MAPK3 (Mitogen-Activated Protein Kinase 3)

RAGE neutralization attenuated GA-induced vimentin upregulation. Altogether, these findings show that GA exerts pro-tumorigenic effects in IDC-derived CSCs and upregulates vimentin protein expression via RAGE, highlighting the GA-RAGE axis as a potential therapeutic target and supporting vimentin as a promising prognostic marker for invasive BC in patients with DM.

Integrated multi-omics analyses suggest that the antitumor effects of SB-SD may involve the modulation of key gut microbes like Bacteroides caccae and Lactobacillus, the promotion of choline metabolism, and the regulation of BCKDK and GATM. Together, these findings not only corroborate the direct antitumor activity of SB-SD against pancreatic cancer but also offer novel mechanistic insights by constructing a microbiota-metabolite-protein interaction network.

In vivo, ZGW suppressed CPZ-induced phosphorylation of ERK1/2, p38, and JNK, reduced Iba-1 expression and M1 markers (iNOS and CD86), but did not significantly alter Arg-1 or CD206. ZGW promotes remyelination in CPZ-induced demyelination by inhibiting MAPK pathway overactivation and attenuating microglial M1 polarization, thereby modulating the neuroinflammatory milieu.

Our findings establish a novel PTBP1/DUSP5/ERK1/2 axis governing glioma stem cell proliferation and differentiation and identify the A2-PLGA/venetoclax nanoparticle as a mechanistically justified therapeutic candidate for glioblastoma.

In vivo experiments used a model combining progesterone injection with UV irradiation...It decreased melanin granules, melanin content, tyrosinase activity, and IL-6 and TNF-α levels in mouse skin tissue. This research indicates that Paeoniflorin can significantly suppress UVB-induced cellular inflammatory responses by inhibiting the TNF signaling pathway, thereby reducing hyperpigmentation.

Future research directions included confirmation of baicalein's efficacy and toxicity through in vivo approaches, as well as to understand its efficacy as a combination chemotherapeutic agent. The online version contains supplementary material available at 10.1007/s10616-026-00917-9.

Fundamental molecular processes underlying bladder cancer pathogenesis include cell cycle control, signal transduction, and genomic stability. These findings provide insight into the molecular regulatory landscape of MIBC and highlight potential targets for diagnostic and prognostic applications.

In silico analysis further suggests that the mutations confer increased GEF-binding ability versus wild-type. Results of the study highlight the need to characterize Ras isoform- and mutation-specific phenotypic effects, which may have repercussions in CRC management.

We confirmed that GLBMY inhibits the development and metastasis of TNBC through the MAPK/Erk and IL6-STAT signalling pathways. GLBMY shows promise as a long-term supplementary or alternative therapy for TNBC, offering new insights for TNBC treatment.

These findings suggest that CacyBP/SIP may play a critical role in urothelial carcinoma progression by modulating ERK1/2 and p38 kinase activity.

We identified circulating ERP29, MCL1, TNXB, DAGLB, FES, TRPM4, MAPK3, and TNF as promising, genetically supported druggable targets for CAD treatment. Notably, MAPK3 and TNF demonstrated strong protein-level interactions and close associations with cardiometabolic disorders.

It can be concluded that, down-regulation of MAPK3 and KIT and up-regulation of BMP4 which are the consequence of microsecond PEF treatment inhibit medulloblastoma. The results exhibited the significant role of MAPK3 in response to microsecond PEF treatment.