<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Campbell B</submitter><funding>Philipps-Universität Marburg</funding><funding>Deutsche Forschungsgemeinschaft</funding><pagination>3000</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9944271</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(1)</volume><pubmed_abstract>SAM domain-containing protein 1 (SAMD1) has been implicated in atherosclerosis, as well as in chromatin and transcriptional regulation, suggesting a versatile and complex biological function. However, its role at an organismal level is currently unknown. Here, we generated SAMD1&lt;sup>-/-&lt;/sup> and SAMD1&lt;sup>+/-&lt;/sup> mice to explore the role of SAMD1 during mouse embryogenesis. Homozygous loss of SAMD1 was embryonic lethal, with no living animals seen after embryonic day 18.5. At embryonic day 14.5, organs were degrading and/or incompletely developed, and no functional blood vessels were observed, suggesting failed blood vessel maturation. Sparse red blood cells were scattered and pooled, primarily near the embryo surface. Some embryos had malformed heads and brains at embryonic day 15.5. I</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Investigation of SAMD1 ablation in mice.</pubmed_title><pmcid>PMC9944271</pmcid><funding_grant_id>109546710</funding_grant_id><pubmed_authors>Bourassa P</pubmed_authors><pubmed_authors>Engle SJ</pubmed_authors><pubmed_authors>Weber LM</pubmed_authors><pubmed_authors>Liefke R</pubmed_authors><pubmed_authors>Campbell B</pubmed_authors><pubmed_authors>Aiello R</pubmed_authors><pubmed_authors>Ozolins TRS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Investigation of SAMD1 ablation in mice.</name><description>SAM domain-containing protein 1 (SAMD1) has been implicated in atherosclerosis, as well as in chromatin and transcriptional regulation, suggesting a versatile and complex biological function. However, its role at an organismal level is currently unknown. Here, we generated SAMD1&lt;sup>-/-&lt;/sup> and SAMD1&lt;sup>+/-&lt;/sup> mice to explore the role of SAMD1 during mouse embryogenesis. Homozygous loss of SAMD1 was embryonic lethal, with no living animals seen after embryonic day 18.5. At embryonic day 14.5, organs were degrading and/or incompletely developed, and no functional blood vessels were observed, suggesting failed blood vessel maturation. Sparse red blood cells were scattered and pooled, primarily near the embryo surface. Some embryos had malformed heads and brains at embryonic day 15.5. I</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2026-05-29T08:15:25.217Z</modification><creation>2024-11-20T02:15:58.033Z</creation></dates><accession>S-EPMC9944271</accession><cross_references><pubmed>36810619</pubmed><doi>10.1038/s41598-023-29779-3</doi></cross_references></HashMap>