MAP2K4 (Mitogen-Activated Protein Kinase Kinase 4)

Collectively, these findings demonstrate that 20(S)-Ginsenoside Rg3 suppresses CAF activation and function associated with the IL-17RD-FGF-MAP2K4-JNK-c-Jun signaling pathway, highlighting its potential as a tumor microenvironment-targeted therapeutic agent in NSCLC. The online version contains supplementary material available at 10.1007/s10616-026-00957-1.

The therapeutic potential of SHCZF was evaluated in alpha-naphthylisothiocyanate (ANIT)-induced IC rat model, with ursodeoxycholic acid (UDCA) used as positive control...Importantly, GW6471 altered the regulatory effects of SHCZF on MKK4/JNK pathway and bile acid homeostasis. SHCZF improves IC by regulating PPARα-mediated bile acid homeostasis and MKK4/JNK pathway.

This mini-review synthesizes recent mechanistic advances, emphasizes regional and cell-type heterogeneity of YTHDF2 function, and proposes a "dose-target dependency" framework to reconcile its bidirectional effects. We also outline emerging translational strategies aimed at evaluating YTHDF2 as a mechanistic biomarker and a selectively tractable therapeutic target in neurological disease.

As we enter the era of precision medicine, classifying cancers by molecular markers will become increasingly valuable. Our investigation enriches the literature by identifying novel mutations and mutations exclusive to certain demographic groups. These findings support a shift beyond histology toward molecularly informed diagnostics and pathway-directed therapeutic hypotheses for MFS. Next steps should validate candidate markers in independent cohorts and link genomic profiles to clinicopathologic features, disease course, and treatment response to improve clinical translation. These observations will help shape diagnostics and targeted therapies against MFS.

Alterations in the PI3K/AKT/mTOR and JUN pathways can induce resistance to multiple combinations of MAPK pathway inhibitors, and may serve as biomarkers for sensitivity/resistance in clinical trials exploring such combinations in KRAS-mutant PDAC.

Although not associated with immune subtypes, IBC showed differences in HER2 and P53 pathways. The association of IBC with rurality and poverty underscores the importance of health care access for timely diagnosis and treatment of IBC.

This international study identifies recurrent IM driver genes, IM-specific mutational signatures, and alterations in IM-associated immune landscapes and microbiomes. Our results highlight a role for nonepithelial somatic alterations (CH) in IM progression to gastric cancer, offering new translational opportunities for early cancer detection and interception.

Moreover, elevated MAPK8 gene expression was linked to an increased incidence of regional lymph node metastasis. Furthermore, bioinformatics analysis confirmed that MAP2K7 and MAPK8 appear to promote tumor aggressiveness and metastasis, whereas MAPK9 and MAP2K4 may have a protective or regulatory role in early stages of the disease.

Our findings establish MAP2K4 as a Mendelian neurodevelopmental disorder gene and identify impaired JNK signaling as the underlying mechanism. More broadly, this work expands the spectrum of JNK-pathway disorders and underscores the critical role of JNK signaling in human brain development.

This integrated transcriptomic and miRNA profiling study reveals subtype-specific dysregulation of MAPK-associated genes and their miRNA regulators in BC, with TNBC exhibiting the most profound alterations. These findings provide insight into potential targets for personalized therapeutic strategies.

Our findings establish MAP3K1 and MAP2K4 as key tumor suppressors in BRCA that operate via the JNK2-p53-FOSL1 axis. Their inactivation provides an alternative mechanism for p53 pathway disruption, adhering to the "minimal necessary alteration" principle in cancer signaling. This study highlights the dual regulatory mechanisms controlling FRA1 expression and offers insights into breast cancer heterogeneity, with potential implications for targeted therapy and patient stratification.

Oral administration of Lactobacillus for six months reduced OS marker levels and inhibited NRF2/KEAP1, p38 MAPK, and JNK signalling pathways in CRC patients after surgery. These findings suggest that Lactobacillus may contribute to CRC management by modulating oxidative stress.