ArticleExperimental animals2020
Deletion of the Tensin2 SH2-PTB domain, but not the loss of its PTPase activity, induces podocyte injury in FVB/N mouse strain.
Article in Experimental animals, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Automated scoring of glomerular injury in TNS2-deficient nephropathy.Experimental animals · 2024Article
- Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023Review
- Genetic background strongly influences the transition to chronic kidney disease of adriamycin nephropathy in mice.Experimental animals · 2023Article
- Tensin 2-deficient nephropathy: mechanosensitive nephropathy, genetic susceptibility.Experimental animals · 2022Review
- The versatile electric condition in mouse embryos for genome editing using a three-step square-wave pulse electroporator.Experimental animals · 2022Article
- Tensins - emerging insights into their domain functions, biological roles and disease relevance.Journal of cell science · 2021Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tensin2 (TNS2) is a focal adhesion-localized protein possessing N-terminal tandem protein tyrosine phosphatase (PTPase) and C2 domains, and C-terminal tandem Src homology 2 (SH2) and phosphotyrosine binding (PTB) domains. Genetic deletion of Tns2 in a susceptible murine strain leads to podocyte alterations after birth. To clarify the domain contributions to podocyte maintenance, we generated two Tns2-mutant mice with the genetic background of the susceptible FVB/NJ strain, Tns2
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