Mitogen-activated protein kinase 8 (MAPK8)
Mitogen-activated protein kinase 8 (MAPK8), commonly known as c-Jun N-terminal kinase 1 (JNK1), is a stress-responsive mitogen-activated protein kinase investigated as a regulator of inflammation, apoptosis, cellular stress responses, and epithelial–mesenchymal transition (EMT).
Mitogen-activated protein kinase 8 (MAPK8), commonly known as c-Jun N-terminal kinase 1 (JNK1), is a stress-responsive mitogen-activated protein kinase investigated as a regulator of inflammation, apoptosis, cellular stress responses, and epithelial–mesenchymal transition (EMT). In the studies summarized here, MAPK8/JNK1 appears within signaling networks involving NF-κB, p53, reactive oxygen species (ROS), transforming growth factor beta (TGF-β), and EGFR/SRC-mediated EMT. These associations place MAPK8 at the intersection of inflammatory signaling, cell-survival decisions, and tissue-remodeling processes.
MAPK8 has been examined both as a mechanistic readout and as a potential pharmacological target. Reported approaches include pathway inhibition, molecular docking and molecular dynamics, network-pharmacology target prediction, exosome-based intervention, and the design of hydrophobic-tag degraders. The supplied literature particularly extends themes of inflammation and apoptosis, airway inflammation and T-cell biology, and EGFR/SRC-mediated EMT. Related entities appearing in these contexts include NF-κB, caspase-3, BAX, BCL2 apoptosis regulator, endoplasmic reticulum stress, the unfolded protein response, ERN1, glucose-regulated protein 78, and oxidative stress.
Rebuilt from PubMed 7 Sept 2026 · no new papers today
Where the papers sit
11 papers study mitogen-activated protein kinase 8 (mapk8) directly. Those 11 are one subject: JNK Signaling in Disease. JNK signaling recurs as a link between stress, inflammation and cell death, including NF-κB activation, unfolded protein response, PANoptosis and ROS-driven apoptosis. Natural products are repeatedly examined as pathway modulators across allergic, metabolic, neurodegenerative and cancer contexts, without a single therapeutic direction. No way of splitting those 11 scores better than chance.
Recent Findings on mitogen-activated protein kinase 8 (MAPK8)
These studies place JNK/MAPK signaling at the intersection of inflammation, oxidative stress, and apoptosis. Turmeric volatile oil, Lawsone, and human iPSC-derived exosomes suppressed JNK-associated NF-κB signaling, proinflammatory cytokine production, or apoptotic markers in disease models 42310315Jun42105996May41846052Mar. In contrast, santamarine activated ROS-dependent JNK signaling with cisplatin, increasing DNA damage, CASP3 activation, and apoptosis in oral cancer cells 42187533May. The field is therefore moving toward context-specific JNK modulation, supported by multi-omics, serum metabolic profiles, proteomics, and pathway-inhibition experiments.
These studies connect JNK signaling with immune-cell differentiation, stress-induced cell death, and inflammatory tissue injury. α-Cyperone inhibited the PAK1-JNK/NF-κB axis, reducing dendritic cell maturation and Th2/Th9 differentiation in lung tissue and mediastinal lymph nodes 42596835Aug. Yangweishu granules similarly reduced JNK and ERK phosphorylation while restoring the CD4+/CD8+ T-cell ratio and limiting T and B cell proliferation 41985642Apr. JNK inhibition protected human and mouse β cells from IRE1-driven ER-stress death, whereas molecular dynamics and deep-learning analyses now define JNK1 substrate interfaces for pathogenicity assessment and drug discovery 42544575Aug42427025Jul.
These studies identify MAPK8/JNK1 as both a predicted hub target and a direct intervention point in oxidative stress and TGF-β1-induced EMT. Network pharmacology and molecular docking implicated MAPK8, SRC, and IGF1 in the antioxidant effects of Yinxingye tablets, although the study did not experimentally establish MAPK8-dependent activity 42104588May. By contrast, the hydrophobic-tag degrader HY12 directly induced JNK1 degradation through the ubiquitin-proteasome system and autophagy-lysosome pathway, inhibiting TGF-β1-induced EMT 41856067Mar. This work shifts the field from computational target prediction toward targeted protein degradation for EMT-associated disorders.
Written from 11 PubMed abstracts, each one cited by PMID above. Published: 2026-09-06. Last written: 2026-09-07 by GPT. Drafted by language models from published abstracts; not medical advice.