ArticleThe Journal of veterinary medical science2016
Functional validation of tensin2 SH2-PTB domain by CRISPR/Cas9-mediated genome editing.
Article in The Journal of veterinary medical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Tensin2 deficiency transiently accelerates early-phase regenerative myofiber growth following cardiotoxin-induced injury in mice.Experimental animals · 2026Article
- Automated scoring of glomerular injury in TNS2-deficient nephropathy.Experimental animals · 2024Article
- Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023Review
- Tensin 2-deficient nephropathy: mechanosensitive nephropathy, genetic susceptibility.Experimental animals · 2022Review
- Tensins - emerging insights into their domain functions, biological roles and disease relevance.Journal of cell science · 2021Review
- Lycopene attenuates high glucose-mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway.Experimental and therapeutic medicine · 2020Article
- Article
- Deletion of the Tensin2 SH2-PTB domain, but not the loss of its PTPase activity, induces podocyte injury in FVB/N mouse strain.Experimental animals · 2020Article
- Novel murine model of congenital diabetes: The insulin hyposecretion mouse.Journal of diabetes investigation · 2019Article
- Genetics of Childhood Steroid Sensitive Nephrotic Syndrome: An Update.Frontiers in pediatrics · 2019Review
- Precision gene editing technology and applications in nephrology.Nature reviews. Nephrology · 2018Review
- Genetic loci for resistance to podocyte injury caused by the tensin2 gene deficiency in mice.BMC genetics · 2018Article
- C1-Ten is a PTPase of nephrin, regulating podocyte hypertrophy through mTORC1 activation.Scientific reports · 2017Article
- CRISPR/Cas9 targeting events cause complex deletions and insertions at 17 sites in the mouse genome.Nature communications · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes are terminally differentiated and highly specialized cells in the glomerulus, and they form a crucial component of the glomerular filtration barrier. The ICGN mouse is a model of glomerular dysfunction that shows gross morphological changes in the podocyte foot process, accompanied by proteinuria. Previously, we demonstrated that proteinuria in ICR-derived glomerulonephritis mouse ICGN mice might be caused by a deletion mutation in the tensin2 (Tns2) gene (designated Tns2
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.