{"title":"EFTUD2 在大脑中的保护作用","authors":"Marie-Claude Beauchamp, Loydie A Jerome-Majewska","doi":"10.1016/j.neuron.2024.10.003","DOIUrl":null,"url":null,"abstract":"<p><p>In this issue of Neuron, Yang et al.<sup>1</sup> report MFDM-like phenotypes in mice with deletion of Eftud2 in their Purkinje cells (PCs), namely cerebellar atrophy alongside motor and social deficits, similar to phenotypes observed in MFDM patients. The absence of Eftud2 caused mis-splicing of Atf4, reduced Scd1 and Gch1, and promoted ferroptosis-regulated PC death.</p>","PeriodicalId":19313,"journal":{"name":"Neuron","volume":"112 20","pages":"3378-3380"},"PeriodicalIF":14.7000,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A protective role for EFTUD2 in the brain.\",\"authors\":\"Marie-Claude Beauchamp, Loydie A Jerome-Majewska\",\"doi\":\"10.1016/j.neuron.2024.10.003\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>In this issue of Neuron, Yang et al.<sup>1</sup> report MFDM-like phenotypes in mice with deletion of Eftud2 in their Purkinje cells (PCs), namely cerebellar atrophy alongside motor and social deficits, similar to phenotypes observed in MFDM patients. The absence of Eftud2 caused mis-splicing of Atf4, reduced Scd1 and Gch1, and promoted ferroptosis-regulated PC death.</p>\",\"PeriodicalId\":19313,\"journal\":{\"name\":\"Neuron\",\"volume\":\"112 20\",\"pages\":\"3378-3380\"},\"PeriodicalIF\":14.7000,\"publicationDate\":\"2024-10-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuron\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.neuron.2024.10.003\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuron","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.neuron.2024.10.003","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
In this issue of Neuron, Yang et al.1 report MFDM-like phenotypes in mice with deletion of Eftud2 in their Purkinje cells (PCs), namely cerebellar atrophy alongside motor and social deficits, similar to phenotypes observed in MFDM patients. The absence of Eftud2 caused mis-splicing of Atf4, reduced Scd1 and Gch1, and promoted ferroptosis-regulated PC death.
期刊介绍：
Established as a highly influential journal in neuroscience, Neuron is widely relied upon in the field. The editors adopt interdisciplinary strategies, integrating biophysical, cellular, developmental, and molecular approaches alongside a systems approach to sensory, motor, and higher-order cognitive functions. Serving as a premier intellectual forum, Neuron holds a prominent position in the entire neuroscience community.
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