ArticleNature communications2018
Histone demethylase JMJD1A coordinates acute and chronic adaptation to cold stress via thermogenic phospho-switch.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 105 citations in OpenAlex.
- CRONDEX: a web-based platform for exploring links between chromatin-related genes and neurodevelopmental disorders.Clinical epigenetics · 2026Article
- Article
- Gene Expression Profiling of Adipose Tissue in Enshi Black Pigs Subjected to Cold Stress.Veterinary sciences · 2026Article
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Decoding the Adipocyte Epigenome: Differentiation, Metabolic Memory, and Obesity.Journal of obesity & metabolic syndrome · 2025Review
- Molecular mediators of cold adaptation in mammalian cells.Communications biology · 2025Review
- Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury.Nature immunology · 2025Article
- Iron-Dependent JMJD1A-Mediated Demethylation of H3K9me2 Regulates Gene Expression During Adipogenesis in a Spatial Genome Organization-Dependent Manner.Genes to cells : devoted to molecular & cellular mechanisms · 2025Article
- Promoting health and survival through lowered body temperature.Nature aging · 2025Review
- Pre-fertilization-origin preservation of brown fat-mediated energy expenditure in humans.Nature metabolism · 2025Article
- Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways.Biomedicines · 2024Article
- The Different Shades of Thermogenic Adipose Tissue.Current obesity reports · 2024Review
- Epigenetic roles of KDM3B and KDM3C in tumorigenesis and their therapeutic implications.Cell death & disease · 2024Review
- Mitochondrial biogenesis in white adipose tissue mediated by JMJD1A-PGC-1 axis limits age-related metabolic disease.iScience · 2024Article
- Plasticity of Adipose Tissues: Interconversion among White, Brown, and Beige Fat and Its Role in Energy Homeostasis.Biomolecules · 2024Review
- β-Adrenergic Signal and Epigenomic Regulatory Process for Adaptive Thermogenesis.Advances in experimental medicine and biology · 2024Review
- RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression.Molecular cell · 2023Article
- Crucial role of iron in epigenetic rewriting during adipocyte differentiation mediated by JMJD1A and TET2 activity.Nucleic acids research · 2023Article
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- Comprehensive Analyses of Prognostic Values and Immune Infiltration of KDM3 Gene Family in Hepatocellular Carcinoma.Molecular biotechnology · 2023Article
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
In acute cold stress in mammals, JMJD1A, a histone H3 lysine 9 (H3K9) demethylase, upregulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals have another mechanism to cope with long-term cold stress by inducing the browning of the subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic-dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation-independent acute Ucp1 induction in BAT and demethylation-dependent chronic Ucp1 expression in beige scWAT provides complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namely, β-adrenergic receptor and peroxisome proliferator-activated receptor-γ (PPARγ) activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis. S265 phosphorylation of JMJD1A, and the following demethylation of H3K9me2 might prove to be a novel molecular target for the treatment of metabolic disorders, via promoting beige adipogenesis.
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