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Human Polyclonal WWTR1 Primary Antibody für WB - ABIN153163
Chan, Lim, Guo, Ng, Lee, Hunziker, Zeng, Hong: A role for TAZ in migration, invasion, and tumorigenesis of breast cancer cells. in Cancer research 2008
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Human Polyclonal WWTR1 Primary Antibody für ChIP, ICC - ABIN258561
Strakova, Reed, Ihnatovych: Human transcriptional coactivator with PDZ-binding motif (TAZ) is downregulated during decidualization. in Biology of reproduction 2010
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Human Polyclonal WWTR1 Primary Antibody für ICC, IF - ABIN4357944
Bhat, Salazar, Balasubramaniyan, Wani, Heathcock, Hollingsworth, James, Gumin, Diefes, Kim, Turski, Azodi, Yang, Doucette, Colman, Sulman, Lang, Rao, Copray, Vaillant, Aldape: The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma. in Genes & development 2011
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Polyclonal WWTR1 Primary Antibody für IP, WB - ABIN540238
Hong, Hwang, McManus, Amsterdam, Tian, Kalmukova, Mueller, Benjamin, Spiegelman, Sharp, Hopkins, Yaffe: TAZ, a transcriptional modulator of mesenchymal stem cell differentiation. in Science (New York, N.Y.) 2005
Human Polyclonal WWTR1 Primary Antibody für ICC, IF - ABIN4357945
Pathak, Meng, Zhang, Gnosa, Nandy, Adell, Holmlund, Sun: Tafazzin protein expression is associated with tumorigenesis and radiation response in rectal cancer: a study of Swedish clinical trial on preoperative radiotherapy. in PLoS ONE 2014
The authors show that the Hippo pathway transcriptional coactivators Yap1 and Wwtr1 are specifically localized to the presumptive epidermis and notochord, and play a critical and unexpected role in posterior body extension by regulating Fibronectin assembly underneath the presumptive epidermis and surrounding the notochord.
Altogether, the data suggest that Wwtr1 establishes the compact wall architecture necessary for trabeculation, and that Nrg/Erbb2 signaling negatively regulates its nuclear localization and therefore its activity.
Yap/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt retinal pigment epithelium identity in zebrafish.
Taz is required in the anteroposterior patterning of the pronephric progenitor domain in the intermediate mesoderm, acting in part by regulating retinoic acid signaling in the pronephric progenitor field in the intermediate mesoderm.
Taz-depleted larvae displayed patterning defects in ventral cranial vessels that correlate with lateral displacement of thyroid follicles
When transcriptional coactivators Yap and Taz were restricted from interacting with Tead transcription factors through expression of a dominant negative transgene, cardiac precursors failed to migrate completely to the midline.
TAZ has a critical role in osteoblast differentiation in vivo
MRTF is essential for TAZ expression; TAZ and MRTF inhibit each other's cytosolic mobility and stimulus-induced nuclear accumulation; they antagonize each other's stimulatory effect on the alpha-smooth muscle actin promoter, which harbours nearby cis-elements for both, but synergize on isolated TEAD-elements.
YAP/TAZ mechanotransduction integrates with cell-cell communication pathways for fine-grained orchestration of stem cell decisions.
The TAZ WW domain exhibits a binding preference for the second of the two PPxY motifs of LATS1 in vitro. We modelled the structure of the domain in complex with LATS1 PPxY2 peptide and, through molecular dynamics simulations, show that WW domain-PPxY2 complex is stable with some flexibility in the peptide region.
In the present review, we focus on the functions of YAP/TAZ in cancer, discuss their potential as new therapeutic target for tumor treatment, and provide valuable suggestions for further study in this field.
functional evaluation of a HTM cell monolayer using a permeability assay demonstrated that the inhibition of YAP and TAZ attenuated the DEX-induced impairment of permeability. These findings suggest that YAP and TAZ play pivotal roles in the DEX-induced cytoskeletal changes of HTM cells, and reveal novel potential mechanisms for the development and progression of glaucoma
WWTR1 promotes cell proliferation and inhibits apoptosis of GC cells by regulating cell cycle/apoptosisassociated factors, and effectors in the TGFbeta pathway.
EphA2-mediates glutaminolysis through YAP/TAZ activation in HER2-positive breast cancer and may serve as potential therapeutic targets in patients.
Depletion of either YES-associated protein (YAP) or transcriptional coactivator with PDZ-motif (TAZ) sensitised cancer cell lines to MLN8237, resulting in apoptosis and reduction in aurora-A.
High TAZ expression is associated with breast cancer.
Nuclear localization of YAP and TAZ was reduced in DMOG-treated primary tubular epithelial cells.
SnoN interacts with multiple components of the Hippo pathway to inhibit the binding of Lats2 to TAZ and the subsequent phosphorylation of TAZ, leading to TAZ stabilization.
Results show that YAP and TAZ transcription are regulated by Cbx7 inhibiting glioblasoma cell migration.
