The DUSP26 Knockout HAP1 Polyclonal Cells are a pooled CRISPR/Cas9-edited population of HAP1 cells harboring a targeted disruption of the DUSP26 gene. This polyclonal knockout model eliminates functional DUSP26 protein, providing a robust loss-of-function system in a near-haploid background for studies of MAPK phosphatase regulation.
HAP1 is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells, exhibiting adherent, fibroblast-like morphology. Its simplified genome facilitates gene editing and genetic screening, making it a preferred host for knockout validation and functional genomics. HAP1 cells retain intact MAPK pathways and are widely used to investigate signaling, proliferation, and apoptosis.
DUSP26 is a dual-specificity phosphatase that negatively regulates MAPK signaling by dephosphorylating p38, JNK, and ERK1/2. It is induced by oxidative stress and pro-inflammatory cytokines and acts as a feedback regulator to modulate downstream transcription factors such as ATF2, c-Jun, and Elk-1. In the MAPK cascade, upstream kinases including MKK3, MKK6, and MKK4 phosphorylate the terminal MAPKs, which are counteracted by DUSP26. Through this activity, DUSP26 controls cell cycle progression, apoptotic sensitivity, and cellular stress responses.
In the HAP1 near-haploid context, DUSP26 knockout leads to hyperactivation of p38, JNK, and ERK pathways, offering a defined model to interrogate MAPK feedback circuits and their impact on cancer cell behavior. The polyclonal nature of this knockout pool mitigates clonal variation, ensuring consistent phenotypes for high-throughput applications. This system is especially suited for exploring how phosphatase loss influences drug resistance and apoptotic signaling in a leukemia-derived background.
These cells are suited for CRISPR knockout confirmation, MAPK signaling dissection, and functional genomics screens in cancer and neuroinflammation research. Common experimental workflows include phospho-p38/JNK/ERK western blotting, AP-1 luciferase reporter assays, RT-qPCR of MAPK-driven genes, immunofluorescence for phospho-MAPK localization, and flow cytometry for apoptosis (Annexin V) and viability. For further details or technical inquiries, please reach out to Ascent Research.
