<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luo Z</submitter><funding>Science and Technology Planning Project of Guangdong Province</funding><funding>Strategic Priority Research Program of the Chinese Academy of Sciences</funding><funding>Guangzhou Science and Technology Program</funding><funding>Guangdong Province Science and Technology Program</funding><funding>Zhujiang Talents-Overseas Young Talents Postdoctoral Fellowship</funding><funding>National Key Research and Development Program of China</funding><funding>National Natural Science Foundation of China</funding><pagination>21-29</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6557759</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>Class IIa histone deacetylases (HDACs) are a subfamily of HDACs with important functions in development and adult tissue homeostasis. As opposed to other HDACs, they lack catalytic function and bind transcription factors to recruit transcriptional co-regulators, mostly co-repressors such as nuclear receptor co-repressor (NCoR)/silencing mediator of retinoid and thyroid hormone receptor (SMRT). Class IIa HDACs enhance mouse somatic cell reprogramming to induced pluripotent stem cells (iPSCs) by repressing the function of the pro-mesenchymal transcription factor myocyte enhancer factor 2 (MEF2), which is upregulated during this process. Here, we describe, using HDAC4 and 7 as examples, that class IIa HDACs exhibit nuclear-cytoplasmic trafficking in reprogramming, being mostly cytoplasmic in </pubmed_abstract><journal>Cell regeneration (London, England)</journal><pubmed_title>Nuclear-cytoplasmic shuttling of class IIa histone deacetylases regulates somatic cell reprogramming.</pubmed_title><pmcid>PMC6557759</pmcid><funding_grant_id>2014A030312001</funding_grant_id><funding_grant_id>XDA16030502</funding_grant_id><funding_grant_id>81571238</funding_grant_id><funding_grant_id>2016B030229007</funding_grant_id><funding_grant_id>31671537</funding_grant_id><funding_grant_id>201807010066</funding_grant_id><funding_grant_id>2017B050506007</funding_grant_id><funding_grant_id>2017B030314056</funding_grant_id><funding_grant_id>31571524</funding_grant_id><funding_grant_id>2018YFA0106903</funding_grant_id><funding_grant_id>2016YFA0100102</funding_grant_id><pubmed_authors>Luo Z</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Volpe G</pubmed_authors><pubmed_authors>Zhuang Q</pubmed_authors><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Zhong X</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Esteban MA</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Lai Y</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Huang Z</pubmed_authors><pubmed_authors>Qing X</pubmed_authors><pubmed_authors>Benda C</pubmed_authors><pubmed_authors>Ward C</pubmed_authors><pubmed_authors>Qin B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nuclear-cytoplasmic shuttling of class IIa histone deacetylases regulates somatic cell reprogramming.</name><description>Class IIa histone deacetylases (HDACs) are a subfamily of HDACs with important functions in development and adult tissue homeostasis. As opposed to other HDACs, they lack catalytic function and bind transcription factors to recruit transcriptional co-regulators, mostly co-repressors such as nuclear receptor co-repressor (NCoR)/silencing mediator of retinoid and thyroid hormone receptor (SMRT). Class IIa HDACs enhance mouse somatic cell reprogramming to induced pluripotent stem cells (iPSCs) by repressing the function of the pro-mesenchymal transcription factor myocyte enhancer factor 2 (MEF2), which is upregulated during this process. Here, we describe, using HDAC4 and 7 as examples, that class IIa HDACs exhibit nuclear-cytoplasmic trafficking in reprogramming, being mostly cytoplasmic in </description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jun</publication><modification>2025-04-04T22:09:07.956Z</modification><creation>2019-07-24T07:13:51Z</creation></dates><accession>S-EPMC6557759</accession><cross_references><pubmed>31205685</pubmed><doi>10.1016/j.cr.2018.11.001</doi></cross_references></HashMap>