ArticleBMB reports2019
JNK activation induced by ribotoxic stress is initiated from 80S monosomes but not polysomes.
Article in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- USP36 stabilizes nucleolar Snail1 to promote ribosome biogenesis and cancer cell survival upon ribotoxic stress.Nature communications · 2023Article
- Phosphorylation of rpS3 by Lyn increases translation of Multi-Drug Resistance (MDR1) gene.BMB reports · 2023Article
- Ribosomes in poxvirus infection.Current opinion in virology · 2022Review
- RACK1 Regulates Poxvirus Protein Synthesis Independently of Its Role in Ribosome-Based Stress Signaling.Journal of virology · 2022Article
- Negative charge in the RACK1 loop broadens the translational capacity of the human ribosome.Cell reports · 2021Article
- Development of Carbazole Derivatives Compounds againstJournal of fungi (Basel, Switzerland) · 2021Article
- A potential role for a novel ZC3H5 complex in regulating mRNA translation inThe Journal of biological chemistry · 2020Article
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Translation is a costly, but inevitable, cell maintenance process. To reduce unnecessary ATP consumption in cells, a fine-tuning mechanism is needed for both ribosome biogenesis and translation. Previous studies have suggested that the ribosome functions as a hub for many cellular signals such as ribotoxic stress response, mammalian target of rapamycin (mTOR), and ribosomal S6 kinase (RSK) signaling. Therefore, we investigated the relationship between ribosomes and mitogen-activated protein kinase (MAPK) activation under ribotoxic stress conditions and found that the activation of c-Jun N-terminal kinases (JNKs) was suppressed by ribosomal protein knockdown but that of p38 was not. In addition, we found that JNK activation is driven by the association of inactive JNK in the 80S monosomes rather than the polysomes. Overall, these data suggest that the activation of JNKs by ribotoxic stress is attributable to 80S monosomes. These 80S monosomes are active ribosomes that are ready to initiate protein translation, rather than polysomes that are already acting ribosomes involved in translation elongation. [BMB Reports 2019; 52(8): 502-507].
Indexed as
Identifiers
30670151PMC6726213W2971873439What OpenQuestion holds
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.