ArticleMolecular & cellular proteomics : MCP2012
Brainstem deficiency of the 14-3-3 regulator of serotonin synthesis: a proteomics analysis in the sudden infant death syndrome.
Article in Molecular & cellular proteomics : MCP, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Serotonergic receptor binding in the brainstem in the Sudden Infant Death Syndrome in a high-risk population.PloS one · 2025Article
- Platelet Pathophysiology: Unexpected New Research Directions.Seminars in thrombosis and hemostasis · 2024Article
- Dysregulation of platelet serotonin, 14-3-3, and GPIX in sudden infant death syndrome.Scientific reports · 2024Article
- Altered 5-HT2A/C receptor binding in the medulla oblongata in the sudden infant death syndrome (SIDS): Part II. Age-associated alterations in serotonin receptor binding profiles within medullary nuclei supporting cardiorespiratory homeostasis.Journal of neuropathology and experimental neurology · 2024Article
- Proteomics: A New Research Frontier in Forensic Pathology.International journal of molecular sciences · 2023Article
- Review
- Sudden infant death syndrome revisited: serotonin transporter gene, polymorphisms and promoter methylation.Pediatric research · 2022Article
- Proteomic differences in hippocampus and cortex of sudden unexplained death in childhood.Acta neuropathologica · 2022Article
- Cryo-EM Structure and Activator Screening of Human Tryptophan Hydroxylase 2.Frontiers in pharmacology · 2022Article
- Sudden Infant Death Syndrome: Beyond Risk Factors.Life (Basel, Switzerland) · 2021Review
- Sudden infant death syndrome: Melatonin, serotonin, and CD34 factor as possible diagnostic markers and prophylactic targets.PloS one · 2021Article
- Omics era in forensic medicine: towards a new ageTurkish journal of medical sciences · 2020Review
- Revisiting the Neuropathology of Sudden Infant Death Syndrome (SIDS).Frontiers in neurology · 2020Article
- The Serotonin Brainstem Hypothesis for the Sudden Infant Death Syndrome.Journal of neuropathology and experimental neurology · 2019Review
- Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.The Journal of physiology · 2018Review
- Promotion of the Unfolding Protein Response in Orexin/Dynorphin Neurons in Sudden Infant Death Syndrome (SIDS): Elevated pPERK and ATF4 Expression.Molecular neurobiology · 2017Article
- Embryonic hindbrain patterning genes delineate distinct cardio-respiratory and metabolic homeostatic populations in the adult.Scientific reports · 2017Article
- Medullary 5-HT neurons: Switch from tonic respiratory drive to chemoreception during postnatal development.Neuroscience · 2017Article
- Sudden Unexpected Death in Fetal Life Through Early Childhood.Pediatrics · 2016Article
- Microbiome-Gut-Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS-A Novel Hypothesis.Frontiers in pediatrics · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
Impaired brainstem responses to homeostatic challenges during sleep may result in the sudden infant death syndrome (SIDS). Previously we reported a deficiency of serotonin (5-HT) and its key biosynthetic enzyme, tryptophan hydroxylase (TPH2), in SIDS infants in the medullary 5-HT system that modulates homeostatic responses during sleep. Yet, the underlying basis of the TPH2 and 5-HT deficiency is unknown. In this study, we tested the hypothesis that proteomics would uncover previously unrecognized abnormal levels of proteins related to TPH2 and 5-HT regulation in SIDS cases compared with controls, which could provide novel insight into the basis of their deficiency. We first performed a discovery proteomic analysis of the gigantocellularis of the medullary 5-HT system in the same data set with deficiencies of TPH2 and 5-HT levels. Analysis in 6 SIDS cases and 4 controls revealed a 42-75% reduction in abundance in 5 of the 6 isoforms identified of the 14-3-3 signal transduction family, which is known to influence TPH2 activity (p < 0.07). These findings were corroborated in an additional SIDS and control sample using an orthogonal MS(E)-based quantitative proteomic strategy. To confirm these proteomics results in a larger data set (38 SIDS, 11 controls), we applied Western blot analysis in the gigantocellularis and found that 4/7 14-3-3 isoforms identified were significantly reduced in SIDS cases (p ≤ 0.02), with a 43% reduction in all 14-3-3 isoforms combined (p < 0.001). Abnormalities in 5-HT and TPH2 levels and 5-HT(1A) receptor binding were associated with the 14-3-3 deficits in the same SIDS cases. These data suggest a potential molecular defect in SIDS related to TPH2 regulation, as 14-3-3 is critical in this process.
Indexed as
Identifiers
What OpenQuestion holds
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.