Glomerular diseases: genetic causes and future therapeutics.
about
PodocytesMYO1E mutations and childhood familial focal segmental glomerulosclerosis.Xenopus as a model system for the study of GOLPH2/GP73 function: Xenopus GOLPH2 is required for pronephros development.Using zebrafish to study podocyte genesis during kidney development and regeneration.MAGI-2 scaffold protein is critical for kidney barrier function.Next-generation sequencing to dissect hereditary nephrotic syndrome in mice identifies a hypomorphic mutation in Lamb2 and models Pierson's syndromeMolecular Mechanisms of Podocyte Development Revealed by Zebrafish Kidney ResearchAlpha-actinin-4 and CLP36 protein deficiencies contribute to podocyte defects in multiple human glomerulopathies.Sirtuin1 Maintains Actin Cytoskeleton by Deacetylation of Cortactin in Injured Podocytes.Angiotensin II induces endoplasmic reticulum stress in podocyte, which would be further augmented by PI3-kinase inhibitionGenetic Ablation of Calcium-independent Phospholipase A2γ Induces Glomerular Injury in Mice.Functional screening in Drosophila identifies Alzheimer's disease susceptibility genes and implicates Tau-mediated mechanisms.Childhood nephrotic syndrome--current and future therapies.Facing glycosphingolipid-Shiga toxin interaction: dire straits for endothelial cells of the human vasculature.The renal biopsy in the genomic era.Proteostasis in endoplasmic reticulum--new mechanisms in kidney disease.Thrombin-Induced Podocyte Injury Is Protease-Activated Receptor Dependent.Stress Signal Network between Hypoxia and ER Stress in Chronic Kidney Disease.Deletion of inositol-requiring enzyme-1α in podocytes disrupts glomerular capillary integrity and autophagyAngiopoietin-like 3 induces podocyte F-actin rearrangement through integrin α(V)β₃/FAK/PI3K pathway-mediated Rac1 activation.Podocyte Injury Associated with Mutant α-Actinin-4RNA-seq of serial kidney biopsies obtained during progression of chronic kidney disease from dogs with X-linked hereditary nephropathy.Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases.Successful production of genome-edited rats by the rGONAD method.Endoplasmic reticulum stress signal impairs erythropoietin production: a role for ATF4.
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Glomerular diseases: genetic causes and future therapeutics.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on 20 July 2010
@en
vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Glomerular diseases: genetic causes and future therapeutics.
@en
Glomerular diseases: genetic causes and future therapeutics.
@nl
type
label
Glomerular diseases: genetic causes and future therapeutics.
@en
Glomerular diseases: genetic causes and future therapeutics.
@nl
prefLabel
Glomerular diseases: genetic causes and future therapeutics.
@en
Glomerular diseases: genetic causes and future therapeutics.
@nl
P2860
P356
P1476
Glomerular diseases: genetic causes and future therapeutics
@en
P2093
Reiko Inagi
P2860
P2888
P304
P356
10.1038/NRNEPH.2010.103
P407
P577
2010-07-20T00:00:00Z