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TAZ encodes a protein that is expressed at high levels in cardiac and skeletal muscle. Zusätzlich bieten wir Ihnen TAZ Proteine (13) und TAZ Kits (6) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 144 products:
Human Monoclonal TAZ Primary Antibody für BI, WB - ABIN967665
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
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Human Monoclonal TAZ Primary Antibody für ELISA, WB - ABIN520708
Raghunathan, Morgan, Dreier, Reilly, Thomasy, Wood, Ly, Tuyen, Hughbanks, Murphy, Russell: Role of substratum stiffness in modulating genes associated with extracellular matrix and mechanotransducers YAP and TAZ. in Investigative ophthalmology & visual science 2013
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Human Polyclonal TAZ Primary Antibody für IF (p), IHC (p) - ABIN1713913
Sun, Chen, Shi, Qi, Zhao, Zhang: Prognostic impact of TAZ and ?-catenin expression in adenocarcinoma of the esophagogastric junction. in Diagnostic pathology 2014
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Human Polyclonal TAZ Primary Antibody für ELISA, WB - ABIN269827
Brandner, Mick, Frazier, Taylor, Meisinger, Rehling: Taz1, an outer mitochondrial membrane protein, affects stability and assembly of inner membrane protein complexes: implications for Barth Syndrome. in Molecular biology of the cell 2005
During vascular regression, Yap/Taz is activated by blood circulation in the endothelial cells. This leads to induction of Ctgf and actin polymerization. Interference with Yap/Taz activation decreased Ctgf production, which decreased actin polymerization and vascular regression.
knockdown phenotype demonstrates that abnormal cardiac development, with a linear, nonlooped heart, and hypomorphic tail and eye development proves that tafazzin is essential for overall zebrafish development, especially of the heart.
High TAZ expression is associated with breast cancer.
Together, these data illustrate that YAP (zeige YAP1 Antikörper)/TAZ signaling is responsive to hydrogel stiffness and degradability, but the outcome is dependent on the dimensionality of cell-biomaterial interactions.
Data indicate that injury reduced YAP (zeige YAP1 Antikörper) and TAZ activity in cultured podocyte cell line grown on stiff substrates.
factors YAP (zeige YAP1 Antikörper) and TAZ as mechanotransducers started to fill this gap. YAP (zeige YAP1 Antikörper) and TAZ read a broad range of mechanical cues, from shear stress to cell shape and extracellular matrix rigidity, and translate them into cell-specific transcriptional programmes.
Collectively, our study identified an unexpected transcriptional repression function of the BET bromodomain and a novel mechanism for TAZ upregulation.
Nuclear localization of YAP (zeige YAP1 Antikörper) and TAZ was reduced in DMOG-treated primary tubular epithelial cells.
mechanistic study revealed that miR (zeige MLXIP Antikörper)-224 functions by inhibiting the tumor suppressor, SMAD4 (zeige SMAD4 Antikörper), to support the proliferation and migration of osteosarcoma (OS) cells. Our findings indicate that targeting TAZ and miR (zeige MLXIP Antikörper)-224 could be a promising approach for the treatment of OS.
TAZ was positively correlated with EGFR (zeige EGFR Antikörper) signaling, and coexpression of TAZ/EGFR (zeige EGFR Antikörper) conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR (zeige EGFR Antikörper)-wild-type non-small-cell lung cancer .
TAZ mutation-confirmed diagnosis of Barth syndrome (BTHS) was available for 39/42 of the participants. Of 39 patients, 13 have a missense mutation, 6 have a nonsense mutation, 8 have a splicing mutation, 6 have a small out-of-frame insertion or deletion, 2 have a small in-frame insertion, and 4 have a large deletion encompassing several exons
establish a new cancer stem cell signalling pathway downstream of mtp53 in which AKT2 (zeige AKT2 Antikörper) regulates WIP (zeige WIPF1 Antikörper) and controls YAP (zeige YAP1 Antikörper)/TAZ stability.
identify the mesenchymal requirement of YAP (zeige YAP1 Antikörper)/TAZ in the gastrointestinal tract and highlight the functional interplays between Hippo and Hedgehog (zeige SHH Antikörper) signaling underlying temporal and spatial control of tissue growth and specification in developing gut (zeige GUSB Antikörper)
The results uncover an important aspect of the cross-talk between TGFbeta (zeige TGFB1 Antikörper) and Hippo signaling, showing that TGFbeta (zeige TGFB1 Antikörper) induces TAZ via a Smad3 (zeige SMAD3 Antikörper)-independent, p38 (zeige CRK Antikörper)- and MRTF-mediated and yet MRTF translocation-independent mechanism.
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 (zeige YAP1 Antikörper)/TAZ orchestrate an immunosuppressive response following myocardial infarction
Yap (zeige YAP1 Antikörper) and Taz are activated in Schwann cells by mechanical stimuli and regulate Schwann cell proliferation and transcription of basal lamina receptor genes
transient expression of exogenous YAP (zeige YAP1 Antikörper) or its closely related paralogue TAZ in primary differentiated mouse cells can induce conversion to a tissue-specific stem/progenitor cell state.
The impact of endurance training on the cardiac and skeletal muscle phenotype in young TAZ knock-down mice.
impaired Taz-function with onset at adult age does not enhance susceptibility to ischemia-reperfusion injury.
A novel role for Taz in helping to maintain genome integrity in spermatocyte meiosis and facilitating germ cell differentiation.
Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress
This gene encodes a protein that is expressed at high levels in cardiac and skeletal muscle. Mutations in this gene have been associated with a number of clinical disorders including Barth syndrome, dilated cardiomyopathy (DCM), hypertrophic DCM, endocardial fibroelastosis, and left ventricular noncompaction (LVNC). Multiple transcript variants encoding different isoforms have been described. A long form and a short form of each of these isoforms is produced\; the short form lacks a hydrophobic leader sequence and may exist as a cytoplasmic protein rather than being membrane-bound. Other alternatively spliced transcripts have been described but the full-length nature of all these transcripts is not known.
, protein G4.5
, Barth syndrome)
, endocardial fibroelastosis 2
, tafazzin (cardiomyopathy, dilated 3A (X-linked)
, tafazzin (cardiomyopathy, dilated 3A (X-linked); endocardial fibroelastosis 2; Barth syndrome)