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http://purl.uniprot.org/citations/34293353http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34293353http://www.w3.org/2000/01/rdf-schema#comment"Persistent chronic inflammation and delayed epithelialization lead to stalled healing in diabetic ulcers (DUs). PD-L1 shows anti-inflammatory and proliferative activities in healing defects, whereas its function in DU pathogenesis remains unknown. Lower levels of PD-L1 were found in DU tissues, and exogenous PD-L1 has therapeutic effects in the healing process by accelerating re-epithelialization and attenuating prolonged inflammation, which contributed to the delayed wound closure. We detected the downstream effectors of PD-L1 using transcriptional profiles and screened the interacting proteins using immunoprecipitation in combination with mass spectrometry and coimmunoprecipitation assays. The biological functions of eIF3I‒PD-L1‒IRS4 axis were tested both in vivo and in vitro. Finally, we validated the expression levels of eIF3I, PD-L1, and IRS4 in DU tissues from human clinical samples by immunohistochemistry staining. Mechanistically, PD-L1 binds to eIF3I and promotes cutaneous diabetic wound healing by downregulating IRS4. These findings identify that the eIF3I‒PD-L1‒IRS4 axis contributes to wound healing defects, which can serve as a potential therapeutic target in DUs."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.org/dc/terms/identifier"doi:10.1016/j.jid.2021.06.028"xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Luo Y."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Li B."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Ru Y."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Lu B."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Song J.K."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Kuai L."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Yin S.Y."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Chen Q.L."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Luo Y.'"xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Xiang Y.W."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/author"Jiang J.S."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/name"J Invest Dermatol"xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/pages"220-231.e8"xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/title"PD-L1 Triggered by Binding eIF3I Contributes to the Amelioration of Diabetes-Associated Wound Healing Defects by Regulating IRS4."xsd:string
http://purl.uniprot.org/citations/34293353http://purl.uniprot.org/core/volume"142"xsd:string
http://purl.uniprot.org/citations/34293353http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34293353
http://purl.uniprot.org/citations/34293353http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34293353
http://purl.uniprot.org/uniprot/#_Q3U472-mappedCitation-34293353http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34293353
http://purl.uniprot.org/uniprot/#_Q9EP73-mappedCitation-34293353http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34293353
http://purl.uniprot.org/uniprot/Q3U472http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34293353