http://purl.uniprot.org/citations/30905411 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/30905411 | http://www.w3.org/2000/01/rdf-schema#comment | "Lysyl hydroxylase 2 (LH2) is an endoplasmic reticulum (ER)-resident enzyme that catalyzes the hydroxylation of lysine residues in the telopeptides of fibrillar collagens. This is a critical modification to determine the fate of collagen cross-linking pathway that contributes to the stability of collagen fibrils. Studies have demonstrated that the aberrant LH2 function causes various diseases including osteogenesis imperfecta, fibrosis, and cancer metastasis. However, surprisingly, a LH2-deficient animal model has not been reported. In the current study, to better understand the function of LH2, we generated LH2 gene knockout mice by CRISPR/Cas9 technology. LH2 deficiency was confirmed by genotyping polymerase chain reaction (PCR), reverse transcriptase-PCR, and immunohistochemical analyses. Homozygous LH2 knockout (LH2-/-) embryos failed to develop normally and died at early embryonic stage E10.5 with abnormal common ventricle in a heart, i.e., an insufficient wall, a thin ventricular wall, and loosely packed cells. In the LH2-/- mice, the ER stress-responsive genes, ATF4 and CHOP were significantly up-regulated leading to increased levels of Bax and cleaved caspase-3. These data indicate that LH2 plays an essential role in cardiac development through an ER stress-mediated apoptosis pathway."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2019.03.091"xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Kimura Y."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Miki T."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Saito T."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Oka N."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Hayashi F."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Kita A."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Okubo Y."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Ito C."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Kasamatsu A."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Yamauchi M."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Toshimori K."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Miyamoto I."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Uzawa K."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Shiiba M."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/author | "Tanzawa H."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/pages | "486-491"xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/title | "Deficiency of lysyl hydroxylase 2 in mice causes systemic endoplasmic reticulum stress leading to early embryonic lethality."xsd:string |
http://purl.uniprot.org/citations/30905411 | http://purl.uniprot.org/core/volume | "512"xsd:string |
http://purl.uniprot.org/citations/30905411 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/30905411 |
http://purl.uniprot.org/citations/30905411 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/30905411 |