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1 tumor mass, suggesting a pathogenic role for renalase.
2 mmon single nucleotide polymorphism in human renalase 3'-UTR (C/T; rs10749571) creates a binding site
3 -29a/b/c and miR-146a/b with mouse and human renalase 3'-UTR (untranslated region) in cultured cells.
4 consistently, miR-146a down-regulated human renalase 3'-UTR/luciferase activity in case of the T all
9 rge of epinephrine lasting <2 minutes causes renalase activity to increase from 48+/-18 to 2246+/-98
11 nohistochemistry, and immunofluorescence for renalase and its binding partners, PMCA4b and PZP, were
13 ase signaling using siRNA or inhibitory anti-renalase antibodies decreased the viability of cultured
14 We have identified the catalytic activity of renalase as an alpha-NAD(P)H oxidase/anomerase, whereby
19 d plasma catecholamine levels were higher in renalase-deficient mice subjected to renal ischemia repe
20 erall survival was inversely correlated with renalase expression in the tumor mass, suggesting a path
22 e estimated miR-29b and miR-146a, as well as renalase expression, in genetically hypertensive blood p
23 terleukin-2 (IL-2), IL2/4q27 (rs2069763) and renalase, FAD-dependent amine oxidase (RNLS)/10q23.31 (r
25 dence for post-transcriptional regulation of renalase gene by miR-29 and miR-146 and has implications
32 eveal a previously unrecognized role for the renalase in cancer: its expression may serve as a progno
36 ion injury had significantly lower levels of renalase in the plasma and kidney compared with sham-ope
38 onal antibody m28-RNLS or shRNA knockdown of renalase inhibited pancreatic ductal adenocarcinoma grow
46 ministration of either native or recombinant renalase lowers blood pressure, heart rate, and cardiac
47 ney and metabolizes catecholamines in vitro (renalase metabolizes dopamine most efficiently, followed
49 In two xenograft mouse models, either the renalase monoclonal antibody m28-RNLS or shRNA knockdown
50 h mice showed diminished (~1.6- to 1.8-fold) renalase mRNA/protein levels and elevated (~2.2-fold) mi
55 vels, cardiac hypertrophy, and hypertension, renalase replacement is an attractive therapeutic modali
56 ed that the kidney-secreted survival protein renalase (RNLS) and an agonist peptide protected mice fr
61 1390 located to a region 58.8 kb upstream of renalase (RNLS) with eGFR was detected in the Ludwigshaf
64 denine dinucleotide-dependent amine oxidase (renalase) that is secreted into the blood by the kidney