ArticleMolecular and cellular biology2012
TAZ suppresses NFAT5 activity through tyrosine phosphorylation.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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
26 citing papers in PubMed, 43 citations in OpenAlex.
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Multi-Functional Regulation by YAP/TAZ Signaling Networks in Tumor Progression and Metastasis.Cancers · 2023Review
- NEK1-Mediated Phosphorylation of YAP1 Is Key to Prostate Cancer Progression.Biomedicines · 2023Article
- TAZ promotes PDX1-mediated insulinogenesis.Cellular and molecular life sciences : CMLS · 2022Article
- RB1CC1 functions as a tumor-suppressing gene in renal cell carcinoma via suppression of PYK2 activity and disruption of TAZ-mediated PDL1 transcription activation.Cancer immunology, immunotherapy : CII · 2021Article
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- TAZ ControlsCells · 2020Article
- Hippo-Yap/Taz signaling: Complex network interactions and impact in epithelial cell behavior.Wiley interdisciplinary reviews. Developmental biology · 2020Review
- A gain-of-functional screen identifies the Hippo pathway as a central mediator of receptor tyrosine kinases during tumorigenesis.Oncogene · 2020Article
- The Hippo Pathway in Innate Anti-microbial Immunity and Anti-tumor Immunity.Frontiers in immunology · 2020Review
- A TAZ-AXL-ABL2 Feed-Forward Signaling Axis Promotes Lung Adenocarcinoma Brain Metastasis.Cell reports · 2019Article
- Regulation of Inflammatory Functions of Macrophages and T Lymphocytes by NFAT5.Frontiers in immunology · 2019Review
- PYK2 negatively regulates the Hippo pathway in TNBC by stabilizing TAZ protein.Cell death & disease · 2018Article
- Farnesoid X receptor is essential for the survival of renal medullary collecting duct cells under hypertonic stress.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A Novel S100A8/A9 Induced Fingerprint of Mesenchymal Stem Cells associated with Enhanced Wound Healing.Scientific reports · 2018Article
- The Role of Hippo Pathway in Cancer Stem Cell Biology.Molecules and cells · 2018Review
- Reciprocal stabilization of ABL and TAZ regulates osteoblastogenesis through transcription factor RUNX2.The Journal of clinical investigation · 2016Article
- Outside the mainstream: novel collecting duct proteins regulating water balance.American journal of physiology. Renal physiology · 2016Review
- Regulation of TAZ in cancer.Protein & cell · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional coactivator with PDZ-binding motif (TAZ) physically interacts with a variety of transcription factors and modulates their activities involved in cell proliferation and mesenchymal stem cell differentiation. TAZ is highly expressed in the kidney, and a deficiency of this protein results in multiple renal cysts and urinary concentration defects; however, the molecular functions of TAZ in renal cells remain largely unknown. In this study, we examined the effects of osmotic stress on TAZ expression and activity in renal cells. We found that hyperosmotic stress selectively increased protein phosphorylation at tyrosine 316 of TAZ and that this was enhanced by c-Abl activation in response to hyperosmotic stress. Interestingly, phosphorylated TAZ physically interacted with nuclear factor of activated T cells 5 (NFAT5), a major osmoregulatory transcription factor, and subsequently suppressed DNA binding and transcriptional activity of NFAT5. Furthermore, TAZ deficiency elicited an increase in NFAT5 activity in vitro and in vivo, which then reverted to basal levels following restoration of wild-type TAZ but not mutant TAZ (Y316F). Collectively, the data suggest that TAZ modulates cellular responses to hyperosmotic stress through fine-tuning of NFAT5 activity via tyrosine phosphorylation.
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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.