Tafazzin (TAZ) ELISA Kits

TAZ encodes a protein that is expressed at high levels in cardiac and skeletal muscle. Additionally we are shipping TAZ Antibodies (163) and TAZ Proteins (13) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
TAZ 6901 Q16635
Anti-Mouse TAZ TAZ 66826  
Anti-Rat TAZ TAZ 363521  
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Top TAZ ELISA Kits at antibodies-online.com

Showing 3 out of 7 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Delivery Price Details
Human 0.057 ng/mL 0.15 ng/mL - 10 ng/mL 96 Tests 13 to 16 Days
$736.84
Details
Human
  96 Tests 26 to 36 Days
$899.80
Details
Human < 0.054 ng/mL 0.156 ng/mL - 10 ng/mL   96 Tests 11 to 18 Days
$902.56
Details

More ELISA Kits for 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. intrinsic mitochondrial localization sequences in the human TAZ protein, were identified.

  2. Analysis of enzymes that mediate the conversion of glutamate to alpha-ketoglutarate shows that TAZ/YAP induce glutamic-oxaloacetic transaminase (GOT1) and phosphoserine aminotransferase (PSAT1) expression and that TAZ/YAP activity positively correlates with transaminase expression in breast cancer patients.

  3. Nuclear TAZ expression correlates with increased collagen abundance in melanoma.

  4. TAZ(Q233del) plays a major role in regulating malignancy of cancer cells by hijacking Hippo pathway.

  5. 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.

  6. 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.

  7. 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.

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

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

  10. 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.

  11. 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

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

  13. TAZ mutation is associated with Barth syndrome.

  14. 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.

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

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

  17. 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

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

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

  20. 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.

Mouse (Murine) Tafazzin (TAZ) interaction partners

  1. in vitro studies demonstrate that mitochondria-targeted antioxidants improve contractile capacity in TAZ-deficient cardiomyocytes. The purpose of the present study was to determine if resolving mitochondrial oxidative stress would be sufficient to prevent cardiomyopathy and skeletal myopathy in vivo using a mouse model of Barth Syndrome

  2. Tafazzin was elevated in the hearts of high-fat-diet fed mice.Increased tafazzin contributes to insulin resistance via mediating Drp-1 translocation to the mitochondria.

  3. Findings demonstrate that TAZ-mediated remodeling of cardiolipin (CL) contributes significantly to the expansive distribution of CL molecular species in the brain, plays a key role in mitochondria respiratory activity, maintains normal cognitive function.

  4. targeting mTORC2 retards fibroblast activation and kidney fibrosis through suppressing Yap/Taz activation.

  5. 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.

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

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

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

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

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

  11. 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

  12. 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 Antigen Profile

Antigen 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 (TAZ) ELISA Kits

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

Protein level used designations for Tafazzin (TAZ) ELISA Kits

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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