<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>41</volume><submitter>Gassler A</submitter><funding>Bundesministerium für Bildung und Forschung</funding><pubmed_abstract>&lt;h4>Objective&lt;/h4>Altered gene expression contributes to the development of type 2 diabetes (T2D); thus, the analysis of differentially expressed genes between diabetes-susceptible and diabetes-resistant mouse models is an important tool for the determination of candidate genes that participate in the pathology. Based on RNA-seq and array data comparing pancreatic gene expression of diabetes-prone New Zealand Obese (NZO) mice and diabetes-resistant B6.V-ob/ob (B6-ob/ob) mice, the gap junction protein beta 4 (Gjb4) was identified as a putative novel T2D candidate gene.&lt;h4>Methods&lt;/h4>Gjb4 was overexpressed in primary islet cells derived from C57BL/6 (B6) mice and INS-1 cells via adenoviral-mediated infection. The proliferation rate of cells was assessed by BrdU incorporation, and insulin se</pubmed_abstract><journal>Molecular metabolism</journal><pagination>101042</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7365933</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Overexpression of Gjb4 impairs cell proliferation and insulin secretion in primary islet cells.</pubmed_title><pmcid>PMC7365933</pmcid><pubmed_authors>Jonas W</pubmed_authors><pubmed_authors>Vogel H</pubmed_authors><pubmed_authors>Stadion M</pubmed_authors><pubmed_authors>Mayer F</pubmed_authors><pubmed_authors>Helms A</pubmed_authors><pubmed_authors>Spranger J</pubmed_authors><pubmed_authors>Quiclet C</pubmed_authors><pubmed_authors>Schwerbel K</pubmed_authors><pubmed_authors>Kluth O</pubmed_authors><pubmed_authors>Wilhelmi I</pubmed_authors><pubmed_authors>Gassler A</pubmed_authors><pubmed_authors>Gottmann P</pubmed_authors><pubmed_authors>Ouni M</pubmed_authors><pubmed_authors>Schurmann A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Overexpression of Gjb4 impairs cell proliferation and insulin secretion in primary islet cells.</name><description>&lt;h4>Objective&lt;/h4>Altered gene expression contributes to the development of type 2 diabetes (T2D); thus, the analysis of differentially expressed genes between diabetes-susceptible and diabetes-resistant mouse models is an important tool for the determination of candidate genes that participate in the pathology. Based on RNA-seq and array data comparing pancreatic gene expression of diabetes-prone New Zealand Obese (NZO) mice and diabetes-resistant B6.V-ob/ob (B6-ob/ob) mice, the gap junction protein beta 4 (Gjb4) was identified as a putative novel T2D candidate gene.&lt;h4>Methods&lt;/h4>Gjb4 was overexpressed in primary islet cells derived from C57BL/6 (B6) mice and INS-1 cells via adenoviral-mediated infection. The proliferation rate of cells was assessed by BrdU incorporation, and insulin se</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Nov</publication><modification>2026-07-16T02:56:41.274Z</modification><creation>2025-04-04T13:38:25.255Z</creation></dates><accession>S-EPMC7365933</accession><cross_references><pubmed>32565358</pubmed><doi>10.1016/j.molmet.2020.101042</doi></cross_references></HashMap>