Results 191 to 200 of about 3,950 (204)

Drosophila Mitochondrial Membrane‐bound Tafazzin Protein Is A Transacylase

The FASEB Journal, 2007
Barth syndrome is an X‐linked mitochondria disorder with skeleton myopathy, cardiomyopathy and neutropenia, resulting from the tafazzin mutation. As demonstrated previously [Xu et al.: PNAS 103:11584, 2006], the mutation of full length Drosophila ...
Yang Xu, Mindong Ren, Ashim Malhotra, Louis Lee, Jin Zhang, Thomas JJ Blanck, Michael Schlame   +6 more
openaire   +1 more source

Tafazzin knockdown interrupts cell cycle progression in cultured neonatal ventricular fibroblasts

American Journal of Physiology-Heart and Circulatory Physiology, 2013
Mutation of the mitochondrial protein tafazzin causes dilated cardiomyopathy in Barth syndrome. Previous studies have shown that tafazzin knockdown promotes hypertrophy of neonatal cardiac myocytes. The current investigation was designed to show whether tafazzin knockdown affects cardiac fibroblast proliferation and collagen secretion, which contribute
Quan, He, Miao, Wang, Nicole, Harris, Xianlin, Han   +3 more
openaire   +2 more sources

Tafazzin contributes to IgE‐mediated mast cell degranulation and cytokine secretion

The FASEB Journal, 2020
Prevalence of allergic pathologies, such as food allergies, asthma, and atopic dermatitis, have been on the rise over the past several decades with approximately 40% of children in developed nations suffering one of these chronic inflammatory diseases. These pathologies, driven largely by
Aindriu R. R. Maguire, Robert W. E. Crozier, Paul J. LeBlanc, Adam J. MacNeil   +3 more
openaire   +1 more source

Abstract 18250: Tafazzin-Knockdown Mice: Heart Mitochondrial Structure and Function

Circulation, 2013
Barth syndrome is a genetic disorder with mutations in the tafazzin gene resulting in cardiomyopathy, hypotonia, growth delays, and cyclic neutropenia. Mitochondria have been examined for functional defects in Barth syndrome and defects found in oxidative phosphorylation, a decreased content and abnormal composition of cardiolipin, and an increased ...
Junhwas Kim, Hisashi Fujioka, Bernard Tandler, Charles Hoppel   +3 more
openaire   +1 more source

Cardiac Pathology in a Patient with a Novel Pathogenic Variant c.703del (p.Ile235SerfsTer4) of the TAFAZZIN Gene.

Cardiovascular pathology
M. Prasanpanich, Majid Husain, N. Halnon, Richard Chang, Neda Zadeh, Jason Knight, Gregory A. Fishbein   +6 more
semanticscholar   +1 more source

Tafazzin-Mediated Cardiolipin Remodeling Controls Metabolic Stress Response and Effector Function of Inflammatory T Cells

bioRxiv
Xiufeng Zhao, Sophia M. Hochrein, Miriam Eckstein, Hao Wu, Katrin Sinning, Katharina J. Ermer, Sarah-Lena Puhl, Martin Eilers, Werner Schmitz, Christian Stigloher, S. Claypool, Christoph Maack, Jan Dudek, Martin Vaeth   +13 more
semanticscholar   +1 more source

Tafazzin deficiency attenuates anti-cluster of differentiation 40 and interleukin-4 activation of mouse B lymphocytes

Cell and Tissue Research, 2022
Hana M. Zegallai, Ejlal Abu-El-Rub, Edgard M. Mejia, G. Sparagna, L. Cole, A. Marshall, G. Hatch   +6 more
semanticscholar   +1 more source

The role of cardiolipin in molecular assemblies of tafazzin

Mitochondrion, 2011
Ashim Malhotra⁎, Devrim Acehan, Mindong Ren, Michael Schlame   +3 more
openaire   +1 more source

A linear algebra model of the tafazzin reaction

Chemistry and Physics of Lipids, 2008
openaire   +1 more source

Defective cardiomyocyte mitophagy in TAFAZZIN deficiency: New implications for cellular pathogenesis in Barth syndrome

Molecular Genetics and Metabolism
Olivia Sniezek Carney, Kyuna Lee, K. Harris, Grant Butschek, A. Anzmann, Anne Hammacher-Brady, Hilary Vernon   +6 more
semanticscholar   +1 more source