{"corpus_id":44885716,"paper_sha":"95423616b92e72ab930d16f0f42873eac6fee00a","doi":"10.4161/cib.3.3.11414","arxiv_id":null,"pmid":20714405,"pmcid":"PMC2918768","mag_id":2073969666,"dblp_id":null,"acl_id":null,"title":"Neuronal JNK pathway activation by IL-1 is mediated through IL1RAPL1, a protein required for development of cognitive functions","year":2010,"publication_date":"2010-05-01","venue":"Communicative & Integrative Biology","journal":{"name":"Communicative & Integrative Biology","pages":"15 - 245 - 247","volume":"3"},"journal_issn":null,"journal_title":null,"publication_types":["JournalArticle"],"pubmed_pub_types":["Journal Article"],"s2_fields_of_study":["Biology","Medicine"],"reference_count":15,"citation_count":38,"influential_citation_count":4,"is_open_access":true,"arxiv_categories":null,"arxiv_license":null,"arxiv_journal_ref":null,"mesh_headings":null,"chemicals":null,"comments_corrections":null,"source_flags":5,"s2_open_access_pdf_url":"https://www.tandfonline.com/doi/pdf/10.4161/cib.3.3.11414?needAccess=true","s2_open_access_landing_url":"https://www.semanticscholar.org/paper/95423616b92e72ab930d16f0f42873eac6fee00a","s2_open_access_license":"CCBYNC","s2_open_access_status":"GOLD","pmc_open_access_pdf_url":null,"pmc_open_access_landing_url":null,"pmc_open_access_license":null,"pmc_open_access_status":null,"unpaywall_open_access_pdf_url":null,"unpaywall_open_access_landing_url":null,"unpaywall_open_access_license":null,"unpaywall_open_access_status":null,"abstract":"Interleukin-1-Receptor Accessory Protein Like 1 (IL1RAPL1) gene mutations are associated to cognitive impairment ranging from non-syndromic X-linked mental retardation to autism. Functionally IL1RAPL1 belongs to a novel family of Toll/ IL-1 Receptors, but its ligand is unknown. In a recent study, we have shown that IL1RAPL1 is present in dendritic spine where it interacts with PSD-95, a major scaffold protein of excitatory post-synaptic density. We demonstrated that IL1RAPL1 regulates the synaptic localization of PSD-95 by controlling JNK (c-Jun terminal Kinase) activity and PSD-95 phosphorylation. Loss of IL1RAPL1 in mouse not only led to a reduction of excitatory synapses but also to specific deficits in hippocampal long-term synaptic plasticity. Here we report that activation of JNK pathway in neurons by Interleukin-1 (IL-1) is mediated by IL1RAPL1. The interaction of IL1RAPL1 with PSD-95 discloses a novel pathophysiological mechanism underlying cognitive impairment associated with alterations of the JNK pathway in response to IL-1 and leading to the mis-localization of PSD-95, that subsequently result in abnormal synaptic organization and function.","claims":[{"public_id":"cl_739ff2eed526831282450ef5ac4cfa55","status":"active","text":"Activation of the neuronal JNK pathway by interleukin-1 is mediated by IL1RAPL1.","confidence":0.98,"contributors":[{"id":1,"public_id":"12632b8b5f","public_label":"Anonymous (12632b8b5f)","roles":["extraction"],"url":"https://sah.borca.ai/u/12632b8b5f"}],"url":"https://sah.borca.ai/claims/cl_739ff2eed526831282450ef5ac4cfa55"},{"public_id":"cl_70b25413b133bee3eb3287be6f18bcf3","status":"active","text":"IL1RAPL1 controls PSD-95 synaptic localization by regulating JNK activity and PSD-95 phosphorylation.","confidence":0.97,"contributors":[{"id":1,"public_id":"12632b8b5f","public_label":"Anonymous 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