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Literatura científica selecionada sobre o tema "Transcriptional co-activator with PDZ-Binding motif (TAZ)"

Autor: Grafiati

Publicado: 5 de abril de 2025

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Artigos de revistas sobre o assunto "Transcriptional co-activator with PDZ-Binding motif (TAZ)"

1

Wu, Chia-Lin, Chia-Chu Chang, Tao-Hsiang Yang, et al. "Tubular transcriptional co-activator with PDZ-binding motif protects against ischemic acute kidney injury." Clinical Science 134, no. 13 (2020): 1593–612. http://dx.doi.org/10.1042/cs20200223.

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Abstract Transcriptional co-activator with PDZ-binding motif (TAZ) is a key downstream effector of the Hippo tumor-suppressor pathway. The functions of TAZ in the kidney, especially in tubular epithelial cells, are not well-known. To elucidate the adaptive expression, protective effects on kidney injury, and signaling pathways of TAZ in response to acute kidney injury (AKI), we used in vitro (hypoxia-treated human renal proximal tubular epithelial cells [RPTECs]) and in vivo (mouse ischemia–reperfusion injury [IRI]) models of ischemic AKI. After ischemic AKI, TAZ was up-regulated in RPTECs and

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2

Huang, Yao, Xueqian Ouyang, Jinghua Tan, Zhenyu Meng, Xiuwen Ma, and Yiguo Yan. "The physiological and pathogenic roles of yes-associated protein/transcriptional co-activator with PDZ-binding motif in bone or skeletal motor system-related cells." Cytojournal 22 (February 8, 2025): 13. https://doi.org/10.25259/cytojournal_237_2024.

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Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) are the primary downstream effectors of the Hippo signaling pathway. This pathway plays a crucial role in regulating organ size, maintaining tissue homeostasis, and controlling cellular processes such as fate determination and tissue development. This review provides an overview of the current understanding of how the transcriptional regulators YAP and TAZ contribute to the physiological and pathological processes in tissues and cells associated with the skeletal motor system. The underlying molecular me

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3

Liu, Tao, Jiaojiao Zhou, Yanmin Chen, et al. "Genome-Wide Characterization of TAZ Binding Sites in Mammary Epithelial Cells." Cancers 15, no. 19 (2023): 4713. http://dx.doi.org/10.3390/cancers15194713.

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The transcriptional co-activator with PDZ binding motif (TAZ) is a key effector of the Hippo signaling pathway. We and others previously reported that high expression levels of TAZ are positively associated with decreased survival rates and shorter times to relapse in basal-like breast cancer (BLBC) patients. The oncogenic activity of TAZ involves the regulation of diverse signal transduction pathways that direct processes such as cell proliferation, migration, and resistance to apoptosis, albeit through poorly characterized gene expression programs. Here, using a tet-inducible system in mamma

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4

Salem and Hansen. "The Hippo Pathway in Prostate Cancer." Cells 8, no. 4 (2019): 370. http://dx.doi.org/10.3390/cells8040370.

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Despite recent efforts, prostate cancer (PCa) remains one of the most common cancers in men. Currently, there is no effective treatment for castration-resistant prostate cancer (CRPC). There is, therefore, an urgent need to identify new therapeutic targets. The Hippo pathway and its downstream effectors—the transcriptional co-activators, Yes-associated protein (YAP) and its paralog, transcriptional co-activator with PDZ-binding motif (TAZ)—are foremost regulators of stem cells and cancer biology. Defective Hippo pathway signaling and YAP/TAZ hyperactivation are common across various cancers. H

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5

Tiffon, Camille, Julie Giraud, Silvia Elena Molina-Castro, et al. "TAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Properties." Cells 9, no. 6 (2020): 1462. http://dx.doi.org/10.3390/cells9061462.

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Helicobacter pylori infection, the main risk factor for gastric cancer (GC), leads to an epithelial–mesenchymal transition (EMT) of gastric epithelium contributing to gastric cancer stem cell (CSC) emergence. The Hippo pathway effectors yes-associated protein (YAP) and transcriptional co-activator with PDZ binding motif (TAZ) control cancer initiation and progression in many cancers including GC. Here, we investigated the role of TAZ in the early steps of H. pylori-mediated gastric carcinogenesis. TAZ implication in EMT, invasion, and CSC-related tumorigenic properties were evaluated in three

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6

MAHONEY, William M., Jeong-Ho HONG, Michael B. YAFFE, and Iain K. G. FARRANCE. "The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members." Biochemical Journal 388, no. 1 (2005): 217–25. http://dx.doi.org/10.1042/bj20041434.

