Linked Life Data

12372253

Source:http://linkedlifedata.com/resource/pubmed/id/12372253

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2002-10-9
pubmed:abstractText
Gridlock (grl) is one of the first mutations characterized from the large zebrafish mutagenesis screens, and it results in an arterial (aortic) maturation defect, which was proposed to resemble aortic coarctation, a clinically important human malformation. While the grl mutation appears to be a hypomorph, grl knockdown experiments have shown even stronger effects on arterial development. We have generated a knockout of the murine Hey2 (gridlock) gene to analyze the mammalian phenotype. Surprisingly, Hey2 loss does not affect aortic development, but it instead leads to a massive postnatal cardiac hypertrophy with high lethality during the first 10 days of life. This cardiomyopathy is ameliorated with time in surviving animals that do not appear to be manifestly impaired during adult life. These differences in phenotypes suggest that changes in expression or function of genes during evolution may lead to quite different pathological phenotypes, if impaired.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0960-9822
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1601-4
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Mouse gridlock: no aortic coarctation or deficiency, but fatal cardiac defects in Hey2 -/- mice.
pubmed:affiliation
Theodor-Boveri-Institute of the University of Wuerzburg, Physiological Chemistry I, Am Hubland, D-97074 Wuerzburg, Germany. gessler@biozentrum.uni-wuerzburg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't