Changli (David) Wei to Proteinuria
This is a "connection" page, showing publications Changli (David) Wei has written about Proteinuria.
Connection Strength
0.758
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SuPAR mediates viral response proteinuria by rapidly changing podocyte function. Nat Commun. 2023 07 21; 14(1):4414.
Score: 0.212
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Bone marrow-derived immature myeloid cells are a main source of circulating suPAR contributing to proteinuric kidney disease. Nat Med. 2017 01; 23(1):100-106.
Score: 0.134
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Reduction of proteinuria through podocyte alkalinization. J Biol Chem. 2014 Jun 20; 289(25):17454-67.
Score: 0.112
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Proteolytic processing of dynamin by cytoplasmic cathepsin L is a mechanism for proteinuric kidney disease. J Clin Invest. 2007 Aug; 117(8):2095-104.
Score: 0.070
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Induction of TRPC6 channel in acquired forms of proteinuric kidney disease. J Am Soc Nephrol. 2007 Jan; 18(1):29-36.
Score: 0.067
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The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5. Kidney Int. 2023 06; 103(6):1056-1062.
Score: 0.051
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Soluble Urokinase Receptor and Chronic Kidney Disease. N Engl J Med. 2015 Nov 12; 373(20):1916-25.
Score: 0.031
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A Podocyte-Based Automated Screening Assay Identifies Protective Small Molecules. J Am Soc Nephrol. 2015 Nov; 26(11):2741-52.
Score: 0.030
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Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy. Transplantation. 2013 Oct 15; 96(7):649-56.
Score: 0.027
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CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival. J Clin Invest. 2011 Oct; 121(10):3965-80.
Score: 0.023