Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The 129 genetic background affects susceptibility to glomerulosclerosis in tensin2-deficient mice.

Biomedical research (Tokyo, Japan) - 1 Feb 2012

Nishino Tomohiro, Sasaki Nobuya, Nagasaki Ken-Ichi, Ichii Osamu, Kon Yasuhiro, Agui Takashi

Abstract excerpt

The ICGN mouse strain is a glomerulosclerosis (GS) model that shows significant proteinuria, podocyte morphological abnormalities and increased extracellular matrix accumulation in the glomeruli, which represent the final common pathology associated with a variety of kidney diseases leading to end-stage renal failure. Previously, we demonstrated that GS in ICGN mice can be attributed to the deletion mutation of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Albuminuria
Share to Disease Models, Animal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Kidney Diseases

Share to Kidney Failure, Chronic

Share to Mice, Inbred Strains

Share to Phosphoprotein Phosphatases

Share to Podocytes

Share to Proteinuria

Source

Identifiers

PMID: 22361887
DOI: 10.2220/biomedres.33.53

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The 129 genetic background affects susceptibility to glomerulosclerosis in tensin2-deficient mice.PMID 22361887Read ↗

Genetic background strongly influences the severity of glomerulosclerosis in mice.Semantic proximity Read ↗

Quantitative trait Loci for resistance to the congenital nephropathy in tensin 2-deficient mice.Semantic proximity Read ↗

Deficiency of the tensin2 gene in the ICGN mouse: an animal model for congenital nephrotic syndromeSemantic proximity Read ↗

Functional validation of tensin2 SH2-PTB domain by CRISPR/Cas9-mediated genome editing.Semantic proximity Read ↗

Proteinuria-induced chronic kidney disease in the ICGN/Oa mice with a mutation of Tensin2 gene.Semantic proximity Read ↗

Tensin 2-deficient nephropathy: mechanosensitive nephropathy, genetic susceptibility.Semantic proximity Read ↗

Non-Transgenic Mouse Models of Kidney Disease.Semantic proximity Read ↗

Identification of nephropathy candidate genes by comparing sclerosis-prone and sclerosis-resistant mouse strain kidney transcriptomes.Semantic proximity Read ↗

Renal phenotype of the cystinosis mouse model is dependent upon genetic background.Semantic proximity Read ↗

Model of robust induction of glomerulosclerosis in mice: importance of genetic background.Semantic proximity Read ↗

Knockout of the TauT gene predisposes C57BL/6 mice to streptozotocin-induced diabetic nephropathy.Semantic proximity Read ↗

Col4a3-/- Mice on Balb/C Background Have Less Severe Cardiorespiratory Phenotype and SGLT2 Over-Expression Compared to 129x1/SvJ and C57Bl/6 Backgrounds.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.