<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lu L</submitter><funding>Foundation of Zhejiang Health Science and Technology</funding><pagination>1172795</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8977338</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2022</volume><pubmed_abstract>&lt;i>β&lt;/i> cell dysfunction is the leading cause of diabetes. Adult &lt;i>β&lt;/i> cells have matured glucose-stimulated insulin secretion (GSIS), whereas fetal and neonatal &lt;i>β&lt;/i> cells are insensitive to glucose and are functionally immature. However, how &lt;i>β&lt;/i> cells mature and acquire robust GSIS is not fully understood. Here, we explored the potential regulatory proteins of &lt;i>β&lt;/i> cell maturation process and the capacity for GSIS. Combined with the data from public databases, we found that the gene expression of &lt;i>Mitofusin2&lt;/i> (&lt;i>Mfn2&lt;/i>) showed an increasing trend from mouse neonatal &lt;i>β&lt;/i> cells to mature &lt;i>β&lt;/i> cells. Moreover, its protein expression increased during mouse embryonic pancreas development and &lt;i>β&lt;/i> cell differentiation from mouse embryonic stem cells. Knock</pubmed_abstract><journal>Stem cells international</journal><pubmed_title>Mitofusin2 Promotes &lt;i>β&lt;/i> Cell Maturation from Mouse Embryonic Stem Cells via Sirt3/Idh2 Activation.</pubmed_title><pmcid>PMC8977338</pmcid><funding_grant_id>LYY21H310003</funding_grant_id><funding_grant_id>LYY20H280004</funding_grant_id><funding_grant_id>2020381061</funding_grant_id><funding_grant_id>81703578</funding_grant_id><pubmed_authors>Lu L</pubmed_authors><pubmed_authors>Dongsheng H</pubmed_authors><pubmed_authors>Mingzhu H</pubmed_authors><pubmed_authors>Zongfu P</pubmed_authors><pubmed_authors>Xiaoyang L</pubmed_authors><pubmed_authors>Xiaoping H</pubmed_authors><pubmed_authors>Nannan C</pubmed_authors><pubmed_authors>Zhitao L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitofusin2 Promotes &lt;i>β&lt;/i> Cell Maturation from Mouse Embryonic Stem Cells via Sirt3/Idh2 Activation.</name><description>&lt;i>β&lt;/i> cell dysfunction is the leading cause of diabetes. Adult &lt;i>β&lt;/i> cells have matured glucose-stimulated insulin secretion (GSIS), whereas fetal and neonatal &lt;i>β&lt;/i> cells are insensitive to glucose and are functionally immature. However, how &lt;i>β&lt;/i> cells mature and acquire robust GSIS is not fully understood. Here, we explored the potential regulatory proteins of &lt;i>β&lt;/i> cell maturation process and the capacity for GSIS. Combined with the data from public databases, we found that the gene expression of &lt;i>Mitofusin2&lt;/i> (&lt;i>Mfn2&lt;/i>) showed an increasing trend from mouse neonatal &lt;i>β&lt;/i> cells to mature &lt;i>β&lt;/i> cells. Moreover, its protein expression increased during mouse embryonic pancreas development and &lt;i>β&lt;/i> cell differentiation from mouse embryonic stem cells. Knock</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-06-18T08:48:40.153Z</modification><creation>2025-04-19T21:50:11.352Z</creation></dates><accession>S-EPMC8977338</accession><cross_references><pubmed>35386849</pubmed><doi>10.1155/2022/1172795</doi></cross_references></HashMap>