ArticleCell death & disease2019
Hyperactivity of Mek in TNS1 knockouts leads to potential treatments for cystic kidney diseases.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Development and characterization of an inducible Tensin1 deficient transgenic murine model.Scientific reports · 2026Article
- A novel isoform of tensin-1 promotes actin filament assembly for efficient erythroblast enucleation.Blood advances · 2025Article
- Kinase suppressor of Ras 1 (KSR1) promotes liver carcinogenesis via activation of the RAS/RAF/MEK/ERK signaling pathway.JHEP reports : innovation in hepatology · 2025Article
- Targeting AXL Inhibits the Growth and Metastasis of Prostate Cancer in Bone.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023Review
- C-terminal tensin-like (Genes & diseases · 2023Article
- Phase transition of tensin-1 during the focal adhesion disassembly and cell division.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- NUSAP1 Binds ILF2 to Modulate R-Loop Accumulation and DNA Damage in Prostate Cancer.International journal of molecular sciences · 2023Article
- Tensins - emerging insights into their domain functions, biological roles and disease relevance.Journal of cell science · 2021Review
- ROS-ERK Pathway as Dual Mediators of Cellular Injury and Autophagy-Associated Adaptive Response in Urinary Protein-Irritated Renal Tubular Epithelial Cells.Journal of diabetes research · 2021Article
- GDNF drives rapid tubule morphogenesis in a novel 3DJournal of cell science · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cystic kidney disease is the progressive development of multiple fluid-filled cysts that may severely compromise kidney functions and lead to renal failure. TNS1 (tensin-1) knockout mice develop cystic kidneys and die from renal failure. Here, we have established TNS1-knockout MDCK cells and applied 3D culture system to investigate the mechanism leading to cyst formation. Unlike wild-type MDCK cells, which form cysts with a single lumen, TNS1-knockout cysts contain multiple lumens and upregulated Mek/Erk activities. The multiple lumen phenotype and Mek/Erk hyperactivities are rescued by re-expression of wild-type TNS1 but not the TNS1 mutant lacking a fragment essential for its cell-cell junction localization. Furthermore, Mek inhibitor treatments restore the multiple lumens back to single lumen cysts. Mek/Erk hyperactivities are also detected in TNS1-knockout mouse kidneys. Treatment with the Mek inhibitor trametinib significantly reduces the levels of interstitial infiltrates, fibrosis and dilated tubules in TNS1-knockout kidneys. These studies establish a critical role of subcellular localization of TNS1 in suppressing Mek/Erk signaling and maintaining lumenogenesis, and provide potential therapeutic strategies by targeting the Mek/Erk pathway for cystic kidney diseases.
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