The DUSP23 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from HEK293T cells, designed for disruption of the DUSP23 gene. This knockout model eliminates expression of the dual-specificity phosphatase DUSP23, enabling investigation of negative regulation of MAPK signaling. The polyclonal population consists of a heterogeneous pool of edited cells carrying distinct DUSP23 locus mutations, ensuring robust analysis free of monoclonal expansion artifacts.
HEK293T host cells originate from female human embryonic kidney tissue, exhibit epithelial-like morphology, and were transformed with sheared adenovirus type 5 DNA. They constitutively express the SV40 large T antigen, allowing episomal replication of plasmids containing the SV40 origin of replication. Known for high transfection efficiency and rapid growth, HEK293T cells are a premier model for transient gene expression, recombinant protein production, and viral packaging, making them an ideal background for CRISPR/Cas9-mediated gene knockout studies.
DUSP23 is an atypical dual-specificity phosphatase that dephosphorylates phosphotyrosine and phosphothreonine/serine residues on MAPKs, including ERK1/2, JNK, and p38. This activity negatively regulates MAPK pathway signaling, suppressing downstream activation of c-Jun, ATF2, and the AP-1 complex. DUSP23 expression is regulated by p53 and potentially E2F1 following cellular stress, linking it to cell cycle and apoptosis. Functioning downstream of RAS, RAF, and MEK1/2, DUSP23 directly opposes terminal kinase phosphorylation, providing a critical feedback mechanism that modulates signal duration and amplitude.
In the HEK293T background, DUSP23 knockout allows dissection of its role in MAPK pathway dynamics without endogenous interference. This model is particularly relevant for studying hepatocellular carcinoma, colorectal cancer, and neurodegenerative diseases where DUSP23 dysfunction is implicated. The rapid proliferation and transformability of HEK293T cells facilitate investigation of cell cycle perturbations, apoptotic thresholds, and stress responses. Researchers can examine how DUSP23 deficiency alters phosphorylation of ERK1/2, JNK, and p38 in response to stimuli.
This polyclonal knockout cell product supports diverse applications: western blotting for DUSP23 and phospho-MAPK detection, RT-qPCR for transcript analysis, flow cytometry for cell cycle/apoptosis profiling, proliferation assays, RNA-seq, and co-immunoprecipitation for substrate validation. It enables drug target validation for phosphatase inhibitors and functional genomics screens. For further information, contact Ascent Research.
