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http://purl.uniprot.org/citations/27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27019035http://www.w3.org/2000/01/rdf-schema#comment"Autism is one of the most common subtypes of autism spectrum disorder (ASD). Recent studies suggested a relationship between immune-dependent coding genes and ASD, indicating that long term neuroimmunological anomalies affect brain development and synaptic transmission among neural networks. Furthermore, various studies focused on biomarker potential of TNF-α in autism. Ionotropic receptors are also studied as potential marker for autism since altered gene expression levels are observed in autistic patients. GRID2 is a candidate ionotropic receptor which is involved glutamate transfer. In this study, to propose TNF-α dependent cellular processes involved in autism aetiology in relation to GRID2 we performed a bioinformatic network analysis and identified potential pathways and genes that are involved in TNF-α induced changes at GRID2 receptor levels. As a result, we ascertained the GRID2 receptor gene as a candidate gene and further studied the association between GRID2 expression levels and TNF-induced neurodegeneration. Our bioinformatic analyses and experimental results revealed that TNF-α regulates GRID2 gene expression by activating Cdc42 and GOPC genes. Moreover, increased TNF-α levels leads to increase of caspase-3 protein levels triggering neuronal apoptosis leading to neuronal deficiency, which is one of the major symptoms of autism. The study is the first to show the role of TNF-α in regulation of GRID2 gene expression and its signalling pathway. As a result, GRID2 gene can be a suppressor in TNF-induced neurodegeneration which may help to understand the main factors leading to autism."xsd:string
http://purl.uniprot.org/citations/27019035http://purl.org/dc/terms/identifier"doi:10.1016/j.neulet.2016.03.043"xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/author"Sezerman U."xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/author"Atasever-Arslan B."xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/author"Durasi I.M."xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/author"Kalkan Z."xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/name"Neurosci Lett"xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/pages"62-69"xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/title"Potential of GRID2 receptor gene for preventing TNF-induced neurodegeneration in autism."xsd:string
http://purl.uniprot.org/citations/27019035http://purl.uniprot.org/core/volume"620"xsd:string
http://purl.uniprot.org/citations/27019035http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27019035
http://purl.uniprot.org/citations/27019035http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27019035
http://purl.uniprot.org/uniprot/#_A0A0G2YPN5-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_A0A411D318-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_A0A1U9X8M9-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_A0A510GFL8-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_B5BUQ6-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_A0A977WMN2-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_B4DYB9-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_C1K3N5-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_P01375-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_O43424-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035
http://purl.uniprot.org/uniprot/#_Q4W5L9-mappedCitation-27019035http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27019035