Linked Life Data

19372430

Source:http://linkedlifedata.com/resource/pubmed/id/19372430

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5925
pubmed:dateCreated
2009-4-17
pubmed:abstractText
Oxygen deprivation is rapidly deleterious for most organisms. However, Caenorhabditis elegans has developed the ability to survive anoxia for at least 48 hours. Mutations in the DAF-2/DAF-16 insulin-like signaling pathway promote such survival. We describe a pathway involving the HYL-2 ceramide synthase that acts independently of DAF-2. Loss of the ceramide synthase gene hyl-2 results in increased sensitivity of C. elegans to anoxia. C. elegans has two ceramide synthases, hyl-1 and hyl-2, that participate in ceramide biogenesis and affect its ability to survive anoxic conditions. In contrast to hyl-2(lf) mutants, hyl-1(lf) mutants are more resistant to anoxia than normal animals. HYL-1 and HYL-2 have complementary specificities for fatty acyl chains. These data indicate that specific ceramides produced by HYL-2 confer resistance to anoxia.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1095-9203
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
324
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
381-4
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Protection of C. elegans from anoxia by HYL-2 ceramide synthase.
pubmed:affiliation
Department of Cell Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural