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http://purl.uniprot.org/citations/25790768http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25790768http://www.w3.org/2000/01/rdf-schema#comment"Inflammation is closely related to the extent of damage following cerebral ischaemia, and the targeting of this inflammation has emerged as a promising therapeutic strategy. Here, we present that hypoxia-induced glial T-cell immunoglobulin and mucin domain protein (TIM)-3 can function as a modulator that links inflammation and subsequent brain damage after ischaemia. We find that TIM-3 is highly expressed in hypoxic brain regions of a mouse cerebral hypoxia-ischaemia (H/I) model. TIM-3 is distinctively upregulated in activated microglia and astrocytes, brain resident immune cells, in a hypoxia-inducible factor (HIF)-1-dependent manner. Notably, blockade of TIM-3 markedly reduces infarct size, neuronal cell death, oedema formation and neutrophil infiltration in H/I mice. Hypoxia-triggered neutrophil migration and infarction are also decreased in HIF-1α-deficient mice. Moreover, functional neurological deficits after H/I are significantly improved in both anti-TIM-3-treated mice and myeloid-specific HIF-1α-deficient mice. Further understanding of these insights could serve as the basis for broadening the therapeutic scope against hypoxia-associated brain diseases."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.org/dc/terms/identifier"doi:10.1038/ncomms7340"xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Kim H.S."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Yoon H.J."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Johnson R.S."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Park E.J."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Chang C.Y."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Ahn Y.H."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Kim I.H."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Koh H.S."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Jeon S.B."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/author"Jeon S.H."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/name"Nat Commun"xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/pages"6340"xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/title"The HIF-1/glial TIM-3 axis controls inflammation-associated brain damage under hypoxia."xsd:string
http://purl.uniprot.org/citations/25790768http://purl.uniprot.org/core/volume"6"xsd:string
http://purl.uniprot.org/citations/25790768http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25790768
http://purl.uniprot.org/citations/25790768http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25790768
http://purl.uniprot.org/uniprot/#_A0A077S2U6-mappedCitation-25790768http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25790768
http://purl.uniprot.org/uniprot/#_A0A0R4J1E9-mappedCitation-25790768http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25790768
http://purl.uniprot.org/uniprot/#_A0A0R4J1F0-mappedCitation-25790768http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25790768
http://purl.uniprot.org/uniprot/#_D3Z3I4-mappedCitation-25790768http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25790768
http://purl.uniprot.org/uniprot/#_P08905-mappedCitation-25790768http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25790768