ArticleNucleic acids research2011
Stress induced gene expression: a direct role for MAPKAP kinases in transcriptional activation of immediate early genes.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- MK2/p38/p53 Suppress Basal IL-1β and Non-Canonical NF-κB Signaling in Macrophages.International journal of molecular sciences · 2026Article
- Chronic activation of p38α in skeletal muscle causes necrotic changes, but also abolishes expression of MK2, MK3, and MKK6 and the muscle recovers.The Journal of biological chemistry · 2026Article
- Oxidized Low-Density Lipoprotein as a Potential Target for Enhancing Immune Checkpoint Inhibitor Therapy in Microsatellite-Stable Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- 5-Iodotubercidin sensitizes cells to RIPK1-dependent necroptosis by interfering with NFκB signaling.Cell death discovery · 2023Article
- p38Frontiers in immunology · 2023Article
- The MK2 cascade mediates transient alteration in mGluR-LTD and spatial learning in a murine model of Alzheimer's disease.Aging cell · 2022Article
- NR4A1 regulates expression of immediate early genes, suppressing replication stress in cancer.Molecular cell · 2021Article
- Age-related changes in hippocampal-dependent synaptic plasticity and memory mediated by p75 neurotrophin receptor.Aging cell · 2021Article
- The p38Frontiers in cell and developmental biology · 2021Review
- An overview of mammalian p38 mitogen-activated protein kinases, central regulators of cell stress and receptor signaling.F1000Research · 2020Review
- The Role of Extracellular Matrix Expression, ERK1/2 Signaling and Cell Cohesiveness for Cartilage Yield from iPSCs.International journal of molecular sciences · 2019Article
- Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling.Journal of cardiovascular development and disease · 2019Review
- IL-33 regulates cytokine production and neutrophil recruitment via the p38 MAPK-activated kinases MK2/3.Immunology and cell biology · 2019Article
- Differential regulation of cytokine and chemokine expression by MK2 and MK3 in airway smooth muscle cells.Pulmonary pharmacology & therapeutics · 2018Article
- Pharmacological and genetic inhibition of downstream targets of p38 MAPK in experimental nephrotic syndrome.American journal of physiology. Renal physiology · 2018Article
- Anti-proliferative Effect of C3 Exoenzyme in Fibroblasts is Mediated by c-Jun Phosphorylation.Journal of molecular signaling · 2017Article
- Role of p38Toxins · 2016Article
- Stress-dependent phosphorylation of myocardin-related transcription factor A (MRTF-A) by the p38(MAPK)/MK2 axis.Scientific reports · 2016Article
- Model-Based Characterization of Inflammatory Gene Expression Patterns of Activated Macrophages.PLoS computational biology · 2016Article
- Coordination of stress signals by the lysine methyltransferase SMYD2 promotes pancreatic cancer.Genes & development · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Immediate early gene (IEG) expression is coordinated by multiple MAP kinase signaling pathways in a signal specific manner. Stress-activated p38α MAP kinase is implicated in transcriptional regulation of IEGs via MSK-mediated CREB phosphorylation. The protein kinases downstream to p38, MAPKAP kinase (MK) 2 and MK3 have been identified to regulate gene expression at the posttranscriptional levels of mRNA stability and translation. Here, we analyzed stress-induced IEG expression in MK2/3-deficient cells. Ablation of MKs causes a decrease of p38α level and p38-dependent IEG expression. Unexpectedly, restoration of p38α does not rescue the full-range IEG response. Instead, the catalytic activity of MKs is necessary for the major transcriptional activation of IEGs. By transcriptomics, we identified MK2-regulated genes and recognized the serum response element (SRE) as a common promoter element. We show that stress-induced phosphorylation of serum response factor (SRF) at serine residue 103 is significantly reduced and that induction of SRE-dependent reporter activity is impaired and can only be rescued by catalytically active MK2 in MK2/3-deficient cells. Hence, a new function of MKs in transcriptional activation of IEGs via the p38α-MK2/3-SRF-axis is proposed which probably cooperates with MKs' role in posttranscriptional gene expression in inflammation and 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.