ArticleNature communications2024
Stress pathway outputs are encoded by pH-dependent clustering of kinase components.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Tetramethylpyrazine modulates the Nrf2/JNK axis to intervene in ferroptosis and neuroinflammation after spinal cord injury: an integrated perspective from antioxidant to regenerative therapy.Molecular biology reports · 2026Review
- Noninvasive methods to monitor dynamic single-cell events.Trends in cell biology · 2026Review
- Review
- Optogenetic BlueGENEs engineered into a human safe harbor locus.Nucleic acids research · 2026Article
- Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.Cell death & disease · 2025Review
- Comprehensive landscape of cell death mechanisms: from molecular cross-talk to therapeutic innovation in oncology.Frontiers in cell and developmental biology · 2025Review
- Stress pathway outputs are encoded by pH-dependent clustering of kinase components.Nature communications · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Signal processing by intracellular kinases controls near all biological processes but how signal pathway functions evolve with changed cellular context is poorly understood. Functional specificity of c-Jun N-terminal Kinases (JNK) are partly encoded by signal strength. Here we reveal that intracellular pH (pHi) is a significant component of the JNK network and defines signal response to specific stimuli. We show pHi regulates JNK activity in response to cell stress, with the relationship between pHi and JNK activity dependent on specific stimuli and upstream kinases activated. Using the optogenetic clustering tag CRY2, we show that an increase in pHi promotes the light-induced phase transition of ASK1 to augment JNK activation. While increased pHi similarly promoted CRY2-tagged JNK2 to form light-induced condensates, this attenuated JNK activity. Mathematical modelling of feedback signalling incorporating pHi and differential contributions by ASK1 and JNK2 condensates was sufficient to delineate signal responses to specific stimuli. Taking pHi and ASK1/JNK2 signal contributions into consideration may delineate oncogenic versus tumour suppressive JNK functions and cancer cell drug responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.