| http://purl.uniprot.org/citations/15289604 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15289604 | http://www.w3.org/2000/01/rdf-schema#comment | "Advanced glycation endproducts (AGE) contribute to kidney disease due to diabetes or aging by means of mesangial cell (MC) receptors, such as the receptor for AGE (RAGE), which promote oxidant-stress-dependent NF-kappaB activation and inflammatory gene expression. MC also express scavenger receptors SR-I and SR-II and AGE receptors 1, 2, and 3 (AGE-R1, -R2, and -R3), some of which are linked to AGE turnover. Because AGE-R1 expression is found suppressed in severe diabetic kidney disease, as other receptors increase, we investigated whether his molecule has a protective role against AGE-induced MC injury. A stable murine MC line overexpressing AGE-R1 (R1-MC) was generated, exhibiting a 1.8-to 2.7-fold increase in (125)I-AGE-specific binding, uptake, and degradation, compared with mock-MC. However, AGE-stimulated NF-kappaB activity and mitogen-activated protein kinase (MAPK) (p44/42) phosphorylation were found markedly suppressed in R1-MC. Additionally, AGE-stimulated macrophage chemotaxis protein 1 and RAGE overexpression were abolished in R1-MC. The effect of R1 on RAGE signaling was investigated after overexpressing RAGE in Chinese hamster ovary cells, which lack RAGE. AGE stimulation elicited NF-kappaB and MAPK activities in RAGE-Chinese hamster ovary cells; however, after cotransfection with R1, these responses were suppressed. Also, after silencing endogenous R1 in wild-type MC by R1 small interfering RNA, AGE-mediated MAPK/p44/42 activation exceeded by >2-fold that of mock-MC, consistent with loss of the activation-inhibitory properties of native AGE-R1. AGE-R1, although enhancing AGE removal, is also a distinct receptor in that it suppresses AGE-mediated MC inflammatory injury through negative regulation of RAGE, a previously uncharacterized pathway that may protect renal and other tissue injury due to diabetes and aging."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0401588101"xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/author | "Liu H."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/author | "Lu C."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/author | "Zhu L."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/author | "Cai W."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/author | "He J.C."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/author | "Vlassara H."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/pages | "11767-11772"xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/title | "Advanced glycation endproduct (AGE) receptor 1 is a negative regulator of the inflammatory response to AGE in mesangial cells."xsd:string |
| http://purl.uniprot.org/citations/15289604 | http://purl.uniprot.org/core/volume | "101"xsd:string |
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