ArticleMolecular biology of the cell2016
ZO-2 silencing induces renal hypertrophy through a cell cycle mechanism and the activation of YAP and the mTOR pathway.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- ZO-2 is a scaffold at the centriole and mitotic spindle poles that enhances microtubule stability and supports the proper development of mitotic spindles and cilia.Cell and tissue research · 2025Article
- Contact and communication: ZO-2 and the Hippo pathway.The FEBS journal · 2025Article
- The transcriptome of early compensatory kidney growth reveals cell and time specific responses.iScience · 2024Article
- Article
- The Role of ZO-2 in Modulating JAM-A and γ-Actin Junctional Recruitment, Apical Membrane and Tight Junction Tension, and Cell Response to Substrate Stiffness and Topography.International journal of molecular sciences · 2024Article
- The Hippo signalling pathway and its implications in human health and diseases.Signal transduction and targeted therapy · 2022Review
- The Regulation of the Hippo Pathway by Intercellular Junction Proteins.Life (Basel, Switzerland) · 2022Review
- Article
- ZO-2/Tjp2 suppresses Yap and Wwtr1/Taz-mediated hepatocyte to cholangiocyte transdifferentiation in the mouse liver.NPJ Regenerative medicine · 2022Article
- The Hippo pathway and its correlation with acute kidney injury.Zoological research · 2022Review
- Role of zonula occludens in gastrointestinal and liver cancers.World journal of clinical cases · 2022Review
- ZO-2 favors Hippo signaling, and its re-expression in the steatotic liver by AMPK restores junctional sealing.Tissue barriers · 2022Article
- The LINC Complex Assists the Nuclear Import of Mechanosensitive Transcriptional Regulators.Results and problems in cell differentiation · 2022Article
- Article
- Tight junction protein ZO-2 modulates the nuclear accumulation of transcription factor TEAD.Molecular biology of the cell · 2021Article
- From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues.Biomolecules · 2021Review
- Context-dependent roles of YAP/TAZ in stem cell fates and cancer.Cellular and molecular life sciences : CMLS · 2021Review
- An overview of signaling pathways regulating YAP/TAZ activity.Cellular and molecular life sciences : CMLS · 2021Review
- Role ofInternational journal of molecular sciences · 2020Article
- ZO-2 Is a Master Regulator of Gene Expression, Cell Proliferation, Cytoarchitecture, and Cell Size.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal compensatory hypertrophy (RCH) restores normal kidney function after disease or loss of kidney tissue and is characterized by an increase in organ size due to cell enlargement and not to cell proliferation. In MDCK renal epithelial cells, silencing of the tight junction protein zona occludens 2 (ZO-2 KD) induces cell hypertrophy by two mechanisms: prolonging the time that cells spend at the G1 phase of the cell cycle due to an increase in cyclin D1 level, and augmenting the rate of protein synthesis. The latter is triggered by the nuclear accumulation and increased transcriptional activity of Yes-associated protein (YAP), the main target of the Hippo pathway, which results in decreased expression of phosphatase and tensin homologue. This in turn increased the level of phosphatidylinositol (3,4,5)-triphosphate, which transactivates the Akt/mammalian target of rapamycin pathway, leading to activation of the kinase S6K1 and increased synthesis of proteins and cell size. In agreement, in a rat model of uninephrectomy, RCH is accompanied by decreased expression of ZO-2 and nuclear expression of YAP. Our results reveal a novel role of ZO-2 as a modulator of cell size.
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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.