Sökning: WFRF:(Harley H) > Kallikrein genes ar...
Fältnamn | Indikatorer | Metadata |
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000 | 06605naa a2201477 4500 | |
001 | oai:DiVA.org:uu-102839 | |
003 | SwePub | |
008 | 090512s2009 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1028392 URI |
024 | 7 | a https://doi.org/10.1172/JCI367282 DOI |
040 | a (SwePub)uu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Liu, Kui4 aut |
245 | 1 0 | a Kallikrein genes are associated with lupus and glomerular basement membrane-specific antibody-induced nephritis in mice and humans |
264 | 1 | c 2009 |
338 | a print2 rdacarrier | |
520 | a Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that maybe responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family,which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less evidence of disease. Antagonizing the kallikrein pathway augmented disease, while agonists dampened the severity of anti-GBM antibody-induced nephritis. In addition, nephritis-sensitive mouse strains had kallikrein haplotypes that were distinct from those of control strains, including several regulatory polymorphisms,some of which were associated with functional consequences. Indeed, increased susceptibility to anti-GBM antibody-induced nephritis and spontaneous lupus nephritis was achieved by breeding mice with a genetic interval harboring the kallikrein genes onto a disease-resistant background. Finally, both human SLE and spontaneous lupus nephritis were found to be associated with kallikrein genes, particularly KLK1 and the KLK3 promoter, when DNA SNPs from independent cohorts of SLE patients and controls were compared. Collectively, these studies suggest that kallikreins are protective disease-associated genes in anti-GBM antibody-induced nephritis and lupus. | |
653 | a MEDICINE | |
653 | a MEDICIN | |
700 | 1 | a Li, Quan-Zhen4 aut |
700 | 1 | a Delgado-Vega, Angelica M.u Uppsala universitet,Institutionen för genetik och patologi4 aut |
700 | 1 | a Abelson, Anna-Karinu Uppsala universitet,Institutionen för genetik och patologi4 aut0 (Swepub:uu)anive102 |
700 | 1 | a Sánchez, Elena4 aut |
700 | 1 | a Kelly, Jennifer A.4 aut |
700 | 1 | a Li, Li4 aut |
700 | 1 | a Liu, Yang4 aut |
700 | 1 | a Zhou, Jinchun4 aut |
700 | 1 | a Yan, Mei4 aut |
700 | 1 | a Ye, Qiu4 aut |
700 | 1 | a Liu, Shenxi4 aut |
700 | 1 | a Xie, Chun4 aut |
700 | 1 | a Zhou, Xin J.4 aut |
700 | 1 | a Chung, Sharon A.4 aut |
700 | 1 | a Pons-Estel, Bernardo4 aut |
700 | 1 | a Witte, Torsten4 aut |
700 | 1 | a de Ramón, Enrique4 aut |
700 | 1 | a Bae, Sang-Cheol4 aut |
700 | 1 | a Barizzone, Nadia4 aut |
700 | 1 | a Sebastiani, Gian Domenico4 aut |
700 | 1 | a Merrill, Joan T.4 aut |
700 | 1 | a Gregersen, Peter K.4 aut |
700 | 1 | a Gilkeson, Gary G.4 aut |
700 | 1 | a Kimberly, Robert P.4 aut |
700 | 1 | a Vyse, Timothy J.4 aut |
