pubmed-article:21684255 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21684255 | lifeskim:mentions | umls-concept:C0684336 | lld:lifeskim |
pubmed-article:21684255 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:21684255 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:21684255 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:21684255 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:21684255 | lifeskim:mentions | umls-concept:C1523908 | lld:lifeskim |
pubmed-article:21684255 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:21684255 | pubmed:dateCreated | 2011-7-11 | lld:pubmed |
pubmed-article:21684255 | pubmed:abstractText | We have recently shown that in macrophages proper operation of the survival pathways phosphatidylinositol-3-kinase (PI3K)/AKT and nuclear factor kappa B (NFkB) has an obligatory requirement for constitutive, non-regulated Ca(2+) influx. In the present work we examined if Transient Receptor Potential Canonical 3 (TRPC3), a member of the TRPC family of Ca(2+)-permeable cation channels, contributes to the constitutive Ca(2+) influx that supports macrophage survival. We used bone marrow-derived macrophages obtained from TRPC3(-/-) mice to determine the activation status of survival signaling pathways, apoptosis and their efferocytic properties. Treatment of TRPC3(+/+) macrophages with the pro-apoptotic cytokine TNF? induced time-dependent phosphorylation of I?B?, AKT and BAD, and this was drastically reduced in TRPC3(-/-) macrophages. Compared to TRPC3(+/+) cells TRPC3(-/-) macrophages exhibited reduced constitutive cation influx, increased apoptosis and impaired efferocytosis. The present findings suggest that macrophage TRPC3, presumably through its constitutive function, contributes to survival signaling and efferocytic properties. | lld:pubmed |
pubmed-article:21684255 | pubmed:language | eng | lld:pubmed |
pubmed-article:21684255 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21684255 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21684255 | pubmed:month | Jul | lld:pubmed |
pubmed-article:21684255 | pubmed:issn | 1090-2104 | lld:pubmed |
pubmed-article:21684255 | pubmed:author | pubmed-author:LeeRobertR | lld:pubmed |
pubmed-article:21684255 | pubmed:author | pubmed-author:BirnbaumerLut... | lld:pubmed |
pubmed-article:21684255 | pubmed:author | pubmed-author:VazquezGuille... | lld:pubmed |
pubmed-article:21684255 | pubmed:author | pubmed-author:AbramowitzJoe... | lld:pubmed |
pubmed-article:21684255 | pubmed:author | pubmed-author:SmedlundKathr... | lld:pubmed |
pubmed-article:21684255 | pubmed:author | pubmed-author:TanoJean-Yves... | lld:pubmed |
pubmed-article:21684255 | pubmed:copyrightInfo | Copyright © 2011 Elsevier Inc. All rights reserved. | lld:pubmed |
pubmed-article:21684255 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21684255 | pubmed:day | 8 | lld:pubmed |
pubmed-article:21684255 | pubmed:volume | 410 | lld:pubmed |
pubmed-article:21684255 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21684255 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21684255 | pubmed:pagination | 643-7 | lld:pubmed |
pubmed-article:21684255 | pubmed:meshHeading | pubmed-meshheading:21684255... | lld:pubmed |
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pubmed-article:21684255 | pubmed:meshHeading | pubmed-meshheading:21684255... | lld:pubmed |
pubmed-article:21684255 | pubmed:meshHeading | pubmed-meshheading:21684255... | lld:pubmed |
pubmed-article:21684255 | pubmed:meshHeading | pubmed-meshheading:21684255... | lld:pubmed |
pubmed-article:21684255 | pubmed:meshHeading | pubmed-meshheading:21684255... | lld:pubmed |
pubmed-article:21684255 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21684255 | pubmed:articleTitle | Impairment of survival signaling and efferocytosis in TRPC3-deficient macrophages. | lld:pubmed |
pubmed-article:21684255 | pubmed:affiliation | Department of Physiology and Pharmacology and the Center for Diabetes and Endocrine Research, University of Toledo College of Medicine, Health Science Campus, 3000 Arlington Av, Toledo, OH 43614, USA. | lld:pubmed |
pubmed-article:21684255 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21684255 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:22065 | entrezgene:pubmed | pubmed-article:21684255 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21684255 | lld:entrezgene |