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TAZ encodes a protein that is expressed at high levels in cardiac and skeletal muscle. Additionally we are shipping TAZ Antibodies (144) and TAZ Proteins (13) and many more products for this protein.
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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.
Nuclear localization of YAP (show YAP1 ELISA Kits) and TAZ was reduced in DMOG-treated primary tubular epithelial cells.
mechanistic study revealed that miR (show MLXIP ELISA Kits)-224 functions by inhibiting the tumor suppressor, SMAD4 (show SMAD4 ELISA Kits), to support the proliferation and migration of osteosarcoma (OS) cells. Our findings indicate that targeting TAZ and miR (show MLXIP ELISA Kits)-224 could be a promising approach for the treatment of OS.
TAZ was positively correlated with EGFR (show EGFR ELISA Kits) signaling, and coexpression of TAZ/EGFR (show EGFR ELISA Kits) 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 ELISA Kits)-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 ELISA Kits) regulates WIP (show WIPF1 ELISA Kits) and controls YAP (show YAP1 ELISA Kits)/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 ELISA Kits) signaling upregulated WBP2 (show WBP2 ELISA Kits) by disrupting ITCH-WBP2 (show WBP2 ELISA Kits) interactions via EGFR (show EGFR ELISA Kits)-mediated tyrosine phosphorylation of WBP2 (show WBP2 ELISA Kits) and TAZ/YAP (show YAP1 ELISA Kits) competitive binding.
Data suggest that 14-3-3 sigma protein (show SFN ELISA Kits) 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 ELISA Kits)-protein interaction interfaces.
identify the mesenchymal requirement of YAP (show YAP1 ELISA Kits)/TAZ in the gastrointestinal tract and highlight the functional interplays between Hippo and Hedgehog (show SHH ELISA Kits) signaling underlying temporal and spatial control of tissue growth and specification in developing gut (show GUSB ELISA Kits)
The results uncover an important aspect of the cross-talk between TGFbeta (show TGFB1 ELISA Kits) and Hippo signaling, showing that TGFbeta (show TGFB1 ELISA Kits) induces TAZ via a Smad3 (show SMAD3 ELISA Kits)-independent, p38 (show CRK ELISA Kits)- 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 ELISA Kits)/TAZ orchestrate an immunosuppressive response following myocardial infarction
Yap (show YAP1 ELISA Kits) 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 ELISA Kits) 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)