{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T01:58:30Z","timestamp":1785463110832,"version":"3.56.0"},"reference-count":55,"publisher":"Wiley","issue":"19","license":[{"start":{"date-parts":[[2024,8,28]],"date-time":"2024-08-28T00:00:00Z","timestamp":1724803200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2024,8,28]],"date-time":"2024-08-28T00:00:00Z","timestamp":1724803200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      This study investigates the molecular mechanisms behind ischaemia\/reperfusion (I\/R) injury in the brain, focusing on neuronal apoptosis. It scrutinizes the role of the Jun proto\u2010oncogene in apoptosis, involvement of SOCS1 in neural precursor cell accumulation in ischaemic regions, and the upregulation of C\u2010EBP\u03b2 in the hippocampus following I\/R. Key to the study is understanding how Jun controls C\u2010EBP\u03b2 degradation via SOCS1, potentially offering new clinical treatment avenues for I\/R. Techniques such as mRNA sequencing, KEGG enrichment analysis and protein\u2013protein interaction (PPI) in mouse models have indicated involvement of Jun (AP\u20101) in I\/R\u2010induced cerebral damage. The study employs middle cerebral artery occlusion in different mouse models and oxygen\u2013glucose deprivation\/reoxygenation in cortical neurons to examine the impacts of Jun and SOCS1 manipulation on cerebral I\/R injury and neuronal damage. The findings reveal that I\/R reduces Jun expression in the brain, but its restoration lessens cerebral I\/R injury and neuron death. Jun activates SOCS1 transcriptionally, leading to C\u2010EBP\u03b2 degradation, thereby diminishing cerebral I\/R injury through the SOCS1\/C\u2010EBP\u03b2 pathway. These insights provide a deeper understanding of post\u2010I\/R cerebral injury mechanisms and suggest new therapeutic targets for cerebral I\/R injury.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16195-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Jun and SOCS1 are poorly expressed, and C\u2010EBP\u03b2 is highly expressed in ischaemia\/reperfusion mouse brain tissues.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Jun transcriptionally activates SOCS1.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>SOCS1 promotes the ubiquitination\u2010dependent C\u2010EBP\u03b2 protein degradation.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Jun blunts oxygen\u2013glucose deprivation\/reoxygenation\u2010induced neuron apoptosis and alleviates neuronal injury.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This study provides a theoretical basis for the management of post\u2010I\/R brain injury.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp285673","type":"journal-article","created":{"date-parts":[[2024,8,28]],"date-time":"2024-08-28T15:53:32Z","timestamp":1724860412000},"page":"4959-4985","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Jun\u2010activated SOCS1 enhances ubiquitination and degradation of CCAAT\/enhancer\u2010binding protein \u03b2 to ameliorate cerebral ischaemia\/reperfusion injury"],"prefix":"10.1113","volume":"602","author":[{"given":"Chuan","family":"He","sequence":"first","affiliation":[{"name":"Department of Gastroenterology The First Hospital of Jilin University  Changchun P.R. 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