Linked Life Data

12759573

Source:http://linkedlifedata.com/resource/pubmed/id/12759573

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-5-21
pubmed:abstractText
Certain changes in cellular function are characteristic of renal disease. Foremost among these is the excessive proliferation of cells, but other phenotypic changes include dysregulated apoptosis, migration, adhesion, contraction, secretion, and receptor expression. Recent advances in cell biology have revealed an extensive role for the small monomeric GTPases of the Ras superfamily in the control of these cellular events through intracellular signalling cascades. The specific Ras genes appear to play discrete and identifiable roles in a range of complex signalling networks. These insights lead to the possibility of targeting Ras genes in a specific manner in renal therapies. For example, the process of renal cell proliferation might be sensitive to downregulation of Harvey Ras and Kirsten Ras; targeting of Rho A and related species may modulate cell migration, fibrosis, and intrarenal vasoconstriction. Possible strategies for such modulation could include the use of RNA-interacting agents such as antisense DNA and si-RNA and the use of small molecules acting on Ras directly or on related signalling molecules such as Rho kinase and Raf kinase.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1660-2129
pubmed:author
pubmed:copyrightInfo
Copyright 2003 S. Karger AG, Basel
pubmed:issnType
Electronic
pubmed:volume
93
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
e129-33
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Targeting Ras genes in kidney disease.
pubmed:affiliation
Department of Renal Medicine, Guy's King's St. Thomas' School of Medicine, King's College, London, UK. bruce.hendry@kcl.ac.uk
pubmed:publicationType
Journal Article, Review