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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 (5) 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.
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
establish a new cancer stem cell signalling pathway downstream of mtp53 in which AKT2 (show AKT2 Antibodies) regulates WIP (show WIPF1 Antibodies) and controls YAP (show YAP1 Antibodies)/TAZ stability.
High TAZ expression is associated with non-small cell lung cancer.
TAZ is overexpressed in cervical cancer and may promote tumorigenicity of cervical cancer cells and inhibit apoptosis.
TAZ mutation is associated with Barth syndrome.
Wnt (show WNT2 Antibodies) signaling upregulated WBP2 (show WBP2 Antibodies) by disrupting ITCH-WBP2 (show WBP2 Antibodies) interactions via EGFR (show EGFR Antibodies)-mediated tyrosine phosphorylation of WBP2 (show WBP2 Antibodies) and TAZ/YAP (show YAP1 Antibodies) competitive binding.
Data suggest that 14-3-3 sigma protein (show SFN Antibodies) exhibits two individual secondary binding sites for peptide fragments of TAZ protein; these two pockets appear to be part of at least three physiologically relevant and structurally characterized 14-3-3 protein (show YWHAE Antibodies)-protein interaction interfaces.
AXL (show AXL Antibodies)/TAZ/YAP (show YAP1 Antibodies) expression is associated with poor prognosis in male breast cancer patients.
results highlight both CYR61 (show CYR61 Antibodies) 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
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.
Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress
TAZ mutation is necessary and sufficient for the phenotype of sparse and irregular sarcomeres and weak myocaridal contraction foudn in Barth syndrome.
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)