Daniel Turnberg
Overview
Explore the profile of Daniel Turnberg including associated specialties, affiliations and a list of published articles.
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Articles
6
Citations
143
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Recent Articles
1.
Turnberg D, Lewis M, Moss J, Xu Y, Botto M, Cook H
J Immunol
. 2006 Sep;
177(6):4094-102.
PMID: 16951374
Adriamycin nephropathy is a model of focal segmental glomerulosclerosis, characterized by proteinuria and progressive glomerulosclerosis and tubulointerstitial damage. In this study, we examined the role of complement in the etiology...
2.
Trendelenburg M, Fossati-Jimack L, Cortes-Hernandez J, Turnberg D, Lewis M, Izui S, et al.
J Immunol
. 2005 Nov;
175(10):6909-14.
PMID: 16272350
Many forms of glomerulonephritis are triggered by Ab localization in the glomerulus, but the mechanisms by which this induces glomerular inflammation are not fully understood. In this study we investigated...
3.
Turnberg D, Cook H
Curr Opin Nephrol Hypertens
. 2005 Apr;
14(3):223-8.
PMID: 15821414
Purpose Of Review: The last few years have seen a huge increase in our understanding of the role of the complement system and its regulation in glomerular disease. Our aim...
4.
Turnberg D, Botto M, Lewis M, Zhou W, Sacks S, Morgan B, et al.
Am J Pathol
. 2004 Aug;
165(3):825-32.
PMID: 15331407
The terminal complement components C5a and the membrane attack complex are involved in the pathogenesis of ischemia-reperfusion injury in many organs. CD59 is the major regulator of membrane attack complex...
5.
Turnberg D, Botto M, Warren J, Morgan B, Walport M, Cook H
J Am Soc Nephrol
. 2003 Aug;
14(9):2271-9.
PMID: 12937303
CD59 is a complement regulatory protein that inhibits the terminal part of the complement system, the membrane attack complex (MAC), a mediator of renal injury. Mice deficient in the Cd59a...
6.
Turnberg D, Botto M
Mol Immunol
. 2003 Aug;
40(2-4):145-53.
PMID: 12914820
The complement system is very tightly regulated by fluid-phase and membrane-bound factors that prevent injury to self-tissues. The study of genetically engineered animals with targeted deletion or gain of function...