{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yi J"],"funding":["Howard Hughes Medical Institute","NIGMS NIH HHS"],"pagination":["2005-13"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3138404"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["239(7)"],"pubmed_abstract":["SUR-8, a conserved leucine-rich repeats protein, was first identified as a positive regulator of Ras pathway in Caenorhabditis elegans. Biochemical studies indicated that SUR-8 interacts with Ras and Raf, leading to the elevated ERK activity. However, the physiological role of SUR-8 during mammalian development remains unclear. Here we found that germline deletion of SUR-8 in mice resulted in early embryonic lethality. Inactivated SUR-8 specifically in mouse endothelial cells (ECs) revealed that SUR-8 is essential for embryonic heart development. SUR-8 deficiency in ECs resulted in late embryonic lethality, and the mutant mice displayed multiple cardiac defects. The reduced endothelial-mesenchymal transformation (EMT) and the reduced mesenchyme proliferation phase were observed in the atri"],"journal":["Developmental dynamics : an official publication of the American Association of Anatomists"],"pubmed_title":["Endothelial SUR-8 acts in an ERK-independent pathway during atrioventricular cushion development."],"pmcid":["PMC3138404"],"funding_grant_id":["R01 GM047869"],"pubmed_authors":["Yi J","Yang X","Chen M","Han M","Xu R","Xu T","Wu X","Zhuang Y"],"additional_accession":[]},"is_claimable":false,"name":"Endothelial SUR-8 acts in an ERK-independent pathway during atrioventricular cushion development.","description":"SUR-8, a conserved leucine-rich repeats protein, was first identified as a positive regulator of Ras pathway in Caenorhabditis elegans. Biochemical studies indicated that SUR-8 interacts with Ras and Raf, leading to the elevated ERK activity. However, the physiological role of SUR-8 during mammalian development remains unclear. Here we found that germline deletion of SUR-8 in mice resulted in early embryonic lethality. Inactivated SUR-8 specifically in mouse endothelial cells (ECs) revealed that SUR-8 is essential for embryonic heart development. SUR-8 deficiency in ECs resulted in late embryonic lethality, and the mutant mice displayed multiple cardiac defects. The reduced endothelial-mesenchymal transformation (EMT) and the reduced mesenchyme proliferation phase were observed in the atri","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Jul","modification":"2026-04-07T22:14:51.514Z","creation":"2025-06-27T03:05:10.231Z"},"accession":"S-EPMC3138404","cross_references":{"pubmed":["20549726"],"doi":["10.1002/dvdy.22343"]}}