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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 (151) and TAZ Kits (6) 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.
High TAZ expression is associated with cisplatin-resistance in gastric cancer.
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.
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
TAZ is overexpressed in cervical cancer and may promote tumorigenicity of cervical cancer cells and inhibit apoptosis.
TAZ mutation is associated with Barth syndrome.
Molecular analysis of at risk female family members identified the patient's sister and mother as heterozygous carriers. Apparently harmless synonymous variants in the TAZ gene can damage gene expression. Such findings widen our knowledge of molecular heterogeneity in Barth syndrome.
two novel and non-identical TAZ gene rearrangements were found in the offspring of a single female carrier of Barth syndrome.
Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress
ability of CL-ND to elicit a physiological response was examined in an HL60 cell culture model of Barth Syndrome neutropenia. siRNA knockdown of the phospholipid transacylase, tafazzin (TAZ), induced apoptosis in these cells
novel mutation in exon 1 of the TAZ gene and female mosaicism in three generations of a Polish family with Barth syndrome
results suggest that plasmenylcholine, abundant in linoleoyl species, is important in remodeling CL in the heart. Tafazzin deficiency thus has a major impact on the cardiac plasmenylcholine level and thereby its functions.
Therefore, YAP (show YAP1 Proteins)/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 Proteins)/TAZ in the gastrointestinal tract and highlight the functional interplays between Hippo and Hedgehog (show SHH Proteins) signaling underlying temporal and spatial control of tissue growth and specification in developing gut (show GUSB Proteins)
The results uncover an important aspect of the cross-talk between TGFbeta (show TGFB1 Proteins) and Hippo signaling, showing that TGFbeta (show TGFB1 Proteins) induces TAZ via a Smad3 (show SMAD3 Proteins)-independent, p38 (show CRK Proteins)- 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 Proteins)/TAZ orchestrate an immunosuppressive response following myocardial infarction
Yap (show YAP1 Proteins) 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 Proteins) 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.
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)