Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6473
pubmed:dateCreated
1994-5-9
pubmed:abstractText
The endothelin-1 (ET-1) gene was disrupted in mouse embryonic stem cells by homologous recombination to generate mice deficient in ET-1. These ET-1-/- homozygous mice die of respiratory failure at birth and have morphological abnormalities of the pharyngeal-arch-derived craniofacial tissues and organs. ET-1+/- heterozygous mice, which produce lower levels of ET-1 than wild-type mice, develop elevated blood pressure. These results suggest that ET-1 is essential for normal mouse development and may also play a physiological role in cardiovascular homeostasis.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
368
pubmed:geneSymbol
ET-1
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
703-10
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8152482-Animals, pubmed-meshheading:8152482-Base Sequence, pubmed-meshheading:8152482-Blood Pressure, pubmed-meshheading:8152482-Branchial Region, pubmed-meshheading:8152482-DNA Primers, pubmed-meshheading:8152482-Embryonic and Fetal Development, pubmed-meshheading:8152482-Endothelins, pubmed-meshheading:8152482-Female, pubmed-meshheading:8152482-Heterozygote, pubmed-meshheading:8152482-Homozygote, pubmed-meshheading:8152482-Male, pubmed-meshheading:8152482-Mice, pubmed-meshheading:8152482-Mice, Inbred C57BL, pubmed-meshheading:8152482-Mice, Inbred ICR, pubmed-meshheading:8152482-Molecular Sequence Data, pubmed-meshheading:8152482-Organ Culture Techniques, pubmed-meshheading:8152482-Respiratory Insufficiency, pubmed-meshheading:8152482-Skull, pubmed-meshheading:8152482-Stem Cells
pubmed:year
1994
pubmed:articleTitle
Elevated blood pressure and craniofacial abnormalities in mice deficient in endothelin-1.
pubmed:affiliation
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't