Source:http://linkedlifedata.com/resource/pubmed/id/20833976
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
22
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pubmed:dateCreated |
2010-11-26
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pubmed:abstractText |
Within the healthy population, there is substantial, heritable, and interindividual variability in the platelet response. We explored whether a proportion of this variability could be accounted for by interindividual variation in gene expression. Through a correlative analysis of genome-wide platelet RNA expression data from 37 subjects representing the normal range of platelet responsiveness within a cohort of 500 subjects, we identified 63 genes in which transcript levels correlated with variation in the platelet response to adenosine diphosphate and/or the collagen-mimetic peptide, cross-linked collagen-related peptide. Many of these encode proteins with no reported function in platelets. An association study of 6 of the 63 genes in 4235 cases and 6379 controls showed a putative association with myocardial infarction for COMMD7 (COMM domain-containing protein 7) and a major deviation from the null hypo thesis for LRRFIP1 [leucine-rich repeat (in FLII) interacting protein 1]. Morpholino-based silencing in Danio rerio identified a modest role for commd7 and a significant effect for lrrfip1 as positive regulators of thrombus formation. Proteomic analysis of human platelet LRRFIP1-interacting proteins indicated that LRRFIP1 functions as a component of the platelet cytoskeleton, where it interacts with the actin-remodeling proteins Flightless-1 and Drebrin. Taken together, these data reveal novel proteins regulating the platelet response.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/LRRFIP1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Proteome,
http://linkedlifedata.com/resource/pubmed/chemical/RNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Zebrafish Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1528-0020
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pubmed:author |
pubmed-author:ArdissinoDiegoD,
pubmed-author:Bloodomics Consortium,
pubmed-author:BraySarah LSL,
pubmed-author:BurnsPhilippaP,
pubmed-author:DeckmynHansH,
pubmed-author:DudbridgeFrankF,
pubmed-author:FitzgeraldDesmond JDJ,
pubmed-author:GarnerStephen FSF,
pubmed-author:GoodallAlison HAH,
pubmed-author:GusnantoAriefA,
pubmed-author:JonesChris ICI,
pubmed-author:KochKerstinK,
pubmed-author:LangfordCordeliaC,
pubmed-author:MacaulayIain CIC,
pubmed-author:MaguirePatricia BPB,
pubmed-author:O'ConnorMarie NMN,
pubmed-author:OuwehandWillem HWH,
pubmed-author:RiceCatherine MCM,
pubmed-author:SallesIsabelleI,
pubmed-author:SamaniNilesh JNJ,
pubmed-author:StempleDerekD,
pubmed-author:StephensJonathanJ,
pubmed-author:TripMieke DMD,
pubmed-author:WatkinsNicholas ANA,
pubmed-author:ZwagingaJaap-JanJJ,
pubmed-author:de BonoBernardB
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pubmed:issnType |
Electronic
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pubmed:day |
25
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pubmed:volume |
116
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4646-56
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pubmed:meshHeading |
pubmed-meshheading:20833976-Animals,
pubmed-meshheading:20833976-Blood Platelets,
pubmed-meshheading:20833976-Gene Expression Profiling,
pubmed-meshheading:20833976-Gene Silencing,
pubmed-meshheading:20833976-Genotype,
pubmed-meshheading:20833976-Humans,
pubmed-meshheading:20833976-Platelet Activation,
pubmed-meshheading:20833976-Proteome,
pubmed-meshheading:20833976-RNA-Binding Proteins,
pubmed-meshheading:20833976-Repressor Proteins,
pubmed-meshheading:20833976-Thrombosis,
pubmed-meshheading:20833976-Zebrafish,
pubmed-meshheading:20833976-Zebrafish Proteins
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pubmed:year |
2010
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pubmed:articleTitle |
Transcription profiling in human platelets reveals LRRFIP1 as a novel protein regulating platelet function.
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pubmed:affiliation |
Department of Cardiovascular Science, University of Leicester, Clinical Sciences Wing, Glenfield Hospital, Leicester, UK. ahg5@le.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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