agents and explore potential disease mechanisms in a haploid genetic context, where single-gene disruption yields unambiguous phenotypes.
This polyclonal knockout cell population is well-suited for a range of experimental applications, including DNA repair pathway analysis using alkylating agent sensitivity assays with methyl methanesulfonate, immunofluorescence detection of DNA damage foci, and comet assays. It also supports RNA quality control investigations via RNA sequencing and RT-qPCR, and protein interaction studies by co-immunoprecipitation. Researchers studying drug resistance to alkylating chemotherapeutics or the molecular pathology of neurodevelopmental diseases will find this model invaluable. For product inquiries and technical support, please contact Ascent Research.
