<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chiba A</submitter><funding>Takeda Science Foundation</funding><funding>Nishinomiya Basic Research Fund</funding><funding>Japan Society for the Promotion of Science</funding><pagination>516-527</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11529416</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>44(11)</volume><pubmed_abstract>Parkinson's disease (PD) is an age-related progressive neurodegenerative disease. Previously, we identified midnolin (&lt;i>MIDN&lt;/i>) as a genetic risk factor for PD. Although &lt;i>MIDN&lt;/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 &lt;i>Midn&lt;/i> knockout (KO) PC12 cell models. &lt;i>Midn&lt;/i> KO inhibited neurite outgrowth and neurofilament light chain (&lt;i>Nefl&lt;/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</pubmed_abstract><journal>Molecular and cellular biology</journal><pubmed_title>Midnolin, a Genetic Risk Factor for Parkinson's Disease, Promotes Neurite Outgrowth Accompanied by Early Growth Response 1 Activation in PC12 Cells.</pubmed_title><pmcid>PMC11529416</pmcid><funding_grant_id>21K06573</funding_grant_id><pubmed_authors>Nagashima M</pubmed_authors><pubmed_authors>Nakamura K</pubmed_authors><pubmed_authors>Obara Y</pubmed_authors><pubmed_authors>Ishii K</pubmed_authors><pubmed_authors>Hosoi T</pubmed_authors><pubmed_authors>Chiba A</pubmed_authors><pubmed_authors>Nakagawa T</pubmed_authors><pubmed_authors>Kato C</pubmed_authors><pubmed_authors>Osaki T</pubmed_authors><pubmed_authors>Norota I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Midnolin, a Genetic Risk Factor for Parkinson's Disease, Promotes Neurite Outgrowth Accompanied by Early Growth Response 1 Activation in PC12 Cells.</name><description>Parkinson's disease (PD) is an age-related progressive neurodegenerative disease. Previously, we identified midnolin (&lt;i>MIDN&lt;/i>) as a genetic risk factor for PD. Although &lt;i>MIDN&lt;/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 &lt;i>Midn&lt;/i> knockout (KO) PC12 cell models. &lt;i>Midn&lt;/i> KO inhibited neurite outgrowth and neurofilament light chain (&lt;i>Nefl&lt;/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</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024</publication><modification>2025-04-18T12:59:25.968Z</modification><creation>2025-04-04T01:58:21.54Z</creation></dates><accession>S-EPMC11529416</accession><cross_references><pubmed>39264361</pubmed><doi>10.1080/10985549.2024.2399358</doi></cross_references></HashMap>