{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chiba A"],"funding":["Takeda Science Foundation","Nishinomiya Basic Research Fund","Japan Society for the Promotion of Science"],"pagination":["516-527"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11529416"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(11)"],"pubmed_abstract":["Parkinson's disease (PD) is an age-related progressive neurodegenerative disease. Previously, we identified midnolin (<i>MIDN</i>) as a genetic risk factor for PD. Although <i>MIDN</i> copy number loss increases the risk of PD, the molecular function of MIDN remains unclear. To investigate the role of MIDN in PD, we established monoclonal <i>Midn</i> knockout (KO) PC12 cell models. <i>Midn</i> KO inhibited neurite outgrowth and neurofilament light chain (<i>Nefl</i>) gene expression. Although MIDN is mainly localized in the nucleus, it does not encode DNA-binding domains. We therefore hypothesized that MIDN might bind to certain transcription factors and regulate gene expression. Of the candidate transcription factors, we focused on early growth response 1 (EGR1) because it is required for"],"journal":["Molecular and cellular biology"],"pubmed_title":["Midnolin, a Genetic Risk Factor for Parkinson's Disease, Promotes Neurite Outgrowth Accompanied by Early Growth Response 1 Activation in PC12 Cells."],"pmcid":["PMC11529416"],"funding_grant_id":["21K06573"],"pubmed_authors":["Nagashima M","Nakamura K","Obara Y","Ishii K","Hosoi T","Chiba A","Nakagawa T","Kato C","Osaki T","Norota I"],"additional_accession":[]},"is_claimable":false,"name":"Midnolin, a Genetic Risk Factor for Parkinson's Disease, Promotes Neurite Outgrowth Accompanied by Early Growth Response 1 Activation in PC12 Cells.","description":"Parkinson's disease (PD) is an age-related progressive neurodegenerative disease. Previously, we identified midnolin (<i>MIDN</i>) as a genetic risk factor for PD. Although <i>MIDN</i> copy number loss increases the risk of PD, the molecular function of MIDN remains unclear. To investigate the role of MIDN in PD, we established monoclonal <i>Midn</i> knockout (KO) PC12 cell models. <i>Midn</i> KO inhibited neurite outgrowth and neurofilament light chain (<i>Nefl</i>) gene expression. Although MIDN is mainly localized in the nucleus, it does not encode DNA-binding domains. We therefore hypothesized that MIDN might bind to certain transcription factors and regulate gene expression. Of the candidate transcription factors, we focused on early growth response 1 (EGR1) because it is required for","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2025-04-18T12:59:25.968Z","creation":"2025-04-04T01:58:21.54Z"},"accession":"S-EPMC11529416","cross_references":{"pubmed":["39264361"],"doi":["10.1080/10985549.2024.2399358"]}}