Tafazzin Antibody (E-3): sc-377434

Tafazzin Antibody (E-3) is a mouse monoclonal IgG1 antibody that detects Tafazzin in mouse, rat, and human samples through applications such as western blotting (WB), immunoprecipitation (IP), immunofluorescence (IF), and enzyme-linked immunosorbent assay (ELISA). Tafazzin is a crucial single-pass membrane protein predominantly found in cardiac and skeletal muscle, where Tafazzin plays a vital role in maintaining mitochondrial structure and function. Tafazzin (E-3) antibody recognizes various isoforms, with those featuring hydrophobic N-terminal domains being membrane-anchored, while shorter isoforms lacking this domain may be found in the cytoplasm. The presence of these isoforms suggests a diverse functional repertoire of Tafazzin, influencing not only mitochondrial dynamics but also cellular signaling pathways. Mutations in the Tafazzin gene have been linked to several serious conditions, including dilated cardiomyopathy, hypertrophic cardiomyopathy, endocardial fibroelastosis, left ventricular noncompaction, and Barth syndrome, a severe inherited disorder characterized by neutropenia, cardiac and skeletal myopathy, and short stature. Anti-Tafazzin antibody (E-3) serves as an essential tool for researchers investigating this protein in health and disease, providing insights into Tafazzin function and dysregulation.

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Tafazzin Antibody (E-3) References:

1. Tafazzin splice variants and mutations in Barth syndrome.  |  Kirwin, SM., et al. 2014. Mol Genet Metab. 111: 26-32. PMID: 24342716
2. Increased Dynamin-Related Protein 1-Dependent Mitochondrial Fission Contributes to High-Fat-Diet-Induced Cardiac Dysfunction and Insulin Resistance by Elevating Tafazzin in Mouse Hearts.  |  Chang, W., et al. 2019. Mol Nutr Food Res. 63: e1801322. PMID: 30632304
3. Tafazzin-dependent cardiolipin composition in C6 glioma cells correlates with changes in mitochondrial and cellular functions, and cellular proliferation.  |  Gürtler, S., et al. 2019. Biochim Biophys Acta Mol Cell Biol Lipids. 1864: 452-465. PMID: 30639735
4. Tafazzin modulates cellular phospholipid composition to regulate AML stemness.  |  Seneviratne, AK., et al. 2019. Mol Cell Oncol. 6: e1620051. PMID: 31528696
5. Tafazzin deficiency impairs CoA-dependent oxidative metabolism in cardiac mitochondria.  |  Le, CH., et al. 2020. J Biol Chem. 295: 12485-12497. PMID: 32665401
6. Tafazzin Mutation Affecting Cardiolipin Leads to Increased Mitochondrial Superoxide Anions and Mitophagy Inhibition in Barth Syndrome.  |  Petit, PX., et al. 2020. Cells. 9: PMID: 33096711
7. miR‑125a‑5p reverses epithelial‑mesenchymal transition and restores drug sensitivity by negatively regulating TAFAZZIN signaling in breast cancer.  |  Li, D., et al. 2021. Mol Med Rep. 24: PMID: 34549308
8. Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes.  |  Zegallai, HM., et al. 2022. FASEB J. 36: e22443. PMID: 35816277
9. Tafazzin deficiency attenuates anti-cluster of differentiation 40 and interleukin-4 activation of mouse B lymphocytes.  |  Zegallai, HM., et al. 2022. Cell Tissue Res. 390: 429-439. PMID: 36129532
10. Phenotypic Characterization of Female Carrier Mice Heterozygous for Tafazzin Deletion.  |  Tomczewski, MV., et al. 2023. Biology (Basel). 12: PMID: 37759637

The preferred Tafazzin antibody is Tafazzin Antibody (F-7): sc-365810.