The ATRX Knockout HAP1 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 near-haploid human cell line, engineered to disrupt the ATRX gene. This polyclonal format provides a heterogeneous pool of loss-of-function alleles, enabling robust analysis of ATRX deficiency in a consistent genetic background. The cell population is tailored for research into chromatin remodeling, telomere maintenance, and genomic stability.
The HAP1 cell line is a near-haploid, adherent human cell line with fibroblast-like morphology, derived from the KBM-7 chronic myeloid leukemia line. Its near-haploid karyotype (disomic only for part of chromosome 8) facilitates unambiguous interpretation of recessive phenotypes and high-efficiency genetic screens. HAP1 cells are widely used in functional genomics because single-copy gene disruptions directly reveal loss-of-function effects, making them particularly valuable for studying tumor suppressors and DNA repair pathways.
ATRX encodes a SWI/SNF-family ATP-dependent chromatin remodeler that functions with the histone H3.3 chaperone DAXX to deposit H3.3 at pericentric heterochromatin and telomeres. Its activity is regulated by interaction with DAXX and kinases including ATR, ATM, CDK1-cyclin B, and Aurora B. Downstream, ATRX modulates telomere repeat-containing RNA (TERRA) expression, DNA methylation, and gene expression programs. ATRX interacts with HP1??, MeCP2, cohesin components, and histone chaperone ASF1, connecting it to higher-order chromatin architecture and gene silencing. Disruption of ATRX disrupts H3.3 localization, causes telomere dysfunction, and accumulates DNA damage, driving genome instability.
In the HAP1 hematopoietic background, ATRX knockout provides a clean system to dissect tumor-suppressive roles. The near-haploid genome eliminates wild-type allele masking, while intact DNA damage responses allow direct study of ATRX-dependent chromatin dynamics and genome stability. Loss of ATRX in this model recapitulates phenotypes seen in ATR-X syndrome and malignancies like gliomas, sarcomas, and myeloid disorders, enabling assessment of DNA repair, telomere maintenance, and epigenetic regulation without compensation.
This polyclonal knockout product suits a range of applications including functional genomics screens, chromatin remodeling studies, and DNA damage pathway evaluation. Researchers can confirm ATRX loss by Western blot, analyze H3.3 localization by immunofluorescence and ChIP-qPCR, assess telomere integrity by telomere FISH, and profile transcriptomes by RNA-seq. Comet assays, colony formation, and xenograft models support cellular and tumor phenotype studies, while drug sensitivity testing can uncover synthetic lethal interactions. For further details, please contact Ascent Research.
