http://purl.uniprot.org/citations/35235353 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/35235353 | http://www.w3.org/2000/01/rdf-schema#comment | "The involvement of genetic risk and the underlying developmental and neural circuit mechanisms in autism-related social deficit are largely unclear. Here, we report that deletion of AUTS2, a high-susceptibility gene of ASDs, caused postnatal dentate gyrus (DG) hypoplasia, which was closely relevant to social recognition deficit. Furthermore, a previously unknown mechanism for neural cell migration in postnatal DG development was identified, in which Auts2-related signaling played a vital role as the transcription repressor. Moreover, the supramammillary nucleus (SuM)-DG-CA3 neural circuit was found to be involved in social recognition and affected in Auts2-deleted mice due to DG hypoplasia. Correction of DG-CA3 synaptic transmission by using a pharmacological approach or chemo/optogenetic activation of the SuM-DG circuit restored the social recognition deficit in Auts2-deleted mice. Our findings demonstrated the vital role of Auts2 in postnatal DG development, and this role was critical for SuM-DG-CA3 neural circuit-mediated social recognition behavior."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.org/dc/terms/identifier | "doi:10.1126/sciadv.abk1238"xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Meng H."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Sun X."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "You Y."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Sun M."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Zhang T."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Zhao L."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Wei C."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Zhang D."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/author | "Yue W."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/name | "Sci Adv"xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/pages | "eabk1238"xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/title | "Auts2 deletion involves in DG hypoplasia and social recognition deficit: The developmental and neural circuit mechanisms."xsd:string |
http://purl.uniprot.org/citations/35235353 | http://purl.uniprot.org/core/volume | "8"xsd:string |
http://purl.uniprot.org/citations/35235353 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/35235353 |
http://purl.uniprot.org/citations/35235353 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/35235353 |
http://purl.uniprot.org/uniprot/#_A0A087WPF7-mappedCitation-35235353 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35235353 |
http://purl.uniprot.org/uniprot/#_E0CZ47-mappedCitation-35235353 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35235353 |
http://purl.uniprot.org/uniprot/#_A0A7N9VSJ5-mappedCitation-35235353 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35235353 |