700 | 1 | a Kim, Il4 aut |
700 | 1 | a D'Alfonso, Sandra4 aut |
700 | 1 | a Martin, Javier4 aut |
700 | 1 | a Harley, John B.4 aut |
700 | 1 | a Criswell, Lindsey A.4 aut |
700 | 1 | a Wakeland, Edward K.4 aut |
700 | 1 | a Alarcón-Riquelme, Marta E.u Uppsala universitet,Institutionen för genetik och patologi4 aut0 (Swepub:uu)martaala |
700 | 1 | a Mohan, Chandra4 aut |
700 | 1 | a Danieli, M.G.4 aut |
700 | 1 | a Galeazzi, M.4 aut |
700 | 1 | a Querini, P.R.4 aut |
700 | 1 | a Migliaresi, S.4 aut |
700 | 1 | a Scherbarth, H.R.4 aut |
700 | 1 | a Lopez, J.A.4 aut |
700 | 1 | a Motta, E.L.4 aut |
700 | 1 | a Gamron, S.4 aut |
700 | 1 | a Drenkard, C.4 aut |
700 | 1 | a Menso, E.4 aut |
700 | 1 | a Allievi, A.4 aut |
700 | 1 | a Tate, G.A.4 aut |
700 | 1 | a Presas, J.L.4 aut |
700 | 1 | a Palatnik, S.A.4 aut |
700 | 1 | a Abdala, M.4 aut |
700 | 1 | a Bearzotti, M.4 aut |
700 | 1 | a Alvarellos, A.4 aut |
700 | 1 | a Caeiro, F.4 aut |
700 | 1 | a Bertoli, A.4 aut |
700 | 1 | a Paira, S.4 aut |
700 | 1 | a Roverano, S.4 aut |
700 | 1 | a Graf, C.E.4 aut |
700 | 1 | a Bertero, E.4 aut |
700 | 1 | a Caprarulo, C.4 aut |
700 | 1 | a Buchanan, G.4 aut |
700 | 1 | a Guillerón, C.4 aut |
700 | 1 | a Grimaudo, S.4 aut |
700 | 1 | a Manni, J.4 aut |
700 | 1 | a Catoggio, L.J.4 aut |
700 | 1 | a Soriano, E.R.4 aut |
700 | 1 | a Santos, C.D.4 aut |
700 | 1 | a Prigione, C.4 aut |
700 | 1 | a Ramos, F.A.4 aut |
700 | 1 | a Navarro, S.M.4 aut |
700 | 1 | a Berbotto, G.A.4 aut |
700 | 1 | a Jorfen, M.4 aut |
700 | 1 | a Romero, E.J.4 aut |
700 | 1 | a Garcia, M.A.4 aut |
700 | 1 | a Marcos, J.C.4 aut |
700 | 1 | a Marcos, A.I.4 aut |
700 | 1 | a Perandones, C.E.4 aut |
700 | 1 | a Eimon, A.4 aut |
700 | 1 | a Battagliotti, C.G.4 aut |
700 | 1 | a Armadi-Simab, K.4 aut |
700 | 1 | a Gross, W.L.4 aut |
700 | 1 | a Gromica-Ihle, E.4 aut |
700 | 1 | a Peter, H.H.4 aut |
700 | 1 | a Manger, K.4 aut |
700 | 1 | a Schnarr, S.4 aut |
700 | 1 | a Zeidler, H.4 aut |
700 | 1 | a Schmidt, R.E.4 aut |
700 | 1 | a Ortego, N.4 aut |
700 | 1 | a Callejas, J.L.4 aut |
700 | 1 | a Jiménez-Alonso, J.4 aut |
700 | 1 | a Sabio, M.4 aut |
700 | 1 | a Sánchez-Román, J.4 aut |
700 | 1 | a Garcia-Hernandez, F.J.4 aut |
700 | 1 | a Camps, M.4 aut |
700 | 1 | a López-Nevot, M.A.4 aut |
700 | 1 | a González-Escribano, M.F.4 aut |
700 | 1 | a Harley, J.H.4 aut |
700 | 1 | a Riquelme, M.A.4 aut |
700 | 1 | a Kimberly, R.4 aut |
700 | 1 | a Criswell, L.4 aut |
700 | 1 | a Langefeld, C.4 aut |
700 | 1 | a Tsao, B.4 aut |
700 | 1 | a Jacob, C.4 aut |
710 | 2 | a Uppsala universitetb Institutionen för genetik och patologi4 org |
773 | 0 | t Journal of Clinical Investigationg 119:4, s. 911-923q 119:4<911-923x 0021-9738x 1558-8238 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-102839 |
856 | 4 8 | u https://doi.org/10.1172/JCI36728 |
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