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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.
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.
This work sheds light on essential mediators, mechanisms and genome-wide regulatory elements that are responsible for transcriptional addiction in cancer and lays the groundwork for a rational use of BET inhibitors according to YAP/TAZ biology.
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.
SRC-mediated YAP/TAZ activity promotes tumor growth and enhances metastasis and that SRC-dependent tumor progression depends, at least in part, on YAP and TAZ.
Study confirmed the increase of TAZ/YAP in skin biopsies from patients with diffuse systemic sclerosis.
The homologous proteins Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are the key regulators in the Hippo pathway
Novel kindlin-2 signaling axis that senses the mechanical cues of cell microenvironment and controls mesenchymal stem cell fate decision through YAP1/TAZ.
Study shows YAP/TAZ function as key nodes of multiple signaling pathways and play multiple regulatory roles in cancer cells especially in metabolic reprogramming. [review]
The crosstalk between the Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) transcription factors and Notch signaling influences cell self-renewal, stem cell differentiation, cell fate decisions, epithelial-stromal interactions, inflammation, morphogenesis, and large-scale gene oscillations.
Dickkopf-3 (DKK3) is a heat shock transcription factor 1 protein (HSF1) effector that modulates the pro-tumorigenic behaviour of cancer-associated fibroblasts (CAFs), and DKK3 orchestrates a concomitant activation of beta-catenin and YAP oncogene protein (YAP)/tafazzin protein (TAZ).
Molecular mechanisms of TAZ protein in the lung physiological conditions and lung diseases.[review]
TAZ/YAP is highly expressed in malignant melanoma tumor tissues; high expression of TAZ/YAP promotes the progression of malignant melanoma and affects the postoperative survival of patients
The C-terminal NLS of TAZ is necessary and sufficient for efficient nuclear uptake via a RAN-independent mechanism.
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.
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
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.
These data demonstrate that YAP and TAZ combinatorially promote bone development through regulation of osteoblast activity, matrix quality, and osteoclastic remodeling.
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)