Lost in Translation: Cul3-Dependent Pathological Mechanisms in Psychiatric Disorders
In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic tra...
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Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2020-02, Vol.105 (3), p.398-399 |
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description | In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.
In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety. |
doi_str_mv | 10.1016/j.neuron.2020.01.010 |
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In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2020.01.010</identifier><identifier>PMID: 32027827</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Anxiety ; Autism ; Behavior ; Cullin Proteins ; Excitability ; Genes ; Glutamatergic transmission ; Humans ; Mental Disorders ; Morphology ; Mutation ; Neurons ; Physiology ; Protein biosynthesis ; Proteins ; Translation ; Ubiquitin ; Ubiquitin-protein ligase ; Ubiquitin-Protein Ligases</subject><ispartof>Neuron (Cambridge, Mass.), 2020-02, Vol.105 (3), p.398-399</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><rights>2020. Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-2588bd2a9bdbf379309ace74684c91b4a04dc5592c58af776a7b3c614e7692143</citedby><cites>FETCH-LOGICAL-c436t-2588bd2a9bdbf379309ace74684c91b4a04dc5592c58af776a7b3c614e7692143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuron.2020.01.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32027827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Huei-Ying</creatorcontrib><creatorcontrib>Maher, Brady J.</creatorcontrib><title>Lost in Translation: Cul3-Dependent Pathological Mechanisms in Psychiatric Disorders</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.
In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.</description><subject>Anxiety</subject><subject>Autism</subject><subject>Behavior</subject><subject>Cullin Proteins</subject><subject>Excitability</subject><subject>Genes</subject><subject>Glutamatergic transmission</subject><subject>Humans</subject><subject>Mental Disorders</subject><subject>Morphology</subject><subject>Mutation</subject><subject>Neurons</subject><subject>Physiology</subject><subject>Protein biosynthesis</subject><subject>Proteins</subject><subject>Translation</subject><subject>Ubiquitin</subject><subject>Ubiquitin-protein ligase</subject><subject>Ubiquitin-Protein Ligases</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVpaNy0_yCUhV5yWWf0sdKqh0Jx2iTg0hzcs9Bqx7HMWnKk3UL-feQ6zaGHwMBcnved4SHknMKcApWX23nAKcUwZ8BgDrQMvCEzClrVgmr9lsyg1bKWTPFT8j7nLQAVjabvyCkvGdUyNSOrZcxj5UO1SjbkwY4-hi_VYhp4fYV7DD2Gsbqz4yYO8d47O1Q_0W1s8HmXD7G7_Og23o7Ju-rK55h6TPkDOVnbIePH531Gfv_4vlrc1Mtf17eLb8vaCS7HmjVt2_XM6q7v1lxpDto6VEK2wmnaCQuid02jmWtau1ZKWtVxJ6lAJTWjgp-Ri2PvPsWHCfNodj47HAYbME7ZMN4wKUBpVtDP_6HbOKVQvvtLQRHDdaHEkXIp5pxwbfbJ72x6NBTMwbrZmqN1c7BugJaBEvv0XD51O-xfQv80F-DrEcBi44_HZLLzGBz2PqEbTR_96xeeAFDqlBE</recordid><startdate>20200205</startdate><enddate>20200205</enddate><creator>Chen, Huei-Ying</creator><creator>Maher, Brady J.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20200205</creationdate><title>Lost in Translation: Cul3-Dependent Pathological Mechanisms in Psychiatric Disorders</title><author>Chen, Huei-Ying ; Maher, Brady J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-2588bd2a9bdbf379309ace74684c91b4a04dc5592c58af776a7b3c614e7692143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Anxiety</topic><topic>Autism</topic><topic>Behavior</topic><topic>Cullin Proteins</topic><topic>Excitability</topic><topic>Genes</topic><topic>Glutamatergic transmission</topic><topic>Humans</topic><topic>Mental Disorders</topic><topic>Morphology</topic><topic>Mutation</topic><topic>Neurons</topic><topic>Physiology</topic><topic>Protein biosynthesis</topic><topic>Proteins</topic><topic>Translation</topic><topic>Ubiquitin</topic><topic>Ubiquitin-protein ligase</topic><topic>Ubiquitin-Protein Ligases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Huei-Ying</creatorcontrib><creatorcontrib>Maher, Brady J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Huei-Ying</au><au>Maher, Brady J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lost in Translation: Cul3-Dependent Pathological Mechanisms in Psychiatric Disorders</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2020-02-05</date><risdate>2020</risdate><volume>105</volume><issue>3</issue><spage>398</spage><epage>399</epage><pages>398-399</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.
In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>32027827</pmid><doi>10.1016/j.neuron.2020.01.010</doi><tpages>2</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anxiety Autism Behavior Cullin Proteins Excitability Genes Glutamatergic transmission Humans Mental Disorders Morphology Mutation Neurons Physiology Protein biosynthesis Proteins Translation Ubiquitin Ubiquitin-protein ligase Ubiquitin-Protein Ligases |
title | Lost in Translation: Cul3-Dependent Pathological Mechanisms in Psychiatric Disorders |
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