Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
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Three-dimensional electron microscopy reveals the evolution of glomerular barrier injury.Stem cell therapies benefit Alport syndrome.A mouse Col4a4 mutation causing Alport glomerulosclerosis with abnormal collagen α3α4α5(IV) trimers.Upregulated expression of integrin α1 in mesangial cells and integrin α3 and vimentin in podocytes of Col4a3-null (Alport) miceSafety and Efficacy of the ACE-Inhibitor Ramipril in Alport Syndrome: The Double-Blind, Randomized, Placebo-Controlled, Multicenter Phase III EARLY PRO-TECT Alport Trial in Pediatric Patients.Integrin alpha1beta1 regulates matrix metalloproteinases via P38 mitogen-activated protein kinase in mesangial cells: implications for Alport syndrome.Familial hematuriaCell Receptor-Basement Membrane Interactions in Health and Disease: A Kidney-Centric ViewAlbumin contributes to kidney disease progression in Alport syndrome.Biomechanical strain causes maladaptive gene regulation, contributing to Alport glomerular disease.Feasibility of repairing glomerular basement membrane defects in Alport syndrome.The gene or not the gene--that is the question: understanding the genetically engineered mouse phenotype.The biodistribution of [153Gd]Gd-labeled magnetic resonance contrast agents in a transgenic mouse model of renal failure differs greatly from control mice.Plasma leakage through glomerular basement membrane ruptures triggers the proliferation of parietal epithelial cells and crescent formation in non-inflammatory glomerular injury.The 2014 International Workshop on Alport Syndrome.Lymphocytes are dispensable for glomerulonephritis but required for renal interstitial fibrosis in matrix defect-induced Alport renal disease.Genetic background influences cardiac phenotype in murine chronic kidney disease.Osteopontin deficiency ameliorates Alport pathology by preventing tubular metabolic deficits.The triple helix of collagens - an ancient protein structure that enabled animal multicellularity and tissue evolution.Tumour necrosis factor-α drives Alport glomerulosclerosis in mice by promoting podocyte apoptosis.
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P2860
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
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2007 nî lūn-bûn
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2007年の論文
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2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
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2007年论文
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name
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@ast
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@en
type
label
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@ast
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@en
prefLabel
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@ast
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@en
P2093
P356
P1433
P1476
Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis.
@en
P2093
P2888
P304
P356
10.1038/SJ.KI.5002115
P407
P577
2007-02-07T00:00:00Z
P5875
P6179
1038174088