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http://purl.uniprot.org/citations/34373757http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34373757http://www.w3.org/2000/01/rdf-schema#comment"Neuroligin-3 (NLGN3) is necessary and sufficient to promote glioma cell growth. The recruitment of Gαi1/3 to the ligand-activated receptor tyrosine kinases (RTKs) is essential for mediating oncogenic signaling. Methods: Various genetic strategies were utilized to examine the requirement of Gαi1/3 in NLGN3-driven glioma cell growth. Results: NLGN3-induced Akt-mTORC1 and Erk activation was inhibited by decreasing Gαi1/3 expression. In contrast ectopic Gαi1/3 overexpression enhanced NLGN3-induced signaling. In glioma cells, NLGN3-induced cell growth, proliferation and migration were attenuated by Gαi1/3 depletion with shRNA, but facilitated with Gαi1/3 overexpression. Significantly, Gαi1/3 silencing inhibited orthotopic growth of patient-derived glioma xenografts in mouse brain, whereas forced Gαi1/3-overexpression in primary glioma xenografts significantly enhanced growth. The growth of brain-metastatic human lung cancer cells in mouse brain was largely inhibited with Gαi1/3 silencing. It was however expedited with ectopic Gαi1/3 overexpression. In human glioma Gαi3 upregulation was detected, correlating with poor prognosis. Conclusion: Gαi1/3 mediation of NLGN3-induced signaling is essential for neuronal-driven glioma growth."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.org/dc/terms/identifier"doi:10.7150/thno.61452"xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Chen G."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Cao C."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Liu F."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Peng Y."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Liu Y.Y."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Zhang Z.Q."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Cheng K.W."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Li K.R."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Chen M.B."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/author"Qi L.N."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/name"Theranostics"xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/pages"8535-8549"xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/title"Neuronal-driven glioma growth requires Galphai1 and Galphai3."xsd:string
http://purl.uniprot.org/citations/34373757http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/34373757http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34373757
http://purl.uniprot.org/citations/34373757http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34373757
http://purl.uniprot.org/uniprot/#_A0A0S2Z5K2-mappedCitation-34373757http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34373757
http://purl.uniprot.org/uniprot/#_B7Z3P8-mappedCitation-34373757http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34373757
http://purl.uniprot.org/uniprot/#_A0A8I5KSB7-mappedCitation-34373757http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34373757
http://purl.uniprot.org/uniprot/#_A0A8I5QJH8-mappedCitation-34373757http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34373757