<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jones GN</submitter><funding>NCI NIH HHS</funding><pagination>1559-68</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2940464</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(8)</volume><pubmed_abstract>The cranial neural crest (CNC) undergoes complex molecular and morphological changes during embryogenesis in order to form the vertebrate skull, and nearly three quarters of all birth defects result from defects in craniofacial development. The molecular events leading to CNC differentiation have been extensively studied; however, the role of the cAMP-dependent protein kinase [protein kinase A (PKA)] during craniofacial development has only been described in palate formation. Here, we provide evidence that strict PKA regulation in postmigratory CNC cells is essential during craniofacial bone development. Selective inactivation of Prkar1a, a regulatory subunit of the PKA holoenzyme, in the CNC results in perinatal lethality caused by dysmorphic craniofacial development and subsequent asphyx</pubmed_abstract><journal>Molecular endocrinology (Baltimore, Md.)</journal><pubmed_title>Neural crest-specific loss of Prkar1a causes perinatal lethality resulting from defects in intramembranous ossification.</pubmed_title><pmcid>PMC2940464</pmcid><funding_grant_id>P30 CA016058</funding_grant_id><funding_grant_id>CA16058</funding_grant_id><funding_grant_id>R01 CA112268</funding_grant_id><funding_grant_id>CA112268-02</funding_grant_id><pubmed_authors>Kirschner LS</pubmed_authors><pubmed_authors>Weinstein MB</pubmed_authors><pubmed_authors>Toribio RE</pubmed_authors><pubmed_authors>Jones GN</pubmed_authors><pubmed_authors>La Perle KM</pubmed_authors><pubmed_authors>Carlton MM</pubmed_authors><pubmed_authors>Pringle DR</pubmed_authors><pubmed_authors>Powell KA</pubmed_authors><pubmed_authors>Yin Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Neural crest-specific loss of Prkar1a causes perinatal lethality resulting from defects in intramembranous ossification.</name><description>The cranial neural crest (CNC) undergoes complex molecular and morphological changes during embryogenesis in order to form the vertebrate skull, and nearly three quarters of all birth defects result from defects in craniofacial development. The molecular events leading to CNC differentiation have been extensively studied; however, the role of the cAMP-dependent protein kinase [protein kinase A (PKA)] during craniofacial development has only been described in palate formation. Here, we provide evidence that strict PKA regulation in postmigratory CNC cells is essential during craniofacial bone development. Selective inactivation of Prkar1a, a regulatory subunit of the PKA holoenzyme, in the CNC results in perinatal lethality caused by dysmorphic craniofacial development and subsequent asphyx</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Aug</publication><modification>2025-04-05T12:23:39.472Z</modification><creation>2019-03-27T00:34:08Z</creation></dates><accession>S-EPMC2940464</accession><cross_references><pubmed>20534695</pubmed><doi>10.1210/me.2009-0439</doi></cross_references></HashMap>