Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-6-2
pubmed:abstractText
Dysfunction of pancreatic islet beta cells underlies both type 1 and type 2 diabetes and appears to result in part from the local release of proinflammatory cytokines. An improved understanding of the mechanisms that mediate islet responsiveness to proinflammatory cytokines may therefore expand our knowledge of the role of cytokine signaling in the development of diabetes, providing potential new targets for the development of therapeutics to protect pancreatic islets from inflammation. In this issue of the JCI, Maier and colleagues identify eukaryotic translation initiation factor 5A (eIF5A) as a critical regulator of the inflammatory response in mouse pancreatic islets. I believe these data provide new and important insights into the regulatory pathways that contribute to the development of diabetes and deepen our understanding of the function of the, so far, rather enigmatic cellular protein eIF5A.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1558-8238
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
120
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1806-8
pubmed:dateRevised
2011-1-3
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Revisiting an old acquaintance: role for eIF5A in diabetes.
pubmed:affiliation
Heinrich-Pette-Institute for Experimental Virology and Immunology, Hamburg, Germany. joachim.hauber@hpi.uni-hamburg.de
pubmed:publicationType
Journal Article, Comment, Research Support, Non-U.S. Gov't