ArticleCell death discovery2025
RNF144A-VRK2-G3BP1 axis regulates stress granule assembly.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Liquid-liquid phase separation in cancer therapy resistance.iScience · 2026Review
- Dynamic translocation of Inside-Out proteins to the cell surface underlies cellular adaptation to cancer-induced stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- [Expression, Prognostic and Functional Analysis of SRSF Family Proteins in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Under the cellular stress, stress granules (SGs) help survival and proliferation of the cell. Unfortunately, the same SGs help unwanted cancer cells under stressful environment, including anti-cancer chemotherapy treatment. While SGs elevate the cancer cell's resistance to chemotherapy, the mechanism behind the formation of SGs in cancer cell under chemotherapy treatment is still to be revealed. Here, we identified that the level of VRK2 and the phosphorylation of its novel substrate, G3BP1, are reduced when the cellular stress was increased by sodium arsenite (SA) or cisplatin treatment. We also demonstrated that the level of RNF144A is increased in response to the stress and further downregulates VRK2 through proteasomal degradation in various types of cancer cells. Furthermore, inhibition of SG formation by the overexpression of VRK2 sensitized the cells to the stress and chemotherapy. Together, our study establishes an RNF144A-VRK2-G3BP1 axis that regulates SG formation and suggest its potential usage in anti-cancer therapy.
Identifiers
What Socratic 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 Socratic graph.