The DTX3L Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the DTX3L gene has been disrupted in the haploid human HAP1 cell line. This product provides researchers with a versatile loss-of-function model for studying DTX3L-dependent mechanisms in DNA damage repair, interferon signaling, and cell cycle regulation. The polyclonal composition reflects a broad spectrum of edited alleles, making it suitable for pooled functional screens and bulk biochemical analyses without the need for clonal isolation.
The HAP1 host cell line is a near-haploid, adherent cell model originally derived from a male patient with chronic myeloid leukemia. Its haploid karyotype minimizes genetic redundancy, simplifying knockout generation and phenotypic interpretation, and has established HAP1 as a preferred platform for genetic screens and functional genomics studies. The leukemic origin of the line additionally supports cancer-focused research, particularly in leukemia biology, while its stable growth characteristics facilitate robust experimental reproducibility.
DTX3L encodes an interferon-inducible E3 ubiquitin ligase that assembles into a heterodimeric complex with PARP9. This complex functions downstream of JAK-STAT signaling, where DTX3L transcription is strongly upregulated by STAT1 and STAT2 in response to interferon-alpha and interferon-gamma. Once induced, DTX3L?CPARP9 ubiquitinates key substrates such as histone H2B, influencing chromatin architecture and promoting the recruitment of DNA repair factors and non-homologous end joining (NHEJ) components. DTX3L also interacts with STAT1 and other E3 ligases, integrating interferon-mediated innate immunity with ubiquitin-dependent DNA damage responses and cell cycle control.
Disruption of DTX3L in the HAP1 background creates a powerful system to dissect its role in ubiquitin-mediated signaling cascades without the confounding effects of a diploid genome. The polyclonal knockout population enables researchers to assess global changes in DNA repair kinetics, interferon-stimulated gene expression, and ubiquitination profiles in a genetically tractable context. Because the host cell line originates from a leukemia patient, the model is particularly relevant for exploring the intersection of aberrant ubiquitin signaling and leukemogenesis, as well as for screening compounds that modulate DTX3L-related pathways in cancer or viral infection.
These knockout cells are well-suited for a range of targeted assays: western blotting can confirm DTX3L depletion, ubiquitination assays can probe E3 ligase activity, flow cytometry can monitor cell cycle distribution, and ??H2AX immunofluorescence can visualize DNA damage foci. RT-qPCR can quantify changes in interferon-stimulated genes, while co-immunoprecipitation can assess disrupted DTX3L?CPARP9 complex formation. For further information, please contact Ascent Research.
