<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shull LC</submitter><funding>NIDCR NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institutes of Health</funding><pagination>132-144</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7198358</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>461(2)</volume><pubmed_abstract>The formation of the craniofacial skeleton is a highly dynamic process that requires proper orchestration of various cellular processes in cranial neural crest cell (cNCC) development, including cell migration, proliferation, differentiation, polarity and cell death. Alterations that occur during cNCC development result in congenital birth defects and craniofacial abnormalities such as cleft lip with or without cleft palate. While the gene regulatory networks facilitating neural crest development have been extensively studied, the epigenetic mechanisms by which these pathways are activated or repressed in a temporal and spatially regulated manner remain largely unknown. Chromatin modifiers can precisely modify gene expression through a variety of mechanisms including histone modifications </pubmed_abstract><journal>Developmental biology</journal><pubmed_title>The conserved and divergent roles of Prdm3 and Prdm16 in zebrafish and mouse craniofacial development.</pubmed_title><pmcid>PMC7198358</pmcid><funding_grant_id>P30 NS048154</funding_grant_id><funding_grant_id>R01 DE024034</funding_grant_id><funding_grant_id>F32 DE029099</funding_grant_id><pubmed_authors>Shull LC</pubmed_authors><pubmed_authors>Goyama S</pubmed_authors><pubmed_authors>Artinger KB</pubmed_authors><pubmed_authors>Kurokawa M</pubmed_authors><pubmed_authors>Menzel J</pubmed_authors><pubmed_authors>Sen R</pubmed_authors></additional><is_claimable>false</is_claimable><name>The conserved and divergent roles of Prdm3 and Prdm16 in zebrafish and mouse craniofacial development.</name><description>The formation of the craniofacial skeleton is a highly dynamic process that requires proper orchestration of various cellular processes in cranial neural crest cell (cNCC) development, including cell migration, proliferation, differentiation, polarity and cell death. Alterations that occur during cNCC development result in congenital birth defects and craniofacial abnormalities such as cleft lip with or without cleft palate. While the gene regulatory networks facilitating neural crest development have been extensively studied, the epigenetic mechanisms by which these pathways are activated or repressed in a temporal and spatially regulated manner remain largely unknown. Chromatin modifiers can precisely modify gene expression through a variety of mechanisms including histone modifications </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 May</publication><modification>2025-04-05T10:07:36.487Z</modification><creation>2025-02-19T03:42:00.481Z</creation></dates><accession>S-EPMC7198358</accession><cross_references><pubmed>32044379</pubmed><doi>10.1016/j.ydbio.2020.02.006</doi></cross_references></HashMap>