The DUSP14 Knockout HAP1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of HAP1 cells with targeted disruption of the DUSP14 gene. This product provides a loss-of-function model to investigate the negative regulation of mitogen-activated protein kinase (MAPK) signaling pathways. The polyclonal format captures a heterogeneous pool of gene disruptions, obviating the need for single-cell cloning while preserving functional knockout effects.
HAP1 is a fibroblast-like, adherent human cell line derived from the KBM-7 chronic myeloid leukemia line, characterized by a near-haploid karyotype (disomic only for chromosome 8). Its haploid genetics make it an ideal platform for functional genomic screens and gene-trait mapping, as single-gene disruptions yield clear phenotypes without allelic complexity. HAP1 cells are widely used for signaling studies, drug resistance profiling, and high-throughput screening applications.
The DUSP14 gene encodes a dual-specificity phosphatase that dephosphorylates conserved threonine and tyrosine residues in the activation loops of JNK, ERK, and p38 MAP kinases. It functions as a key negative regulator of these cascades, activated by upstream inputs such as T cell receptor engagement, IL-2, and oxidative stress. DUSP14 directly interacts with TRAF2 and NEMO, and its phosphatase activity suppresses the phosphorylation of JNK, ERK, and p38, thereby dampening AP-1-mediated transcription. In T cell receptor signaling, DUSP14 is positioned downstream of the TCR-CD3 complex, ZAP70, and LAT, and attenuates the Raf-MEK-ERK, MKK4/7-JNK, and MKK3/6-p38 modules to fine-tune immune responses.
In HAP1 cells, DUSP14 expression modulates core MAPK signaling responses to extracellular stimuli. Despite their non-lymphoid origin, HAP1 cells retain responsive MAPK cascades, making this knockout population a valuable tool for examining how DUSP14 loss alters phospho-MAPK dynamics and downstream transcriptional activity. The haploid background ensures that a single DUSP14 allele disruption is sufficient to abolish protein function, simplifying phenotype analysis. Typical readouts include western blot-based phospho-JNK/ERK/p38 profiling and AP-1 reporter assays.
This polyclonal knockout model is suited for mechanistic studies of MAPK pathway regulation, functional genomics screens, and validation of potential drug targets in cancer, inflammation, and autoimmunity. Researchers can employ these cells in western blotting to quantify changes in phospho-MAPK levels, AP-1 luciferase assays, RT-qPCR for downstream gene expression, flow cytometry for cell surface markers, and cytokine ELISA for secretory profiles. The DUSP14 Knockout HAP1 Polyclonal Cells thus enable comprehensive dissection of kinase-phosphatase networks. For additional information, please contact Ascent Research.
