ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
The LIM domain only 4 protein is a metabolic responsive inhibitor of protein tyrosine phosphatase 1B that controls hypothalamic leptin signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Subtype-Specific Roles of Anterior Cingulate Cortex Neurons in Pain-Induced Social Deficits in Mice.Theranostics · 2026Article
- An aminosterol breaks the autocatalytic cycle of AβProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Protein Tyrosine Phosphatase 1B (PTP1B): A Comprehensive Review of Its Role in Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Licochalcone A: A Potential Multitarget Drug for Alzheimer's Disease Treatment.International journal of molecular sciences · 2023Review
- Can Allostery Be a Key Strategy for Targeting PTP1B in Drug Discovery? A Lesson from Trodusquemine.International journal of molecular sciences · 2023Review
- Article
- N-methyl-D-aspartate receptor functions altered by neuronal PTP1B activation in Alzheimer's disease and schizophrenia models.Neural regeneration research · 2022Article
- How "Neuronal" Are Human Skin Mast Cells?International journal of molecular sciences · 2022Review
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- From Marine Metabolites to the Drugs of the Future: Squalamine, Trodusquemine, Their Steroid and Triterpene Analogues.International journal of molecular sciences · 2022Review
- Palm Oil-Rich Diet Affects Murine Liver Proteome andInternational journal of molecular sciences · 2021Article
- Article
- Lipid-induced S-palmitoylation as a Vital Regulator of Cell Signaling and Disease Development.International journal of biological sciences · 2021Review
- MicroRNA-139-5p Alleviates High Glucose-Triggered Human Retinal Pigment Epithelial Cell Injury by Targeting LIM-Only Factor 4.Mediators of inflammation · 2021Article
- Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models.Neural regeneration research · 2021Article
- Activation of tyrosine phosphatases in the progression of Alzheimer's disease.Neural regeneration research · 2020Article
- Activation of tyrosine phosphatase PTP1B in pyramidal neurons impairs endocannabinoid signaling by tyrosine receptor kinase trkB and causes schizophrenia-like behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Hyperactivated PTP1B phosphatase in parvalbumin neurons alters anterior cingulate inhibitory circuits and induces autism-like behaviors.Nature communications · 2020Article
- Neuronal Protein Tyrosine Phosphatase 1B Hastens Amyloid β-Associated Alzheimer's Disease in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Dabrafenib, an inhibitor of RIP3 kinase-dependent necroptosis, reduces ischemic brain injury.Neural regeneration research · 2018Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Protein tyrosine phosphatase 1B (PTP1B) counteracts leptin signaling and is a therapeutic target for obesity and diabetes. Here we found that LIM domain only 4 (LMO4) inhibits PTP1B activity by increasing the oxidized inactive form of PTP1B. Mice with neuronal ablation of LMO4 have elevated PTP1B activity and impaired hypothalamic leptin signaling, and a PTP1B inhibitor normalized PTP1B activity and restored leptin control of circulating insulin levels. LMO4 is palmitoylated at its C-terminal cysteine, and deletion of this residue prevented palmitoylation and retention of LMO4 at the endoplasmic reticulum and abolished its inhibitory effect on PTP1B. Importantly, LMO4 palmitoylation is sensitive to metabolic stress; mice challenged with a brief high-fat diet or acute intracerebroventricular infusion of saturated fatty acid had less palmitoylated LMO4, less oxidized PTP1B, and increased PTP1B activity in the hypothalamus. Thus, unleashed PTP1B activity attributable to loss of LMO4 palmitoylation may account for rapid loss of central leptin signaling after acute exposure to saturated fat.
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Registered trials
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