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http://purl.uniprot.org/citations/22778138http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22778138http://www.w3.org/2000/01/rdf-schema#comment"Cell-cell fusion and cell invasion are essential for placental development. Human cytotrophoblasts in the chorionic villi may undergo cell-cell fusion to form syncytiotrophoblasts to facilitate nutrient-gas exchange or differentiate into extravillous trophoblasts (EVTs) to facilitate maternal-fetal circulation. The placental transcription factor glial cells missing 1 (GCM1) regulates syncytin-1 and -2 expression to mediate trophoblast fusion. Interestingly, GCM1 and syncytin-1 are also expressed in EVTs with unknown physiological functions. In this study, we performed chromatin immunoprecipitation-on-chip (ChIP-chip) analysis and identified the gene for high-temperature requirement protein A4 (HtrA4) as a GCM1 target gene, which encodes a serine protease facilitating cleavage of fibronectin and invasion of placental cells. Importantly, HtrA4 is immunolocalized in EVTs at the maternal-fetal interface, and its expression is decreased by hypoxia and in preeclampsia, a pregnancy complication associated with placental hypoxia and shallow trophoblast invasion. We further demonstrate that HtrA4 interacts with syncytin-1 and suppresses cell-cell fusion. Therefore, HtrA4 may be crucial for EVT differentiation by playing a dual role in prevention of cell-cell fusion of EVTs and promotion of their invasion into the uterus. Our study reveals a novel function of GCM1 and HtrA4 in regulation of trophoblast invasion and that abnormal HrtA4 expression may contribute to shallow trophoblast invasion in preeclampsia."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.org/dc/terms/identifier"doi:10.1128/mcb.00223-12"xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/author"Chen H."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/author"Lee Y.S."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/author"Lee M.T."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/author"Wang L.J."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/author"Cheong M.L."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/name"Mol Cell Biol"xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/pages"3707-3717"xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/title"High-temperature requirement protein A4 (HtrA4) suppresses the fusogenic activity of syncytin-1 and promotes trophoblast invasion."xsd:string
http://purl.uniprot.org/citations/22778138http://purl.uniprot.org/core/volume"32"xsd:string
http://purl.uniprot.org/citations/22778138http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22778138
http://purl.uniprot.org/citations/22778138http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22778138
http://purl.uniprot.org/uniprot/#_B4DTF7-mappedCitation-22778138http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22778138
http://purl.uniprot.org/uniprot/#_P83105-mappedCitation-22778138http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22778138
http://purl.uniprot.org/uniprot/#_Q9NP62-mappedCitation-22778138http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22778138
http://purl.uniprot.org/uniprot/P83105http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22778138
http://purl.uniprot.org/uniprot/B4DTF7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22778138
http://purl.uniprot.org/uniprot/Q9NP62http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22778138