ArticleNeurobiology of disease2010
Interactions of peptide amidation and copper: novel biomarkers and mechanisms of neural dysfunction.
Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Exploring Copper's role in stroke: progress and treatment approaches.Frontiers in pharmacology · 2024Review
- Germline loss-of-functionmedRxiv : the preprint server for health sciences · 2023Article
- Germline loss-of-functionFrontiers in endocrinology · 2023Article
- Peptidylglycine α-amidating monooxygenase as a therapeutic target or biomarker for human diseases.British journal of pharmacology · 2022Review
- Crossroads between membrane trafficking machinery and copper homeostasis in the nerve system.Open biology · 2021Review
- Cell-type specific knockout of peptidylglycine α-amidating monooxygenase reveals specific behavioral roles in excitatory forebrain neurons and cardiomyocytes.Genes, brain, and behavior · 2021Article
- Identifying roles for peptidergic signaling in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- 60 YEARS OF POMC: From POMC and α-MSH to PAM, molecular oxygen, copper, and vitamin C.Journal of molecular endocrinology · 2016Review
- Early eukaryotic origins for cilia-associated bioactive peptide-amidating activity.Journal of cell science · 2016Article
- Canine Models for Copper Homeostasis Disorders.International journal of molecular sciences · 2016Review
- Genetic determinants of amidating enzyme activity and its relationship with metal cofactors in human serum.BMC endocrine disorders · 2014Article
- Elimination of Kalrn expression in POMC cells reduces anxiety-like behavior and contextual fear learning.Hormones and behavior · 2014Article
- Pam heterozygous mice reveal essential role for Cu in amygdalar behavioral and synaptic function.Annals of the New York Academy of Sciences · 2014Article
- In vivo and in vitro analyses of amygdalar function reveal a role for copper.Journal of neurophysiology · 2014Article
- Peptidylglycine α-amidating monooxygenase heterozygosity alters brain copper handling with region specificity.Journal of neurochemistry · 2013Article
- Prediction of protein amidation sites by feature selection and analysis.Molecular genetics and genomics : MGG · 2013Article
- Copper signaling in the mammalian nervous system: synaptic effects.Journal of neuroscience research · 2013Review
- Maternal iron supplementation attenuates the impact of perinatal copper deficiency but does not eliminate hypotriiodothyroninemia nor impaired sensorimotor development.The Journal of nutritional biochemistry · 2011Article
- ATP7A-related copper transport diseases-emerging concepts and future trends.Nature reviews. Neurology · 2011Review
- Probing the production of amidated peptides following genetic and dietary copper manipulations.PloS one · 2011Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
Mammalian genomes encode only a small number of cuproenzymes. The many genes involved in coordinating copper uptake, distribution, storage and efflux make gene/nutrient interactions especially important for these cuproenzymes. Copper deficiency and copper excess both disrupt neural function. Using mice heterozygous for peptidylglycine alpha-amidating monooxygenase (PAM), a cuproenzyme essential for the synthesis of many neuropeptides, we identified alterations in anxiety-like behavior, thermoregulation and seizure sensitivity. Dietary copper supplementation reversed a subset of these deficits. Wildtype mice maintained on a marginally copper-deficient diet exhibited some of the same deficits observed in PAM(+/-) mice and displayed alterations in PAM metabolism. Altered copper homeostasis in PAM(+/-) mice suggested a role for PAM in the cell type specific regulation of copper metabolism. Physiological functions sensitive to genetic limitations of PAM that are reversed by supplemental copper and mimicked by copper deficiency may serve as indicators of marginal copper deficiency.
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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.