Linked Life Data

17187949

Source:http://linkedlifedata.com/resource/pubmed/id/17187949

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-2-13
pubmed:abstractText
Small interfering RNA (siRNA) molecules are the functional mediators of a post-transcriptional gene silencing process known as RNA interference (RNAi). The silencing of genes involved in diseases, using siRNA, is considered a very promising therapeutic strategy. However, as for all the nucleic acid based therapeutics, these negatively charged and hydrophilic molecules do not readily cross biological membranes. The use of cationic carriers generally results in positively charged complexes which are taken up by cells through endocytosis. Still, for gene silencing, these complexes need to escape through the endosomal membrane, thereby reaching the cytosol where all the RNAi machinery is present. One of the strategies developed to facilitate endosomal escape mimics the fusion of viral envelopes with host cell endosomal membranes, which occurs during viral infections. Several synthetic fusogenic peptides have been synthesized based on the fusion domain of the influenza virus. In this study we evaluated the effects of the influenza-derived fusogenic peptide diINF-7 on gene silencing efficiency of siRNA targeting the epidermal growth factor receptor (EGFR) and the K-ras oncogenes. For both targets, strong enhancement of gene silencing activity was noted after addition of diINF-7 fusogenic peptide, identifying endosomal escape as a limiting factor for siRNA silencing efficiency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0378-5173
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
331
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
211-4
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Fusogenic peptides enhance endosomal escape improving siRNA-induced silencing of oncogenes.
pubmed:affiliation
Department of Pharmaceutics, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, PO Box 80.082, 3508 TB Utrecht, The Netherlands. S.Oliveira@pharm.uu.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't