| http://purl.uniprot.org/citations/38229308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/38229308 | http://www.w3.org/2000/01/rdf-schema#comment | "Hepatic ischemia-reperfusion (IR) injury is a complex systemic process causing a series clinical problem. C/EBPα is a key transcription factor for hepatocyte function, but its role and mechanism in regulating hepatic IR injury are largely unknown. Occluding portal vein and hepatic artery was used to establish a mouse model of hepatic IR injury. C/EBPα expression was decreased in IR-injured liver compared with the sham, accompanied by increased contents of serum alanine transaminase (ALT), aspartate transaminase (AST), high mobility group box-1, and proportion of hepatic cells. Oxygen and glucose deprivation/recovery (OGD/R) was used to establish a cellular hepatic IR model in WRL-68 hepatocytes in vitro, and C/EBPα was overexpressed in the hepatocytes to evaluate its effect on hepatic IR injury. OGD/R promoted oxidative stress, cell apoptosis and endoplasmic reticulum (ER) stress in hepatocytes, which was reversed by C/EBPα overexpression. Then, we found that C/EBPα promoted histone deacetylase 1 (HDAC1) transcription through binding to HDAC1 promoter. Moreover, HDAC1 deacetylated the activating transcription factor 4 (ATF4), a key positive regulator of ER stress. Trichostatin-A (an HDAC inhibitor) or ATF4 overexpression reversed the improvement of C/EBPα on OGD/R-induced ER stress and hepatocyte dysfunction. 4-Phenylbutyric acid (an endoplasmic reticulum stress inhibitor) also reversed the hepatic IR injury induced by ATF4 overexpression. Finally, lentivirus-mediated C/EBPα overexpression vector was applied to administrate hepatic IR mice, and the results showed that C/EBPα overexpression ameliorated IR-induced hepatic injury, manifesting with reduced ALT/AST, oxidative stress and ER stress. Altogether, our findings suggested that C/EBPα ameliorated hepatic IR injury by inhibiting ER stress via HDAC1-mediated deacetylation of ATF4 promoter."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.org/dc/terms/identifier | "doi:10.1002/jbt.23630"xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Chen S."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Dong L."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Li S."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Li R."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Ren Y."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Shen L."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Xu M."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/author | "Yang L."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/date | "2024"xsd:gYear |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/name | "J Biochem Mol Toxicol"xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/pages | "e23630"xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/title | "C/EBPalpha alleviates hepatic ischemia-reperfusion injury by inhibiting endoplasmic reticulum stress via HDAC1-mediated deacetylation of ATF4."xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://purl.uniprot.org/core/volume | "38"xsd:string |
| http://purl.uniprot.org/citations/38229308 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/38229308 |
| http://purl.uniprot.org/citations/38229308 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/38229308 |
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| http://purl.uniprot.org/uniprot/#_Q06507-mappedCitation-38229308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38229308 |
| http://purl.uniprot.org/uniprot/#_P53566-mappedCitation-38229308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38229308 |
| http://purl.uniprot.org/uniprot/#_Q3TZI8-mappedCitation-38229308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38229308 |
| http://purl.uniprot.org/uniprot/#_Q58E49-mappedCitation-38229308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38229308 |