Kidney injury molecule-1 expression in murine polycystic kidney disease. - Wikidata - wikimedia - TriplyDB

Kidney injury molecule-1 expression in murine polycystic kidney disease.

Kidney injury molecule-1 expression in murine polycystic kidney disease.

http://www.wikidata.org/entity/Q53663851

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Clinical Predictive Factors in Diabetic Kidney Disease Progression Emerging biomarkers and metabolomics for assessing toxic nephropathy and acute kidney injury (AKI) in neonatology Biomarkers in chronic kidney disease, from kidney function to kidney damage Ciliary calcium signaling is modulated by kidney injury molecule-1 (Kim1)Kidney injury molecule-1 is an early noninvasive indicator for donor brain death-induced injury prior to kidney transplantation Tubular expression of KIM-1 does not predict delayed function after transplantation Age-related differences in susceptibility to cisplatin-induced renal toxicity.Kidney injury molecule-1 expression in transplant biopsies is a sensitive measure of cell injury.Human kidney injury molecule-1 is a tissue and urinary tumor marker of renal cell carcinoma Fenofibrate attenuates tubulointerstitial fibrosis and inflammation through suppression of nuclear factor-κB and transforming growth factor-β1/Smad3 in diabetic nephropathy.Effect of treatment on urinary kidney injury molecule-1 in IgA nephropathy Repair of injured proximal tubule does not involve specialized progenitors Chronic nicotine exposure exacerbates acute renal ischemic injury.Glomerular expression of kidney injury molecule-1 and podocytopenia in diabetic glomerulopathy.Urinary biomarkers at early ADPKD disease stage Evaluation of urine biomarkers of kidney injury in polycystic kidney disease.Neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) as predictors of incident CKD stage 3: the Atherosclerosis Risk in Communities (ARIC) Study Human Alpha-1-Antitrypsin (hAAT) therapy reduces renal dysfunction and acute tubular necrosis in a murine model of bilateral kidney ischemia-reperfusion injury.Mechanistic biomarkers for cytotoxic acute kidney injury.Cell therapy with human renal cell cultures containing erythropoietin-positive cells improves chronic kidney injury.Polycystic kidney disease and renal injury repair: common pathways, fluid flow, and the function of polycystin-1.Characterization of kidney injury molecule-1 in cats Urine NGAL and KIM-1 in children and adolescents with hyperuricemia Mammalian Target of Rapamycin Mediates Kidney Injury Molecule 1-Dependent Tubule Injury in a Surrogate Model.The TIM family of cosignaling receptors: emerging targets for the regulation of autoimmune disease and transplantation tolerance.Chronic epithelial kidney injury molecule-1 expression causes murine kidney fibrosis.Reduction of proteinuria in adriamycin-induced nephropathy is associated with reduction of renal kidney injury molecule (Kim-1) over time Kidney Injury Molecule-1 (KIM-1): a specific and sensitive biomarker of kidney injury.Comparison of kidney injury molecule-1 and other nephrotoxicity biomarkers in urine and kidney following acute exposure to gentamicin, mercury, and chromium.High urinary excretion of kidney injury molecule-1 is an independent predictor of graft loss in renal transplant recipients.Renal primary cilia lengthen after acute tubular necrosis.A bioinformatics approach identifies signal transducer and activator of transcription-3 and checkpoint kinase 1 as upstream regulators of kidney injury molecule-1 after kidney injury.Six2creFrs2α knockout mice are a novel model of renal cystogenesis.Kidney injury molecule-1 in renal disease.Biomarkers of acute kidney injury in children: discovery, evaluation, and clinical application.Kidney injury molecule-1: more than just an injury marker of tubular epithelial cells?Haploinsufficiency of Pkd2 is associated with increased tubular cell proliferation and interstitial fibrosis in two murine Pkd2 models.Urinary biomarkers in the early detection and follow-up of tubular injury in childhood urolithiasis.Kidney Injury Molecule-1 Enhances Endocytosis of Albumin in Renal Proximal Tubular Cells.Kidney Injury Molecule-1 Is Specifically Expressed in Cystically-Transformed Proximal Tubules of the PKD/Mhm (cy/+) Rat Model of Polycystic Kidney Disease.

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Kidney injury molecule-1 expression in murine polycystic kidney disease.

http://www.wikidata.org/entity/Q53663851

description

2002 nî lūn-bûn

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2002年の論文

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年學術文章

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2002年學術文章

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name

Kidney injury molecule-1 expression in murine polycystic kidney disease.

@en

Kidney injury molecule-1 expression in murine polycystic kidney disease.

@nl

type

label

Kidney injury molecule-1 expression in murine polycystic kidney disease.

@en

Kidney injury molecule-1 expression in murine polycystic kidney disease.

@nl

prefLabel

Kidney injury molecule-1 expression in murine polycystic kidney disease.

@en

Kidney injury molecule-1 expression in murine polycystic kidney disease.

@nl

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AJPRENAL.00166.2002

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American Journal of Physiology - Renal Physiology

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Kidney injury molecule-1 expression in murine polycystic kidney disease.

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P2093

E Wolfgang Kuehn

http://www.w3.org/2001/XMLSchema#string

Joseph V Bonventre

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Kwon Moo Park

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Stefan Somlo

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P2860

Polycystin-2, the protein mutated in autosomal dominant polycystic kidney disease (ADPKD), is a Ca2+-permeable nonselective cation channel

Polycystin-2 is an intracellular calcium release channel

Identification of Tapr (an airway hyperreactivity regulatory locus) and the linked Tim gene family

The I.M.A.G.E. Consortium: an integrated molecular analysis of genomes and their expression

PKD2, a gene for polycystic kidney disease that encodes an integral membrane protein

Co-assembly of polycystin-1 and -2 produces unique cation-permeable currents

Renal epithelial polarity in health and disease.

The pathogenesis of autosomal dominant polycystic kidney disease: an update.

Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease.

Molecular basis of renal fibrosis.

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