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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 (132) and TAZ Proteins (13) and many more products for this protein.
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Taz is required in the anteroposterior patterning of the pronephric progenitor domain in the intermediate mesoderm, acting in part by regulating retinoic acid signaling in the pronephric progenitor field in the intermediate mesoderm.
Taz-depleted larvae displayed patterning defects in ventral cranial vessels that correlate with lateral displacement of thyroid follicles.
Yap (show YAP1 ELISA Kits)/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt retinal pigment epithelium identity in zebrafish.
When transcriptional coactivators Yap (show YAP1 ELISA Kits) and Taz were restricted from interacting with Tead transcription factors through expression of a dominant negative transgene, cardiac precursors failed to migrate completely to the midline.
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.
ABL (show ABL1 ELISA Kits) kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 (show STAT5A ELISA Kits) signaling.
Results show TAZ functioned as an oncogene (show RAB1A ELISA Kits) and promoted pancreatic cancer epithelial-mesenchymal transition and progression.
A YAP (show YAP1 ELISA Kits)/TAZ-miR (show MLXIP ELISA Kits)-130/301 molecular circuit exerts systems-level control of fibrosis in a network of human diseases and physiologic conditions
these data reveal a previously unknown role for TAZ and the Hippo pathway in the progression of aggressive subtypes of endometrial cancer.
two novel and non-identical TAZ gene rearrangements were found in the offspring of a single female carrier of Barth syndrome.
The TAZ play an essential role in amino acid-induced mTORC1 activation, particularly under nutrient-limiting conditions.
factor:TAZ transcriptional co-activator and activation of sE-Cadherin/proto-oncogene (show RAB1A ELISA Kits) protein HER-2 (show ERBB2 ELISA Kits) signaling could be potential oncogenic pathways for breast cancer (BC) metastasis.
preS2 upregulates TAZ expression by repressing miRNA-338-3p. TAZ is necessary for preS2-promoted HCC (show FAM126A ELISA Kits) proliferation and migration.
Actin remodeling confers BRAF (show BRAF ELISA Kits) inhibitor resistance to melanoma cells through YAP (show YAP1 ELISA Kits)/TAZ activation
Data suggest that activation of TAZ (tafazzin) inhibits adipogenesis in mesenchymal stem cells; interaction of TAZ and protein phosphatases (PP1A (show PPP1CA ELISA Kits), PP2A (show PPP2R4 ELISA Kits)) up-regulates dephosphorylation and transport of TAZ to cell nucleus.
These findings uncover important roles for Yap (show YAP1 ELISA Kits) and Taz in cranial neural crest diversification and development.
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.
Study discovered Ythat AP/TAZ are bona fide downstream effectors of the alternative Wnt (show WNT2 ELISA Kits) signaling pathway.
A novel role for Taz in helping to maintain genome integrity in spermatocyte meiosis and facilitating germ cell differentiation.
Hippo signalling effectors, YAP (show YAP1 ELISA Kits) and TAZ, promote both the proliferation of intestinal stem/progenitor cells and their differentiation into goblet cells.
Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress
This study identifies a novel mechanism of TAZ regulation by YAP (show YAP1 ELISA Kits), which has significant implications for our understanding of Hippo pathway regulation, YAP (show YAP1 ELISA Kits)-isoform specific signaling, and the role of these proteins in cell proliferation, apoptosis, and tumorigenesis.
YAP (show YAP1 ELISA Kits)/TAZ regulate transcriptional elongation from the enhancer elements by recruiting the Mediator complex and promoting phenotypes of overgrowth and tumorigenesis.
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)