ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Mkp1 is a c-Jun target gene that antagonizes JNK-dependent apoptosis in sympathetic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- Review
- Apoptosis signaling is activated as a transient pulse in neurons.Cell death and differentiation · 2025Article
- Stress pathway outputs are encoded by pH-dependent clustering of kinase components.Nature communications · 2024Article
- DUSP1/MKP-1 represents another piece in the P2X7R intracellular signaling puzzle in cerebellar cells: our last journey with Mª Teresa along the purinergic pathways of Eden.Purinergic signalling · 2024Article
- Inhibition of miR‑101‑3p protects against sepsis‑induced myocardial injury by inhibiting MAPK and NF‑κB pathway activation via the upregulation of DUSP1.International journal of molecular medicine · 2021Article
- Phosphorylation Dynamics of JNK Signaling: Effects of Dual-Specificity Phosphatases (DUSPs) on the JNK Pathway.International journal of molecular sciences · 2019Review
- Interferon-Responsive Genes Are Targeted during the Establishment of Human Cytomegalovirus Latency.mBio · 2019Article
- Apoptotic cell death regulation in neurons.The FEBS journal · 2019Review
- Dual-Specificity Phosphatase Regulation in Neurons and Glial Cells.International journal of molecular sciences · 2019Review
- Inhibition of HDAC4 Attenuated JNK/c-Jun-Dependent Neuronal Apoptosis and Early Brain Injury Following Subarachnoid Hemorrhage by Transcriptionally Suppressing MKK7.Frontiers in cellular neuroscience · 2019Article
- 6'-Oxidative medicine and cellular longevity · 2018Article
- A model of the onset of the senescence associated secretory phenotype after DNA damage induced senescence.PLoS computational biology · 2017Article
- Critical Roles of Dual-Specificity Phosphatases in Neuronal Proteostasis and Neurological Diseases.International journal of molecular sciences · 2017Review
- 4-Hydroxy-2-nonenal induces apoptosis by activating ERK1/2 signaling and depleting intracellular glutathione in intestinal epithelial cells.Scientific reports · 2016Article
- JNK Signaling: Regulation and Functions Based on Complex Protein-Protein Partnerships.Microbiology and molecular biology reviews : MMBR · 2016Review
- Adrenergic Stimulation of DUSP1 Impairs Chemotherapy Response in Ovarian Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Eosinophil resistance to glucocorticoid-induced apoptosis is mediated by the transcription factor NFIL3.Apoptosis : an international journal on programmed cell death · 2016Article
- Let-7a gene knockdown protects against cerebral ischemia/reperfusion injury.Neural regeneration research · 2016Article
- DNA Damage Response Is Involved in the Developmental Toxicity of Mebendazole in Zebrafish Retina.Frontiers in pharmacology · 2016Article
- Microarray Analysis Reveals Increased Transcriptional Repression and Reduced Metabolic Activity but Not Major Changes in the Core Apoptotic Machinery during Maturation of Sympathetic Neurons.Frontiers in cellular neuroscience · 2016Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Developing sympathetic neurons depend on NGF for survival. When sympathetic neurons are deprived of NGF in vitro, a well documented series of events, including c-Jun N-terminal kinase (JNK) pathway activation, release of cytochrome c from the mitochondria, and caspase activation, culminates in the death of the neuron by apoptosis within 24-48 h. This process requires de novo gene expression, suggesting that increased expression of specific genes activates the cell death program. Using rat gene microarrays, we found that NGF withdrawal induces the expression of many genes, including mkp1, which encodes a MAPK phosphatase that can dephosphorylate JNKs. The increase in mkp1 mRNA level requires the MLK-JNK-c-Jun pathway, and we show that Mkp1 is an important regulator of JNK-dependent apoptosis in sympathetic neurons. In microinjection experiments, Mkp1 overexpression can inhibit JNK-mediated phosphorylation of c-Jun and protect sympathetic neurons from apoptosis, while Mkp1 knockdown accelerates NGF withdrawal-induced death. Accordingly, the number of superior cervical ganglion (SCG) neurons is reduced in mkp1-/- mice at P1 during the period of developmental sympathetic neuron death. We also show that c-Jun and ATF2 bind to two conserved ATF binding sites in the mkp1 promoter in vitro and in chromatin. Both of these ATF sites contribute to basal promoter activity and are required for mkp1 promoter induction after NGF withdrawal. These results demonstrate that Mkp1 is part of a negative feedback loop induced by the MLK-JNK-c-Jun signaling pathway that modulates JNK activity and the rate of neuronal death in rat sympathetic neurons following NGF withdrawal.
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