ArticleThe EMBO journal2010
CHIP-dependent termination of MEKK2 regulates temporal ERK activation required for proper hyperosmotic response.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- HES1 potentiates high salt stress response as an enhancer of NFAT5-DNA binding.Communications biology · 2024Article
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- Research progress on oncoprotein hepatitis B X‑interacting protein (Review).Molecular medicine reports · 2024Review
- Chaperone-assisted E3 ligase CHIP: A double agent in cancer.Genes & diseases · 2022Review
- High NaBiomedicines · 2021Review
- Oncoprotein HBXIP promotes tumorigenesis through MAPK/ERK pathway activation in non-small cell lung cancer.Cancer biology & medicine · 2021Article
- STUB1 is targeted by the SUMO-interacting motif of EBNA1 to maintain Epstein-Barr Virus latency.PLoS pathogens · 2020Article
- In Situ Single-Cell Western Blot on Adherent Cell Culture.Angewandte Chemie (International ed. in English) · 2019Review
- Nitration-induced ubiquitination and degradation control quality of ERK1.The Biochemical journal · 2019Article
- Feedback inhibition of cAMP effector signaling by a chaperone-assisted ubiquitin system.Nature communications · 2019Article
- Kir2.1 Interaction with Stk38 Promotes Invasion and Metastasis of Human Gastric Cancer by Enhancing MEKK2-MEK1/2-ERK1/2 Signaling.Cancer research · 2018Article
- Identifying the substrate proteins of U-box E3s E4B and CHIP by orthogonal ubiquitin transfer.Science advances · 2018Article
- Symmetry breaking during homodimeric assembly activates an E3 ubiquitin ligase.Scientific reports · 2017Article
- miRNA-106a directly targeting RARB associates with the expression of Na(+)/I(-) symporter in thyroid cancer by regulating MAPK signaling pathway.Journal of experimental & clinical cancer research : CR · 2016Article
- Protection against doxorubicin-induced myocardial dysfunction in mice by cardiac-specific expression of carboxyl terminus of hsp70-interacting protein.Scientific reports · 2016Article
- MEKK2 mediates an alternative β-catenin pathway that promotes bone formation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- High glucose-induced hyperosmolarity contributes to COX-2 expression and angiogenesis: implications for diabetic retinopathy.Cardiovascular diabetology · 2016Article
- A Decade of Boon or Burden: What Has the CHIP Ever Done for Cellular Protein Quality Control Mechanism Implicated in Neurodegeneration and Aging?Frontiers in molecular neuroscience · 2016Review
- Expression and function of aquaporin-1 in hyperoxia-exposed alveolar epithelial type II cells.Experimental and therapeutic medicine · 2014Article
- Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular signal-regulated kinase (ERK) pathway is an important signalling pathway that regulates a large number of cellular processes, including proliferation, differentiation and gene expression. Hyperosmotic stress activates the ERK pathway, whereas little is known about the regulatory mechanisms and physiological functions of ERK activation in hyperosmotic response. Here, we show that MAPK/ERK kinase kinase 2 (MEKK2), a member of the MAPKKK family, mediated the specific and transient activation of ERK, which was required for the induction of aquaporin 1 (AQP1) and AQP5 gene expression in response to hyperosmotic stress. Moreover, we identified the E3 ubiquitin ligase carboxyl terminus of Hsc70-interacting protein (CHIP) as a binding partner of MEKK2. Depletion of CHIP by small-interference RNA or gene targeting attenuated the degradation of MEKK2 and prolonged the ERK activity. Interestingly, hyperosmolality-induced gene expression of AQP1 and AQP5 was suppressed by CHIP depletion and was reversed by inhibition of the prolonged phase of ERK activity. These findings show that transient activation of the ERK pathway, which depends not only on MEKK2 activation, but also on CHIP-dependent MEKK2 degradation, is crucial for proper gene expression in hyperosmotic stress response.
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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.