Tafazzin Proteins (TAZ)

TAZ encodes a protein that is expressed at high levels in cardiac and skeletal muscle. Additionally we are shipping TAZ Antibodies (159) and TAZ Kits (7) and many more products for this protein.

list all proteins Gene Name GeneID UniProt
TAZ 6901 Q16635
TAZ 66826  
TAZ 363521  
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Top TAZ Proteins at antibodies-online.com

Showing 10 out of 13 products:

Catalog No. Origin Source Conjugate Images Quantity Supplier Delivery Price Details
Insect Cells Human rho-1D4 tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 0.5 mg Log in to see 50 to 55 Days
$7,493.38
Details
Escherichia coli (E. coli) Human His tag,T7 tag 100 μg Log in to see 15 to 18 Days
$752.00
Details
Escherichia coli (E. coli) Mouse His tag,T7 tag 100 μg Log in to see 15 to 18 Days
$768.00
Details
Escherichia coli (E. coli) Rat His tag,T7 tag 100 μg Log in to see 15 to 18 Days
$976.00
Details
Wheat germ Human GST tag 10 μg Log in to see 11 to 12 Days
$414.29
Details
Yeast REACT_Squirrel Monkey His tag   1 mg Log in to see 60 to 71 Days
$2,678.50
Details
Yeast Rhesus Monkey His tag   1 mg Log in to see 60 to 71 Days
$2,678.50
Details
Yeast Primate His tag   1 mg Log in to see 60 to 71 Days
$2,678.50
Details
Yeast Chimpanzee His tag   1 mg Log in to see 60 to 71 Days
$2,772.00
Details
Yeast Pongo pygmaeus His tag   1 mg Log in to see 60 to 71 Days
$2,772.00
Details

TAZ Proteins by Origin and Source

Origin Expressed in Conjugate
Human , ,
, ,
Mouse (Murine)

Rat (Rattus)

More Proteins for Tafazzin (TAZ) Interaction Partners

Zebrafish Tafazzin (TAZ) interaction partners

  1. Disrupted gene function in yap1(-/-); taz(+/-) embryos did not disturb liver bud formation, but instead impaired cell proliferation in liver and movement of the neighboring lateral plate mesoderm (LPM). Overexpression of wild type yap1 or taz could rescue the defective liver phenotypes in yap1(-/-); taz(+/-) embryos.

  2. 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.

  3. 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.

Human Tafazzin (TAZ) interaction partners

  1. Study characterized structural and metabolic adaptations in Barth syndrome patients primary skin fibroblasts and provided novel insights into the molecular details of supercomplex destabilization, aberrant cristae morphology and metabolic changes resulting from TAZ mutations.

  2. Molecular mechanisms of TAZ protein in the lung physiological conditions and lung diseases.[review]

  3. 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.

  4. Report left ventricular non-compaction associated with Barth Syndrome due to triple mutations in TAZ, DTNA, and SDHA genes in multiple members of one family.

  5. TAZ overexpression is associated with poor response to chemotherapy in chronic myeloid leukemia.

  6. High TAZ expression is associated with cisplatin-resistance in gastric cancer.

  7. 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.

  8. 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

  9. TAZ is overexpressed in cervical cancer and may promote tumorigenicity of cervical cancer cells and inhibit apoptosis.

  10. TAZ mutation is associated with Barth syndrome.

  11. 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.

  12. two novel and non-identical TAZ gene rearrangements were found in the offspring of a single female carrier of Barth syndrome.

  13. Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress

  14. 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

  15. novel mutation in exon 1 of the TAZ gene and female mosaicism in three generations of a Polish family with Barth syndrome

  16. mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes

  17. 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.

  18. 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.

  19. 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.

  20. data suggest that genes other than G4.5 are responsible for the familial form of noncompaction of the ventricular myocardium

Mouse (Murine) Tafazzin (TAZ) interaction partners

  1. 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.

  2. 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.

  3. Therefore, YAP/TAZ are crucial for Schwann cells to myelinate developing nerve and to maintain myelinated nerve in adulthood.

  4. identify the mesenchymal requirement of YAP/TAZ in the gastrointestinal tract and highlight the functional interplays between Hippo and Hedgehog signaling underlying temporal and spatial control of tissue growth and specification in developing gut

  5. The results uncover an important aspect of the cross-talk between TGFbeta and Hippo signaling, showing that TGFbeta induces TAZ via a Smad3-independent, p38- and MRTF-mediated and yet MRTF translocation-independent mechanism.

  6. Wnt/beta-catenin signaling via Axin2 is required for myogenesis and, together with YAP/Taz and Tead1, active in IIa/IIx muscle fibers

  7. Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarction

  8. Yap and Taz are activated in Schwann cells by mechanical stimuli and regulate Schwann cell proliferation and transcription of basal lamina receptor genes

  9. transient expression of exogenous YAP or its closely related paralogue TAZ in primary differentiated mouse cells can induce conversion to a tissue-specific stem/progenitor cell state.

  10. The impact of endurance training on the cardiac and skeletal muscle phenotype in young TAZ knock-down mice.

  11. impaired Taz-function with onset at adult age does not enhance susceptibility to ischemia-reperfusion injury.

  12. A novel role for Taz in helping to maintain genome integrity in spermatocyte meiosis and facilitating germ cell differentiation.

  13. Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress

  14. TAZ mutation is necessary and sufficient for the phenotype of sparse and irregular sarcomeres and weak myocaridal contraction foudn in Barth syndrome.

  15. 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

  16. 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.

TAZ Protein Profile

Protein Summary

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.

Gene names and symbols associated with Tafazzin Proteins (TAZ)

  • tafazzin (TAZ)
  • tafazzin (taz)
  • tafazzin L homeolog (taz.L)
  • tafazzin homolog (LOC550948)
  • tafazzin (AFUA_2G13960)
  • tafazzin (AOR_1_318014)
  • tafazzin (Tsp_06712)
  • tafazzin (Taz)
  • 5031411C02Rik protein
  • 9130012G04Rik protein
  • Afu2g13960 protein
  • AW107266 protein
  • AW552613 protein
  • BTHS protein
  • CMD3A protein
  • EFE protein
  • EFE2 protein
  • G4.5 protein
  • GB11956 protein
  • LVNCX protein
  • MGC54019 protein
  • taz protein
  • Taz1 protein
  • wu:fb39f12 protein
  • zgc:91803 protein

Protein level used designations for Tafazzin Proteins (TAZ)

tafazzin , Tafazzin , 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)

GENE ID SPECIES
100446947 Pongo abelii
321965 Danio rerio
379259 Xenopus laevis
515177 Bos taurus
549220 Xenopus (Silurana) tropicalis
550948 Apis mellifera
3513201 Aspergillus fumigatus Af293
5993687 Aspergillus oryzae RIB40
10911739 Trichinella spiralis
100137265 Papio anubis
100196028 Salmo salar
100328759 Oryctolagus cuniculus
100528715 Ictalurus punctatus
6901 Homo sapiens
66826 Mus musculus
363521 Rattus norvegicus
612975 Canis lupus familiaris
449590 Pan troglodytes
574297 Macaca mulatta
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