Podocin inactivation in mature kidneys causes focal segmental glomerulosclerosis and nephrotic syndrome (Q28256662)

Géraldine Mollet

1

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Olivia Boyer

Olivia Boyer

3

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Andrea Onetti Muda

Andrea Onetti Muda

4

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Marie-Claire Gubler

Marie-Claire Gubler

11

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Maggie Dallman

Margaret J Dallman

8

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author name string

Julien Ratelade

2

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Ludivine Morisset

5

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Tiphaine Aguirre Lavin

6

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David Kitzis

7

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Laurence Bugeon

9

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Norbert Hubner

10

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Ernie L Esquivel

Journal of the American Society of Nephrology

13

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language of work or name

English

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publication date

October 2009

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published in

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volume

20

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issue

10

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page(s)

2181-9

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describes a project that uses

ImageJ

1 reference

Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC2754108/fullTextXML

inferred from PubMed Central ID database lookup

cites work

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Podocytes are firmly attached to glomerular basement membrane in kidneys with heavy proteinuria

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Patients with mutations in NPHS2 (podocin) do not respond to standard steroid treatment of nephrotic syndrome.

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Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains

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A missense mutation in podocin leads to early and severe renal disease in mice

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12 December 2020

Gene expression analysis in renal biopsies

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12 December 2020

Permanent genetic tagging of podocytes: fate of injured podocytes in a mouse model of glomerular sclerosis

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12 December 2020

HIV-1 genes vpr and nef synergistically damage podocytes, leading to glomerulosclerosis

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Glomerular sclerosis in kidneys with congenital nephrotic syndrome (NPHS1)

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Laser capture microdissection-microarray analysis of focal segmental glomerulosclerosis glomeruli

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12 December 2020