{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Peek SL"],"funding":["NICHD NIH HHS","NCI NIH HHS","NINDS NIH HHS","NIGMS NIH HHS","The University of Iowa Office of the Vice President for Research"],"pagination":["103814"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8844820"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(2)"],"pubmed_abstract":["Proper gene regulation is critical for both neuronal development and maintenance as the brain matures. We previously demonstrated that Akirin2, an essential nuclear protein that interacts with transcription factors and chromatin remodeling complexes, is required for the embryonic formation of the cerebral cortex. Here we show that Akirin2 plays a mechanistically distinct role in maintaining healthy neurons during cortical maturation. Restricting Akirin2 loss to excitatory cortical neurons resulted in progressive neurodegeneration via necroptosis and severe cortical atrophy with age. Comparing transcriptomes from Akirin2-null postnatal neurons and cortical progenitors revealed that targets of the tumor suppressor p53, a regulator of both proliferation and cell death encoded by <i>Trp53</i>,"],"journal":["iScience"],"pubmed_title":["p53-mediated neurodegeneration in the absence of the nuclear protein Akirin2."],"pmcid":["PMC8844820"],"funding_grant_id":["T32 GM008629","P50 HD103556","P30 CA034196","R01 NS055272"],"pubmed_authors":["Manak JR","Bais P","Peek SL","Iverson BJ","Burgess RW","Weiner JA","Parida M","Michaelson JJ","Bosch PJ","Bahl E"],"additional_accession":[]},"is_claimable":false,"name":"p53-mediated neurodegeneration in the absence of the nuclear protein Akirin2.","description":"Proper gene regulation is critical for both neuronal development and maintenance as the brain matures. We previously demonstrated that Akirin2, an essential nuclear protein that interacts with transcription factors and chromatin remodeling complexes, is required for the embryonic formation of the cerebral cortex. Here we show that Akirin2 plays a mechanistically distinct role in maintaining healthy neurons during cortical maturation. Restricting Akirin2 loss to excitatory cortical neurons resulted in progressive neurodegeneration via necroptosis and severe cortical atrophy with age. Comparing transcriptomes from Akirin2-null postnatal neurons and cortical progenitors revealed that targets of the tumor suppressor p53, a regulator of both proliferation and cell death encoded by <i>Trp53</i>,","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-05-30T15:13:54.247Z","creation":"2025-04-19T22:36:40.229Z"},"accession":"S-EPMC8844820","cross_references":{"pubmed":["35198879"],"doi":["10.1016/j.isci.2022.103814"]}}