ArticleThe Journal of clinical investigation2013
Improved regenerative myogenesis and muscular dystrophy in mice lacking Mkp5.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- Dynamic and structural insights into allosteric regulation on MKP5 a dual-specificity phosphatase.Nature communications · 2025Article
- Article
- Mitogen-Activated Protein Kinase Phosphatase-5 is Required for TGF-β Signaling Through a JNK-Dependent Pathway.Molecular and cellular biology · 2025Article
- MAPK Phosphatase-5 is required for TGF-β signaling through a JNK-dependent pathway.bioRxiv : the preprint server for biology · 2024Article
- METTL3 Promotes the Differentiation of Goat Skeletal Muscle Satellite Cells by Regulating MEF2C mRNA Stability in a mInternational journal of molecular sciences · 2023Article
- The Link between Mitochondrial Dysfunction and Sarcopenia: An Update Focusing on the Role of Pyruvate Dehydrogenase Kinase 4.Diabetes & metabolism journal · 2023Review
- Mitogen-Activated Protein Kinase Phosphatases: No Longer Undruggable?Annual review of pharmacology and toxicology · 2023Review
- Defining the structure-activity relationship for a novel class of allosteric MKP5 inhibitors.European journal of medicinal chemistry · 2022Article
- Angiotensin II Induces Cardiac Edema and Hypertrophic Remodeling through Lymphatic-Dependent Mechanisms.Oxidative medicine and cellular longevity · 2022Article
- Functional interrogation and therapeutic targeting of protein tyrosine phosphatases.Biochemical Society transactions · 2021Review
- Review
- MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis.Frontiers in immunology · 2021Article
- Phosphatase orphan 1 inhibits myoblast proliferation and promotes myogenic differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Micronized sacchachitin promotes satellite cell proliferation through TAK1-JNK-AP-1 signaling pathway predominantly by TLR2 activation.Chinese medicine · 2020Article
- An allosteric site on MKP5 reveals a strategy for small-molecule inhibition.Science signaling · 2020Article
- The ties that bind: functional clusters in limb-girdle muscular dystrophy.Skeletal muscle · 2020Review
- Slc20a1/Pit1 and Slc20a2/Pit2 are essential for normal skeletal myofiber function and survival.Scientific reports · 2020Article
- Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Pim1 kinase positively regulates myoblast behaviors and skeletal muscle regeneration.Cell death & disease · 2019Article
- The Dual-Specificity Phosphatase 10 (DUSP10): Its Role in Cancer, Inflammation, and Immunity.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a degenerative skeletal muscle disease caused by mutations in dystrophin. The degree of functional deterioration in muscle stem cells determines the severity of DMD. The mitogen-activated protein kinases (MAPKs), which are inactivated by MAPK phosphatases (MKPs), represent a central signaling node in the regulation of muscle stem cell function. Here we show that the dual-specificity protein phosphatase DUSP10/MKP-5 negatively regulates muscle stem cell function in mice. MKP-5 controlled JNK to coordinate muscle stem cell proliferation and p38 MAPK to control differentiation. Genetic loss of Mkp5 in mice improved regenerative myogenesis and dystrophin-deficient mdx mice lacking Mkp5 exhibited an attenuated dystrophic muscle phenotype. Hence, enhanced promyogenic MAPK activity preserved muscle stem cell function even in the absence of dystrophin and ultimately curtailed the pathogenesis associated with DMD. These results identify MKP-5 as an essential negative regulator of the promyogenic actions of the MAPKs and suggest that MKP-5 may serve as a target to promote muscle stem cell function in the treatment of degenerative skeletal muscle diseases.
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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.