<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ohnishi T</submitter><funding>Ministry of Education, Culture, Sports, Science and Technology</funding><funding>Japan Society for the Promotion of Science</funding><pagination>e12574</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8033514</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(4)</volume><pubmed_abstract>Genomic defects with large effect size can help elucidate unknown pathologic architecture of mental disorders. We previously reported on a patient with schizophrenia and a balanced translocation between chromosomes 4 and 13 and found that the breakpoint within chromosome 4 is located near the LDB2 gene. We show here that Ldb2 knockout (KO) mice displayed multiple deficits relevant to mental disorders. In particular, Ldb2 KO mice exhibited deficits in the fear-conditioning paradigm. Analysis of the amygdala suggested that dysregulation of synaptic activities controlled by the immediate early gene Arc is involved in the phenotypes. We show that LDB2 forms protein complexes with known transcription factors. Consistently, ChIP-seq analyses indicated that LDB2 binds to > 10,000 genomic sites in</pubmed_abstract><journal>EMBO molecular medicine</journal><pubmed_title>Cooperation of LIM domain-binding 2 (LDB2) with EGR in the pathogenesis of schizophrenia.</pubmed_title><pmcid>PMC8033514</pmcid><funding_grant_id>JP19H05435</funding_grant_id><funding_grant_id>17790834</funding_grant_id><funding_grant_id>19H04876</funding_grant_id><funding_grant_id>19H03321</funding_grant_id><funding_grant_id>24591737</funding_grant_id><funding_grant_id>25116505</funding_grant_id><funding_grant_id>20K07934</funding_grant_id><funding_grant_id>16K07017</funding_grant_id><funding_grant_id>23220008</funding_grant_id><funding_grant_id>21591535</funding_grant_id><funding_grant_id>15K01848</funding_grant_id><pubmed_authors>Ogawa I</pubmed_authors><pubmed_authors>Hosoya T</pubmed_authors><pubmed_authors>Toriumi K</pubmed_authors><pubmed_authors>Suzuki K</pubmed_authors><pubmed_authors>Ohnishi T</pubmed_authors><pubmed_authors>Watanabe A</pubmed_authors><pubmed_authors>Balan S</pubmed_authors><pubmed_authors>Kurokawa R</pubmed_authors><pubmed_authors>Toyota T</pubmed_authors><pubmed_authors>Arima-Yoshida F</pubmed_authors><pubmed_authors>Kuraku S</pubmed_authors><pubmed_authors>Itokawa M</pubmed_authors><pubmed_authors>Ohba H</pubmed_authors><pubmed_authors>Bito H</pubmed_authors><pubmed_authors>Iwayama Y</pubmed_authors><pubmed_authors>Toyoshima M</pubmed_authors><pubmed_authors>Yoshikawa A</pubmed_authors><pubmed_authors>Shimamoto-Mitsuyama C</pubmed_authors><pubmed_authors>Tanaka K</pubmed_authors><pubmed_authors>Maekawa M</pubmed_authors><pubmed_authors>Okuno H</pubmed_authors><pubmed_authors>Nakaya A</pubmed_authors><pubmed_authors>Manabe T</pubmed_authors><pubmed_authors>Yamada K</pubmed_authors><pubmed_authors>Kadota M</pubmed_authors><pubmed_authors>Horiuchi Y</pubmed_authors><pubmed_authors>Yoshikawa T</pubmed_authors><pubmed_authors>Nozaki Y</pubmed_authors><pubmed_authors>Kiyama Y</pubmed_authors><pubmed_authors>Arai M</pubmed_authors><pubmed_authors>Ichikawa T</pubmed_authors><pubmed_authors>Miyashita M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cooperation of LIM domain-binding 2 (LDB2) with EGR in the pathogenesis of schizophrenia.</name><description>Genomic defects with large effect size can help elucidate unknown pathologic architecture of mental disorders. We previously reported on a patient with schizophrenia and a balanced translocation between chromosomes 4 and 13 and found that the breakpoint within chromosome 4 is located near the LDB2 gene. We show here that Ldb2 knockout (KO) mice displayed multiple deficits relevant to mental disorders. In particular, Ldb2 KO mice exhibited deficits in the fear-conditioning paradigm. Analysis of the amygdala suggested that dysregulation of synaptic activities controlled by the immediate early gene Arc is involved in the phenotypes. We show that LDB2 forms protein complexes with known transcription factors. Consistently, ChIP-seq analyses indicated that LDB2 binds to > 10,000 genomic sites in</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-26T08:20:52.711Z</modification><creation>2022-02-09T14:51:58.755Z</creation></dates><accession>S-EPMC8033514</accession><cross_references><pubmed>33656268</pubmed><doi>10.15252/emmm.202012574</doi></cross_references></HashMap>