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Study in zebrafish fluorescent transgenic reporter lines of Yap1/Taz provided an in vivo view of Yap1/Taz activity during development and adulthood at the whole organism level. Analysis of vascular development in yap1/taz zebrafish mutants revealed specific defects in posterior cardinal vein formation, with altered expression of arterial/venous markers.
Taz is essential for micropylar cell fate acquisition and subsequent micropyle formation in zebrafish.
ur work identifies a novel role for the Hippo/Taz pathway in micropylar cell specification in zebrafish, and uncovers the molecular basis of micropyle formation in teleosts.
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.
IMP3 also facilitates the transcription of SLUG, which is necessary for TAZ nuclear localization and activation, by a mechanism that is also mediated by WNT5B.
Nuclear TAZ activity associates with lung squamous cell carcinomas (LUSC). Nuclear TAZ activity correlates worse clinical outcomes in LUSC, suggesting a prognostic value for activated TAZ in LUSC. TAZ may be a valuable target for developing therapeutics treating LUSC.
activation of STARD13-correlated ceRNA network was negatively correlated with YAP/TAZ (WWTR1) activity in breast cancer.
Study proposed that the overexpression of YAP and TAZ around the human molluscum contagiosum (MC) virus infected skin lesions supports the hypothesis that the Hippo signaling pathway plays a key role in the development of MC. It is also conceivable that MCV contributes to the development of an infectious environment by increasing the expression of YAP/TAZ and subsequently inhibiting TBK1.
The authors show that TAZ (WWTR1) regulates signaling through the insulin pathway in breast cancer cells.
Data show that hyperactivated WWTR1 (TAZ) protein induced substantial myeloid cell infiltration into the liver and the secretion of proinflammatory cytokines through a TEA domain transcription factor 1 (TEAD)-dependent mechanism.
In this review, we synthesize advances of YAP and WWTR1 (TAZ) function during eye development in different model organisms, introduce their function in different ocular tissues and eye diseases, and highlight the potential for therapeutic interventions
mechanistically, PGC-1alpha maintains bone and fat balance by inducing WWTR1 (TAZ); results suggest that PGC-1alpha is a potentially important therapeutic target in the treatment of osteoporosis and skeletal aging
Hip to the Game: YAP/TAZ is required for nonmelanoma skin cancers.
Since cysteine post-translational regulation plays important roles in redox signalling, tumorigenesis and drug resistance, further studies on the functional effect of this dimerization through post-translational modulation of cysteine residues in YAP2L/ WWTR1 (TAZ) will provide a significant contribution to our understanding of the roles of
Data show that vascular endothelial growth factor (VEGF) -neuropilin 2 (NRP2) signaling contributed to the activation of WWTR1 (TAZ) in various breast cancer cells.
YAP/TAZ function in a developmental checkpoint controlled by signaling from the actin cytoskeleton that prevents differentiation of a progenitor cell until it is in the correct cellular and tissue environment
The data implicate TAZ as a critical downstream effector of fluid flow that regulates proliferation of prostate cancer cells.
YAP/TAZ-TEAD interactions can repress COX-2 transcription and thereby mediate cell density-dependent modulation of proinflammatory responses.
These findings indicate that the oncogenic YAP/TAZ-Wnt crosstalk may be active in gastric cancer.
By elucidating a novel SUMOylation-mediated control mechanism of YAP/TAZ signaling in breast cancer metastasis, we have revealed previously unknown interplay between oncogenic KRAS and EGFR signaling and YAP/TAZ protein stability
All combined hepatocellular (HCC)- cholangiocarcinoma (CCA) and CCA patients showed high expression levels for YAP and TAZ (WWTR1), while only some patients of the HCC group were positive for the YAP-TAZ expression.
Taz (WWTR1) promotes cancer immune evasion through PD-L1.TAZ-induced PD-L1 upregulation in human cancer cells is sufficient to inhibit T-cell function.
An oncogenic role for TAZ (WWTR1) in malignant mesotheliomas via transcriptional induction of distinct pro-oncogenic genes including cytokines.
Inhibition of TAZ (WWTR1) is involved in radiation-induced senescence and might benefit GBM radiotherapy.
Here, the authors show that YAP/TAZ promote stretch-induced proliferation and rearrangements of endothelial cells whilst preventing bleeding in developing vessels.
ARID1A-containing SWI/SNF complex (ARID1A-SWI/SNF) operates as an inhibitor of the pro-oncogenic transcriptional coactivators YAP and TAZ (Wwtr1)
In Yap (wWTR1) transgenic mice, TAZ downregulation in adipose stem cells activated PPARgamma, leading to their differentiation into mature adipocytes and consequently increased adipose tissue. These results highlight the in vivo necessity of TAZ for adipocyte commitment and differentiation
polycystins and TAZ integrate at the molecular level to reciprocally regulate osteoblast and adipocyte differentiation, indicating that the polycystins/TAZ complex may be a potential therapeutic target to increase bone mass.
YAP and TAZ are key determinants of skin cancer initiation, suggesting that targeting the YAP and TAZ signaling pathway might be beneficial for the treatment of skin cancers.
Study establishes a reciprocal antagonism between Hippo-YAP/TAZ and NF-kappaB signaling in regulating the induction of matrix-degrading enzyme expression and cartilage degradation during osteoarthritis pathogenesis.
these results suggest that YAP and TAZ in osteoblast progenitors oppose differentiation towards the osteoblast lineage.
Wnt5a promotes kidney fibrosis by stimulating Yap/Taz (Wwtr1)-mediated macrophage M2 polarization
Novel kindlin-2 signaling axis that senses the mechanical cues of cell microenvironment and controls mesenchymal stem cell fate decision through YAP1/TAZ.
Hippo pathway is inactivated after hepatic ischemia-reperfusion injury and Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) activation is detected in hepatic stellate cells, promoting cell proliferation and liver regeneration.
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.
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)