<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gao Y</submitter><funding>NICHD NIH HHS</funding><pagination>e13791</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11955836</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(2)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Maternal obesity (MO) impairs fetal skeletal muscle development, but the underlying mechanisms remain poorly defined. The regulatory roles of lncRNA H19 and its first exon derived microRNA675 (miR675) in prenatal muscle development remain to be examined. H19/Igf2 are in the same imprinting cluster with H19 expressed from the maternal allele while Igf2 expresses paternally. H19 contains a G-rich loop, and KH-type splicing regulatory protein (KHSRP) mediates the biogenesis of pre-miRNAs containing G-rich loops, which depends on its phosphorylation by AKT, a key mediator of IGF2 signalling. This study aims to depict the elusive function of these regulators that are affected by MO during embryonic myogenesis.&lt;h4>Methods&lt;/h4>Single-cell transcriptomic sequencing and GeoMx spa</pubmed_abstract><journal>Journal of cachexia, sarcopenia and muscle</journal><pubmed_title>Balancing LncRNA H19 and miR-675 Bioconversion as a Key Regulator of Embryonic Myogenesis Under Maternal Obesity.</pubmed_title><pmcid>PMC11955836</pmcid><funding_grant_id>R01 HD067449</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Zhao L</pubmed_authors><pubmed_authors>Hossain MN</pubmed_authors><pubmed_authors>Deavila JM</pubmed_authors><pubmed_authors>Zhu MJ</pubmed_authors><pubmed_authors>Murdoch GK</pubmed_authors><pubmed_authors>Gao Y</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Du M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Balancing LncRNA H19 and miR-675 Bioconversion as a Key Regulator of Embryonic Myogenesis Under Maternal Obesity.</name><description>&lt;h4>Background&lt;/h4>Maternal obesity (MO) impairs fetal skeletal muscle development, but the underlying mechanisms remain poorly defined. The regulatory roles of lncRNA H19 and its first exon derived microRNA675 (miR675) in prenatal muscle development remain to be examined. H19/Igf2 are in the same imprinting cluster with H19 expressed from the maternal allele while Igf2 expresses paternally. H19 contains a G-rich loop, and KH-type splicing regulatory protein (KHSRP) mediates the biogenesis of pre-miRNAs containing G-rich loops, which depends on its phosphorylation by AKT, a key mediator of IGF2 signalling. This study aims to depict the elusive function of these regulators that are affected by MO during embryonic myogenesis.&lt;h4>Methods&lt;/h4>Single-cell transcriptomic sequencing and GeoMx spa</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2026-06-03T02:37:50.338Z</modification><creation>2025-07-09T03:04:41.55Z</creation></dates><accession>S-EPMC11955836</accession><cross_references><pubmed>40162559</pubmed><doi>10.1002/jcsm.13791</doi></cross_references></HashMap>