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Article

Mice with podocyte-specific overexpression of wild type alpha-actinin-4 are healthy controls for K256E-alpha-actinin-4 mutant transgenic mice.

Transgenic research - 1 Apr 2010

Michaud Jean-Louis, Stitt-Cavanaugh Erin, Endlich Nicole, Endlich Karlhans, De Repentigny Yves, Kothary Rashmi, Kennedy Chris R J

Abstract excerpt

Mutations in the gene ACTN4 encoding the actin bundling protein-alpha-actinin-4 underlie an inherited form of kidney lesions known as focal segmental glomerulosclerosis (FSGS). Previously, we developed a model for this condition by generating mice with podocyte-specific overexpression of a diseas...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 19585264
DOI: 10.1007/s11248-009-9305-9

Genes

ACTN4
NPHS1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-19585264-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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Mice with podocyte-specific overexpression of wild type alpha-actinin-4 are healthy controls for K256E-alpha-actinin-4 mutant transgenic mice.PMID 19585264Read ↗

Focal and Segmental Glomerulosclerosis in Mice with Podocyte-Specific Expression of Mutant α-Actinin-4Semantic proximity Read ↗

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Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis.Semantic proximity Read ↗

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Alpha-actinin-4-mediated FSGS: an inherited kidney disease caused by an aggregated and rapidly degraded cytoskeletal protein.Semantic proximity Read ↗

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Mutational and Biological Analysis of alpha-actinin-4 in focal segmental glomerulosclerosis.Semantic proximity Read ↗

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A Bigenic mouse model of FSGS reveals perturbed pathways in podocytes, mesangial cells and endothelial cellsSemantic proximity Read ↗

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