JMJD4 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the JMJD4 gene in the near-haploid human HAP1 cell line. This product provides a loss-of-function model for investigating JMJD4??s roles in translation regulation, oncogenic signaling, and cancer cell proliferation. The polyclonal format generates a heterogeneous knockout pool, enabling robust functional studies without single-cell cloning.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myelogenous leukemia (CML) line, which retains the BCR-ABL fusion oncogene characteristic of CML. Its near-haploid karyotype minimizes genetic redundancy, ensuring that targeted gene disruption yields unambiguous phenotypes. Widely employed in functional genomics and genetic screens, HAP1 cells provide a clean background for dissecting gene function, particularly in pathways relevant to hematologic malignancies.
JMJD4 encodes a lysine demethylase that specifically demethylates eukaryotic translation elongation factor 1 alpha 1 (eEF1A1) at lysine 36, a modification that enhances translation termination and protein synthesis. JMJD4 expression is transcriptionally activated by the ??-catenin/TCF complex downstream of Wnt/??-catenin signaling, with hypoxia serving as an additional upstream inducer. The enzyme requires 2-oxoglutarate and iron cofactors and directly interacts with its substrate eEF1A1. Aberrant Wnt-driven overexpression of JMJD4 promotes proliferation in colorectal and lung cancers, highlighting its role in oncogenic translation. Key signaling nodes in this pathway include ??-catenin, TCF4, AXIN2, and eEF1A1.
In the HAP1 background, which harbors the BCR-ABL oncogene known to modulate translation via mTOR and other effectors, JMJD4 knockout provides a powerful system to examine how leukemogenic signaling intersects with translation termination. The near-haploid genome ensures a clean loss-of-function effect free from allelic compensation, allowing precise characterization of JMJD4-dependent phenotypes in a CML-derived context. This model is particularly suited to explore synthetic vulnerabilities and feedback loops between translation control and oncogenic pathways.
This polyclonal knockout population supports diverse research applications, including functional genomics screens, cancer biology studies, and translation regulation analyses. Specific assays include Western blotting for eEF1A1 methylation, puromycin incorporation to assess global translation rates, and polysome profiling for ribosome occupancy. Wnt pathway activity can be monitored via TCF/LEF luciferase reporters, and cell proliferation can be measured by MTT or CCK8 assays. RNA sequencing may further elucidate JMJD4??s involvement in alternative splicing. For additional product details or technical inquiries, please contact Ascent Research.
