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Wei, Changli (David)
One or more keywords matched the following items that are connected to Wei, Changli (David)
Item TypeName
Concept Kidney Glomerulus
Concept Kidney Transplantation
Concept Kidney Failure, Chronic
Concept Acute Kidney Injury
Concept Kidney
Concept Kidney Diseases
Concept Kidney Tubules
Concept Polycystic Kidney, Autosomal Dominant
Academic Article Induction of TRPC6 channel in acquired forms of proteinuric kidney disease.
Academic Article Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy.
Academic Article Proteolytic processing of dynamin by cytoplasmic cathepsin L is a mechanism for proteinuric kidney disease.
Academic Article Soluble Urokinase Receptor and Chronic Kidney Disease.
Academic Article A Podocyte-Based Automated Screening Assay Identifies Protective Small Molecules.
Academic Article TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function.
Academic Article Modification of kidney barrier function by the urokinase receptor.
Academic Article Bone marrow-derived immature myeloid cells are a main source of circulating suPAR contributing to proteinuric kidney disease.
Academic Article Podocytes exhibit a specialized protein quality control employing derlin-2 in kidney disease.
Academic Article Wnt signaling in bone, kidney, intestine, and adipose tissue and interorgan interaction in aging.
Academic Article uPAR isoform 2 forms a dimer and induces severe kidney disease in mice.
Academic Article Soluble Urokinase Plasminogen Activator Receptor and Decline in Kidney Function in Autosomal Dominant Polycystic Kidney Disease.
Academic Article Soluble Urokinase Receptor and Acute Kidney Injury.
Academic Article suPAR, a Circulating Kidney Disease Factor.
Academic Article suPAR links a dysregulated immune response to tissue inflammation and sepsis-induced acute kidney injury.
Academic Article The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5.
Academic Article The D2D3 form of uPAR acts as an immunotoxin and may cause diabetes and kidney disease.
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