Besides its role in normal tissue development, TAZ plays critical roles in cell proliferation, differentiation, apoptosis, migration, invasion, epithelial-mesenchymal transition (EMT), and stemness in multiple human cancers.
Together, these data illustrate that YAP/TAZ signaling is responsive to hydrogel stiffness and degradability, but the outcome is dependent on the dimensionality of cell-biomaterial interactions.
Wnt signaling upregulated WBP2 by disrupting ITCH-WBP2 interactions via EGFR-mediated tyrosine phosphorylation of WBP2 and TAZ/YAP competitive binding.
results highlight both CYR61 and TAZ genes as potential predictive biomarkers for stratification of the risk for development of adenocarcinoma and suggest a potential mechanistic route for Barrett's esophagus neoplastic progression
Collectively, our study identified an unexpected transcriptional repression function of the BET bromodomain and a novel mechanism for TAZ upregulation.
High TAZ expression is associated with non-small cell lung cancer.
These findings demonstrate sufficiency of TAZ activation for driving fibroblast proliferation, contraction, and soluble profibrotic factor expression, and mechanical context-dependent crosstalk of TAZ with other pathways in regulating Col1a1 expression.
A group of miRNAs have been demonstrated to directly target components of the Hippo signaling pathway, such as YAP, TAZ and LATS1/2 in oncogenesis. (Review)
AXL/TAZ/YAP expression is associated with poor prognosis in male breast cancer patients.
TAZ was activated in fibrosis through TGF-beta1-dependent mechanisms and sustained TAZ signaling promotes epithelial maladaptive repair. TAZ is also a novel non-SMAD downstream effector of renal TGF-beta1 signaling, establishing TAZ as a new antifibrosis target for treatment of CKD.
Taz is not essential for achieving proper liver size during development or in the perinatal period but is required to mount an effective regenerative response following hepatectomy.
During and after liver development, the activation of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epithelial cell lineage.
Wnt/beta-catenin signaling via Axin2 is required for myogenesis and, together with YAP/Taz and Tead1, active in IIa/IIx muscle fibers
Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction
Yap and Taz are activated in Schwann cells by mechanical stimuli and regulate Schwann cell proliferation and transcription of basal lamina receptor genes
YAP/TAZ are crucial for Schwann cells to myelinate developing nerve and to maintain myelinated nerve in adulthood.
transient expression of exogenous YAP or its closely related paralogue TAZ in primary differentiated mouse cells can induce conversion to a tissue-specific stem/progenitor cell state.
The results uncover an important aspect of the cross-talk between TGFbeta and Hippo signaling, showing that TGFbeta induces TAZ via a Smad3-independent, p38- and MRTF-mediated and yet MRTF translocation-independent mechanism.
These data demonstrate that YAP and TAZ combinatorially promote bone development through regulation of osteoblast activity, matrix quality, and osteoclastic remodeling.
MOB1-dependent YAP1/TAZ-TEAD complex functions as a transcriptional repressor of SOX9 and thereby negatively regulates chondrogenesis.
TAZ regulates cell fate depends on not only the cell type but also its subcellular localization.
The results suggested that TAZ may suppress apoptosis and premature senescence in spermatogenic cells by inhibiting the p53-p21 signaling pathway, thus playing important roles in the maintenance and control of reproductive function.
The role of Yap and Wwtr1 in the Hippo signaling pathway and the regulation of spermatogenesis in mice are reported.
Taz and Yap have overlapping functions in promoting myoblast proliferation but Taz then switches to enhance myogenic differentiation.
A crucial role for YAP and TAZ in the maintenance of the postnatal adrenal cortex.
TAZ is a critical factor for SRC kinase-mediated intestinal tumor formation and regeneration.
YAP/TAZ plays multifaceted roles for endothelial cell behaviors, proliferation, junction assembly, and metabolism in sprouting angiogenesis and barrier formation
Yap and Taz leads to impaired epicardial epithelial-to-mesenchymal transition (EMT) and a reduction in epicardial cell proliferation and differentiation into coronary endothelial cells.
This gene encodes a binding protein of the 14-3-3 family of proteins that regulate cell cycle progression, differentiation and apoptosis. The encoded protein is a transcriptional co-activator that binds to the PPXY motif present on transcription factors. The gene product contains a WW domain and, in the C-terminus, a conserved PDZ-binding motif. This gene is distinct from the gene encoding tafazzin. Both genes share the gene symbol Taz. Multiple transcript variants encoding different isoforms have been described.
WW domain containing transcription regulator 1
, WW domain-containing transcription regulator protein 1
, WW domain-containing transcription regulator protein 1-like
, transcriptional co-activator with PDZ-binding motif
, transcriptional coactivator with PDZ-binding motif
, transcriptional coactivator with PDZ binding motif
, transcriptional co-activator with PDZ-binding motif (TA)Z
, transcriptional co-activator with PDZ-binding motif (TAZ)