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TAZ encodes a protein that is expressed at high levels in cardiac and skeletal muscle. 再加上，我们可以发TAZ 蛋白 (13) 和 TAZ 试剂盒 (7)和数多这个蛋白质的别的产品。
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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 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
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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.
We report a novel TAZ gene mutation in male and female siblings with left ventricular noncompaction and hypotonia. Additionally, the brother presented an intermittent neutropenia and increased urinary levels of 3-methylglutaconic and 3-methylglutaric acid. The molecular genetic testing showed that both siblings carry the mutation: c.253insC, p.(Arg85Profs*54) in exon 3 of the TAZ gene. Normal karyotype female.
Report left ventricular non-compaction associated with Barth Syndrome due to triple mutations in TAZ, DTNA (显示 DTNA 抗体), and SDHA (显示 SDHA 抗体) genes in multiple members of one family.
TAZ overexpression is associated with poor response to chemotherapy in chronic myeloid leukemia (显示 BCL11A 抗体).
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.
During and after liver development, the activation of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epithelial cell lineage.
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 (显示 YAP1 抗体)/TAZ are crucial for Schwann cells to myelinate developing nerve and to maintain myelinated nerve in adulthood.
identify the mesenchymal requirement of YAP (显示 YAP1 抗体)/TAZ in the gastrointestinal tract and highlight the functional interplays between Hippo and Hedgehog (显示 SHH 抗体) signaling underlying temporal and spatial control of tissue growth and specification in developing gut (显示 GUSB 抗体)
The results uncover an important aspect of the cross-talk between TGFbeta (显示 TGFB1 抗体) and Hippo signaling, showing that TGFbeta (显示 TGFB1 抗体) induces TAZ via a Smad3 (显示 SMAD3 抗体)-independent, p38 (显示 CRK 抗体)- 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 (显示 YAP1 抗体)/TAZ orchestrate an immunosuppressive response following myocardial infarction
Yap (显示 YAP1 抗体) 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 (显示 YAP1 抗体) 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.
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)