The DUSP16 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the DUSP16 gene in human HAP1 cells. This loss-of-function model enables study of the dual-specificity phosphatase DUSP16, a key regulator of stress-activated MAPK signaling, specifically JNK and p38 inactivation. The polyclonal nature provides a heterogeneous knockout system suitable for robust functional analyses without clonal artifacts.
The HAP1 cell line is a near-haploid chronic myeloid leukemia model derived from KBM-7, carrying the BCR-ABL1 fusion and a haploid karyotype that simplifies gene disruption studies. Its leukemic background and haploidy make it ideal for investigating signaling pathways in cancer-relevant contexts, offering clear genotype-phenotype correlations in stress response and drug sensitivity assays.
DUSP16 encodes a dual-specificity phosphatase that dephosphorylates and inactivates JNK and p38 MAPKs, acting as a negative feedback regulator. It is induced by oxidative stress, TNF-??, and activated JNK/p38, and interacts with MAPK scaffold proteins like JIP. Upstream kinases MKK4 and MKK3/6 activate JNK and p38, which then phosphorylate transcription factors c-Jun and ATF2 to control apoptosis and survival. DUSP16 thus tempers stress and inflammatory signaling.
In the HAP1 leukemic context, DUSP16 knockout allows dissection of how loss of phosphatase restraint on JNK/p38 affects apoptosis, drug resistance, and stress adaptation. The haploid background ensures direct phenotype linkage, making this model valuable for studying the interplay between oncogenic BCR-ABL1 signaling and stress MAPK pathways in CML and other cancers.
Applications include MAPK pathway analysis, stress and drug resistance studies, apoptosis regulation, and inflammation research. Typical assays are western blotting for phospho-JNK/p38, RT-qPCR for c-Jun and ATF2, apoptosis assays, phospho-signaling profiling, and cell viability tests under oxidative stress or TNF-??. This polyclonal knockout population supports both screening and mechanistic investigations. For further details, contact Ascent Research.
