ArticleThe Journal of biological chemistry2014
Gene trap mice reveal an essential function of dual specificity phosphatase Dusp16/MKP-7 in perinatal survival and regulation of Toll-like receptor (TLR)-induced cytokine production.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Regulatory roles of MKP7/DUSP16 in cancer.Medical oncology (Northwood, London, England) · 2025Review
- Dual-Specificity Phosphatases in Regulation of Tumor-Associated Macrophage Activity.International journal of molecular sciences · 2023Review
- Dusp6 deficiency attenuates neutrophil-mediated cardiac damage in the acute inflammatory phase of myocardial infarction.Nature communications · 2022Article
- Ebola Virus Encodes Two microRNAs in Huh7-Infected Cells.International journal of molecular sciences · 2022Article
- Phosphatases in toll-like receptors signaling: the unfairly-forgotten.Cell communication and signaling : CCS · 2021Review
- A novel myeloid cell in murine spleen defined through gene profiling.Journal of cellular and molecular medicine · 2019Article
- Dual-Specificity Phosphatases in Immunity and Infection: An Update.International journal of molecular sciences · 2019Review
- Dynamics of Dual Specificity Phosphatases and Their Interplay with Protein Kinases in Immune Signaling.International journal of molecular sciences · 2019Article
- Dual-specificity MAP kinase phosphatases in health and disease.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Dual-specificity phosphatases regulate mitogen-activated protein kinase signaling in adipocytes in response to inflammatory stress.Cellular signalling · 2019Article
- Alterations of microRNAs and their predicted targeting mRNAs expression in RAW264.7 macrophages infected with Omp25 mutant Brucella melitensis.Innate immunity · 2018Article
- Mitogen-activated protein kinase phosphatase 1 (MKP-1) in macrophage biology and cardiovascular disease. A redox-regulated master controller of monocyte function and macrophage phenotype.Free radical biology & medicine · 2017Review
- Dusp16 Deficiency Causes Congenital Obstructive Hydrocephalus and Brain Overgrowth by Expansion of the Neural Progenitor Pool.Frontiers in molecular neuroscience · 2017Article
- MAP kinase phosphatase 2 deficient mice develop attenuated experimental autoimmune encephalomyelitis through regulating dendritic cells and T cells.Scientific reports · 2016Article
- Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs).Journal of molecular and cellular cardiology · 2016Review
- MAPK phosphatase 7 regulates T cell differentiation via inhibiting ERK-mediated IL-2 expression.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
MAPK activity is negatively regulated by members of the dual specificity phosphatase (Dusp) family, which differ in expression, substrate specificity, and subcellular localization. Here, we investigated the function of Dusp16/MKP-7 in the innate immune system. The Dusp16 isoforms A1 and B1 were inducibly expressed in macrophages and dendritic cells following Toll-like receptor stimulation. A gene trap approach was used to generate Dusp16-deficient mice. Homozygous Dusp16tp/tp mice developed without gross abnormalities but died perinatally. Fetal liver cells from Dusp16tp/tp embryos efficiently reconstituted the lymphoid and myeloid compartments with Dusp16-deficient hematopoietic cells. However, GM-CSF-induced proliferation of bone marrow progenitors in vitro was impaired in the absence of Dusp16. In vivo challenge with Escherichia coli LPS triggered higher production of IL-12p40 in mice with a Dusp16-deficient immune system. In vitro, Dusp16-deficient macrophages, but not dendritic cells, selectively overexpressed a subset of TLR-induced genes, including the cytokine IL-12. Dusp16-deficient fibroblasts showed enhanced activation of p38 and JNK MAPKs. In macrophages, pharmacological inhibition and siRNA knockdown of JNK1/2 normalized IL-12p40 secretion. Production of IL-10 and its inhibitory effect on IL-12 production were unaltered in Dusp16tp/tp macrophages. Altogether, the Dusp16 gene trap mouse model identifies an essential role in perinatal survival and reveals selective control of differentiation and cytokine production of myeloid cells by the MAPK phosphatase Dusp16.
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