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Members of the highly related TEF-1 (transcriptional enhancer factor-1) family (also known as TEAD, for TEF-1, TEC1, ABAA domain) bind to MCAT (muscle C, A and T sites) and A/T-rich sites in promoters active in cardiac, skeletal and smooth muscle, placenta, and neural crest. TEF-1 activity is regulated by interactions with transcriptional co-factors [p160, TONDU (Vgl-1, Vestigial-like protein-1), Vgl-2 and YAP65 (Yes-associated protein 65 kDa)]. The strong transcriptional co-activator YAP65 interacts with all TEF-1 family members, and, since YAP65 is related to TAZ (transcriptional co-activato

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7

Chu, Cong-Qiu, and Taihao Quan. "Fibroblast Yap/Taz Signaling in Extracellular Matrix Homeostasis and Tissue Fibrosis." Journal of Clinical Medicine 13, no. 12 (2024): 3358. http://dx.doi.org/10.3390/jcm13123358.

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Tissue fibrosis represents a complex pathological condition characterized by the excessive accumulation of collagenous extracellular matrix (ECM) components, resulting in impaired organ function. Fibroblasts are central to the fibrotic process and crucially involved in producing and depositing collagen-rich ECM. Apart from their primary function in ECM synthesis, fibroblasts engage in diverse activities such as inflammation and shaping the tissue microenvironment, which significantly influence cellular and tissue functions. This review explores the role of Yes-associated protein (Yap) and Tran

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8

Warren, Janine, Yuxuan Xiao, and John Lamar. "YAP/TAZ Activation as a Target for Treating Metastatic Cancer." Cancers 10, no. 4 (2018): 115. http://dx.doi.org/10.3390/cancers10040115.

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Yes-Associated Protein (YAP) and Transcriptional Co-activator with PDZ-binding Motif (TAZ) have both emerged as important drivers of cancer progression and metastasis. YAP and TAZ are often upregulated or nuclear localized in aggressive human cancers. There is abundant experimental evidence demonstrating that YAP or TAZ activation promotes cancer formation, tumor progression, and metastasis. In this review we summarize the evidence linking YAP/TAZ activation to metastasis, and discuss the roles of YAP and TAZ during each step of the metastatic cascade. Collectively, this evidence strongly sugg

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9

Park, Sangryong, Ho-Young Lee, Jayoung Kim, et al. "Cerebral Cavernous Malformation 1 Determines YAP/TAZ Signaling-Dependent Metastatic Hallmarks of Prostate Cancer Cells." Cancers 13, no. 5 (2021): 1125. http://dx.doi.org/10.3390/cancers13051125.

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Enhanced Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signaling is correlated with the extraprostatic extension of prostate cancer. However, the mechanism by which YAP/TAZ signaling becomes hyperactive and drives prostate cancer progression is currently unclear. In this study, we revealed that higher expression of CCM1, which is uniquely found in advanced prostate cancer, is inversely correlated with metastasis-free and overall survival in patients with prostate cancer. We also demonstrated that CCM1 induces the metastasis of multiple types of prostate

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10

Lauriola, Angela, Elisa Uliassi, Matteo Santucci, et al. "Identification of a Quinone Derivative as a YAP/TEAD Activity Modulator from a Repurposing Library." Pharmaceutics 14, no. 2 (2022): 391. http://dx.doi.org/10.3390/pharmaceutics14020391.

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The transcriptional regulators YAP (Yes-associated protein) and TAZ (transcriptional co-activator with PDZ-binding motif) are the major downstream effectors in the Hippo pathway and are involved in cancer progression through modulation of the activity of TEAD (transcriptional enhanced associate domain) transcription factors. To exploit the advantages of drug repurposing in the search of new drugs, we developed a similar approach for the identification of new hits interfering with TEAD target gene expression. In our study, a 27-member in-house library was assembled, characterized, and screened

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