ArticleThe Journal of biological chemistry2009
TEADs mediate nuclear retention of TAZ to promote oncogenic transformation.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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Who cites it
145 citing papers in PubMed, 240 citations in OpenAlex.
- Molecular Mechanisms of FAT Atypical Cadherin 1 (FAT1), the Hippo Pathway, and the Yes-Associated Protein (YAP) Signaling Pathways in Some Cancers.Asian Pacific journal of cancer prevention : APJCP · 2026Review
- Hippo signaling regulates the nuclear behavior and DNA binding times of YAP and TEAD to control transcription.Science advances · 2025Article
- M-Motif, a potential non-conventional NLS in YAP/TAZ and other cellular and viral proteins that inhibits classic protein import.iScience · 2025Article
- Transcriptional Co-Activator With PDZ Binding Motif (TAZ) Inhibits Dexamethasone-Induced Muscle Atrophy via mTOR Signalling.Journal of cachexia, sarcopenia and muscle · 2025Article
- TAZ interactome analysis using nanotrap-based affinity purification-mass spectrometry.Journal of cell science · 2025Article
- YAP/TAZ Inhibitor-Based Drug Delivery System for Selective Tumor Accumulation and Cancer Combination Therapy.Biomacromolecules · 2025Article
- Intra-tumoral YAP and TAZ heterogeneity drives collective NSCLC invasion that is targeted by SUMOylation inhibitor TAK-981.iScience · 2024Article
- New Horizons in Cancer Progression and Metastasis:Biomedicines · 2024Review
- CDK9 Inhibition by Dinaciclib Is a Therapeutic Vulnerability in Epithelioid Hemangioendothelioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Hippo pathway in non-small cell lung cancer: mechanisms, potential targets, and biomarkers.Cancer gene therapy · 2024Review
- Identification of PTPN12 Phosphatase as a Novel Negative Regulator of Hippo Pathway Effectors YAP/TAZ in Breast Cancer.International journal of molecular sciences · 2024Article
- Role of YAP Signaling in Regulation of Programmed Cell Death and Drug Resistance in Cancer.International journal of biological sciences · 2024Review
- Wnt16 Promotes Vascular Smooth Muscle Contractile Phenotype and Function via Taz (Wwtr1) Activation in Male LDLR-/- Mice.Endocrinology · 2023Article
- Nuclear Import and Export of YAP and TAZ.Cancers · 2023Review
- The Hippo Pathway Effectors YAP/TAZ-TEAD Oncoproteins as Emerging Therapeutic Targets in the Tumor Microenvironment.Cancers · 2023Review
- New insights into the ambivalent role of YAP/TAZ in human cancers.Journal of experimental & clinical cancer research : CR · 2023Review
- The oncogenic roles and clinical implications of YAP/TAZ in breast cancer.British journal of cancer · 2023Review
- YAP1 and WWTR1 expression inversely correlates with neuroendocrine markers in Merkel cell carcinoma.The Journal of clinical investigation · 2023Article
- TAZ/YAP fusion proteins: mechanistic insights and therapeutic opportunities.Trends in cancer · 2022Review
- The Regulation of the Hippo Pathway by Intercellular Junction Proteins.Life (Basel, Switzerland) · 2022Review
85 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional coactivators YAP and TAZ are downstream targets inhibited by the Hippo tumor suppressor pathway. The expression level of TAZ is recently shown to be elevated in invasive breast cancer cells and some primary breast cancers. TAZ is important for breast cancer cell migration, invasion, and tumorigenesis, but the underlying mechanism is not defined. In this study, we show that TAZ interacts with TEAD transcriptional factors. Knockdown of TEADs suppresses TAZ-mediated oncogenic transformation of MCF10A cells. Uncoupling TAZ from Hippo regulation by S89A mutation enhances its transforming ability. Several residues located in the N-terminal region of TAZ are identified to be important for interaction with TEADs, and these same residues are equally important for TAZ to transform MCF10A cells. Mechanistically, TAZ mutants defective in interaction with TEADs fail to accumulate in the nucleus. Live cell imaging of enhanced green fluorescent protein-TAZ and its mutant defective in TEAD interaction suggests that TEAD interaction mediates nuclear retention. These results reveal a novel mechanism for TEADs to regulate nuclear retention and thus the transforming ability of TAZ.
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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 Socratic graph.