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TAZ encodes a protein that is expressed at high levels in cardiac and skeletal muscle. Additionally we are shipping TAZ Proteins (13) and TAZ Kits (6) and many more products for this protein.
Showing 10 out of 144 products:
Human Monoclonal TAZ Primary Antibody for 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 Monoclonal TAZ Primary Antibody for 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 Polyclonal TAZ Primary Antibody for 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
Show all 2 Pubmed References
Human Polyclonal TAZ Primary Antibody for 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.
This is the first report of systematic mutation screening of TAZ in a large cohort of pediatric patients with primary cardiomyopathy using the NGS approach. TAZ mutations were found in 4/114 (3.5%) male patients with primary cardiomyopathy. Our findings indicate that the inclusion of TAZ gene testing in cardiomyopathy genetic testing panels may contribute to the early diagnosis of BTHS.
High TAZ expression is associated with breast cancer.
Together, these data illustrate that YAP (show YAP1 Antibodies)/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 (show YAP1 Antibodies) and TAZ activity in cultured podocyte cell line grown on stiff substrates.
factors YAP (show YAP1 Antibodies) and TAZ as mechanotransducers started to fill this gap. YAP (show YAP1 Antibodies) 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 (show YAP1 Antibodies) and TAZ was reduced in DMOG-treated primary tubular epithelial cells.
mechanistic study revealed that miR (show MLXIP Antibodies)-224 functions by inhibiting the tumor suppressor, SMAD4 (show SMAD4 Antibodies), to support the proliferation and migration of osteosarcoma (OS) cells. Our findings indicate that targeting TAZ and miR (show MLXIP Antibodies)-224 could be a promising approach for the treatment of OS.
TAZ was positively correlated with EGFR (show EGFR Antibodies) signaling, and coexpression of TAZ/EGFR (show EGFR Antibodies) 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 (show EGFR Antibodies)-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
Therefore, YAP (show YAP1 Antibodies)/TAZ are crucial for Schwann cells to myelinate developing nerve and to maintain myelinated nerve in adulthood.
identify the mesenchymal requirement of YAP (show YAP1 Antibodies)/TAZ in the gastrointestinal tract and highlight the functional interplays between Hippo and Hedgehog (show SHH Antibodies) signaling underlying temporal and spatial control of tissue growth and specification in developing gut (show GUSB Antibodies)
The results uncover an important aspect of the cross-talk between TGFbeta (show TGFB1 Antibodies) and Hippo signaling, showing that TGFbeta (show TGFB1 Antibodies) induces TAZ via a Smad3 (show SMAD3 Antibodies)-independent, p38 (show CRK Antibodies)- 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 (show YAP1 Antibodies)/TAZ orchestrate an immunosuppressive response following myocardial infarction
Yap (show YAP1 Antibodies) 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 (show YAP1 Antibodies) 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.
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)