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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 (4) and many more products for this protein.
Showing 10 out of 135 products:
Human Monoclonal TAZ Primary Antibody for ELISA - ABIN394550
Zimmerman, Cox, Lakdawala, Cirino, Mancini-DiNardo, Clark, Leon, Duffy, White, Baxter, Alaamery, Farwell, Weiss, Seidman, Seidman, Ho, Rehm, Funke: A novel custom resequencing array for dilated cardiomyopathy. in Genetics in medicine : official journal of the American College of Medical Genetics 2010
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Human Monoclonal TAZ Primary Antibody for ELISA - ABIN395886
Strakova, Reed, Ihnatovych: Human transcriptional coactivator with PDZ-binding motif (TAZ) is downregulated during decidualization. in Biology of reproduction 2010
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Human Polyclonal TAZ Primary Antibody for WB - ABIN871734
Kanai, Marignani, Sarbassova, Yagi, Hall, Donowitz, Hisaminato, Fujiwara, Ito, Cantley, Yaffe: TAZ: a novel transcriptional co-activator regulated by interactions with 14-3-3 and PDZ domain proteins. in The EMBO journal 2001
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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 EIA, WB - ABIN453847
Gedeon, Wilson, Colley, Sillence, Mulley: X linked fatal infantile cardiomyopathy maps to Xq28 and is possibly allelic to Barth syndrome. in Journal of medical genetics 1995
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Dog (Canine) Polyclonal TAZ Primary Antibody for WB - ABIN374615
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
Human Polyclonal TAZ Primary Antibody for FACS, IHC (p) - ABIN652751
Bione, DAdamo, Maestrini, Gedeon, Bolhuis, Toniolo: A novel X-linked gene, G4.5. is responsible for Barth syndrome. in Nature genetics 1996
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.
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
mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes
Strong expression of TAZ protein seems to be related to rectal cancer development and RT response, it can be a predictive biomarker of distant recurrence in patients with preoperative RT.
Three novel hemizygous mutations in the TAZ gene were found (c.584G>T; c.109+6T>C; c.86G>A). We conclude that Barth syndrome should be included in differential diagnosis of cardiomyopathy in childhood.
Results show that in both healthy controls and in Barth syndrome patients, a greater variety of alternatively spliced forms than previously described was found. It includes a sizeable proportion of minor splice variants besides the four dominant isoforms.
data suggest that genes other than G4.5 are responsible for the familial form of noncompaction of the ventricular myocardium
study reports five new TAZ gene mutations in six unrelated Barth Syndrome patients, including two new gross gene rearrangements
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.
TAZ mutation is necessary and sufficient for the phenotype of sparse and irregular sarcomeres and weak myocaridal contraction foudn in Barth syndrome.
Tafazzin knockdown mice provide a mammalian model system for Barth syndrome in which the pathophysiological relationships between altered content of mitochondrial phospholipids, ultrastructural abnormalities, myocardial and mitochondrial dysfunction
The data suggest that tafazzin deficiency affects cardiolipin in all mitochondria, but significant alterations of the ultrastructure, such as remodeling and aggregation of inner membranes, will only occur after specific 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)