| pubmed-article:16778360 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C0035696 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C0752348 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C0060916 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C1621633 | lld:lifeskim |
| pubmed-article:16778360 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:16778360 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:16778360 | pubmed:dateCreated | 2006-6-21 | lld:pubmed |
| pubmed-article:16778360 | pubmed:abstractText | Overexpression of constitutively active (CA)-G alpha13 significantly increased the expression of interleukin (IL)-1beta and IL-6 mRNAs and proteins in rat cardiac fibroblasts. IL-1beta mRNA induction by CA-G alpha13 was suppressed by diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, but not by BAPTA-AM, an intracellular Ca2+ chelator. In contrast, IL-6 mRNA induction by CA-G alpha13 was suppressed by BAPTA-AM but not by DPI. However, both IL-1beta and IL-6 mRNA induction was suppressed by nuclear factor kappaB (NF-kappaB) inhibitors. The CA-G alpha13-induced NF-kappaB activation was suppressed by DPI and BAPTA-AM, but not C3 toxin and the Rho-kinase inhibitor Y27632. IL-6 mRNA induction by CA-G alpha13 was suppressed by SK&F96365 (1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole hydrochloride), an inhibitor of receptor-activated nonselective cation channels, and the expression of CA-G alpha13 increased basal Ca2+ influx. These results suggest that G alpha13 regulates IL-1beta mRNA induction through the reactive oxygen species-NF-kappaB pathway, while it regulates IL-6 mRNA induction through the Ca2+-NF-kappaB pathway. | lld:pubmed |
| pubmed-article:16778360 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16778360 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16778360 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16778360 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16778360 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16778360 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16778360 | pubmed:issn | 1347-8613 | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:KobayashiHiro... | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:NishidaMotohi... | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:KuroseHitoshi... | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:SatoYojiY | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:MaruyamaYoshi... | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:NagamatsuYuic... | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:OnoharaNaoyaN | lld:pubmed |
| pubmed-article:16778360 | pubmed:author | pubmed-author:FukutomiMasas... | lld:pubmed |
| pubmed-article:16778360 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16778360 | pubmed:volume | 101 | lld:pubmed |
| pubmed-article:16778360 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16778360 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16778360 | pubmed:pagination | 144-50 | lld:pubmed |
| pubmed-article:16778360 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16778360 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16778360 | pubmed:articleTitle | Heterotrimeric G protein G alpha13-induced induction of cytokine mRNAs through two distinct pathways in cardiac fibroblasts. | lld:pubmed |
| pubmed-article:16778360 | pubmed:affiliation | Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan. | lld:pubmed |
| pubmed-article:16778360 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16778360 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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