ArticleMolecular and cellular biology2005
Identification of neuronal enhancers of the proopiomelanocortin gene by transgenic mouse analysis and phylogenetic footprinting.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 97 citations in OpenAlex.
- Scalable hypothalamic neuron differentiation from human pluripotent stem cells suitable for modeling metabolic disorders.Stem cell reports · 2026Article
- Exploring the roles of conserved context-dependent cis-regulatory elements (cdCREs) in multicellularity, human health and disease.The FEBS journal · 2025Review
- Highly Conserved STAT3 Motifs Present in the Neuronal Pomc Enhancer nPE1 are Critical for Maximal Hypothalamic Pomc Expression.Molecular neurobiology · 2025Article
- Article
- Leptin/Melanocortin Pathway in Cholelithiasis Patients: A Diagnostic Perspective.Protein and peptide letters · 2025Article
- The Musashi-1-type 2 deiodinase pathway regulates astrocyte proliferation.The Journal of biological chemistry · 2024Article
- A mammalian tripartite enhancer cluster controls hypothalamicProceedings of the National Academy of Sciences of the United States of America · 2024Article
- (3α,5α)3-Hydroxypregnan-20-one (3α,5α-THP) Regulation of the HPA Axis in the Context of Different Stressors and Sex.Biomolecules · 2022Article
- Enhancer redundancy in development and disease.Nature reviews. Genetics · 2021Review
- Optogenetic stimulation of the liver-projecting melanocortinergic pathway promotes hepatic glucose production.Nature communications · 2020Article
- Comparative Transcriptomic Analyses of Developing Melanocortin Neurons Reveal New Regulators for the Anorexigenic Neuron Identity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The transcriptional regulator PRDM12 is critical for Pomc expression in the mouse hypothalamus and controlling food intake, adiposity, and body weight.Molecular metabolism · 2020Article
- Expression of a hypomorphic Pomc allele alters leptin dynamics during late pregnancy.The Journal of endocrinology · 2020Article
- Decreased sensitivity to the anorectic effects of leptin in mice that lack a Pomc-specific neural enhancer.PloS one · 2020Article
- The Homeodomain Transcription Factor NKX2.1 Is Essential for the Early Specification of Melanocortin Neuron Identity and ActivatesThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Maternal overnutrition programs epigenetic changes in the regulatory regions of hypothalamic Pomc in the offspring of rats.International journal of obesity (2005) · 2018Article
- Activation of temperature-sensitive TRPV1-like receptors in ARC POMC neurons reduces food intake.PLoS biology · 2018Article
- 17α-estradiol acts through hypothalamic pro-opiomelanocortin expressing neurons to reduce feeding behavior.Aging cell · 2018Article
- Molecular and functional genetics of the proopiomelanocortin gene, food intake regulation and obesity.FEBS letters · 2017Review
- SVA retrotransposons as potential modulators of neuropeptide gene expression.Neuropeptides · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The proopiomelanocortin (POMC) gene is expressed in the pituitary and arcuate neurons of the hypothalamus. POMC arcuate neurons play a central role in the control of energy homeostasis, and rare loss-of-function mutations in POMC cause obesity. Moreover, POMC is the prime candidate gene within a highly significant quantitative trait locus on chromosome 2 associated with obesity traits in several human populations. Here, we identify two phylogenetically conserved neuronal POMC enhancers designated nPE1 (600 bp) and nPE2 (150 bp) located approximately 10 to 12 kb upstream of mammalian POMC transcriptional units. We show that mouse or human genomic regions containing these enhancers are able to direct reporter gene expression to POMC hypothalamic neurons, but not the pituitary of transgenic mice. Conversely, deletion of nPE1 and nPE2 in the context of the entire transcriptional unit of POMC abolishes transgene expression in the hypothalamus without affecting pituitary expression. Our results indicate that the nPEs are necessary and sufficient for hypothalamic POMC expression and that POMC expression in the brain and pituitary is controlled by independent sets of enhancers. Our study advances the understanding of the molecular nature of hypothalamic POMC neurons and will be useful to determine whether polymorphisms in POMC regulatory regions play a role in the predisposition to obesity.
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