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Publikováno v:
Journal of Molecular and Cellular Cardiology. 136:42-52
The C-terminal end segment of troponin subunit I (TnI) is a structure highly conserved among the three muscle type-specific isoforms and across vertebrate species. Partial deletion or point mutation in this segment impairs cardiac muscle relaxation.
Autor:
Charles F. McTiernan, Iain Scott, Janet R. Manning, Javier Traba, Catherine Corey, Michael W. Stoner, Dharendra Thapa, Manling Zhang, Michael N. Sack, Sruti Shiva
Publikováno v:
Journal of Molecular and Cellular Cardiology. 129:69-78
GCN5L1 regulates mitochondrial protein acetylation, cellular bioenergetics, reactive oxygen species (ROS) generation, and organelle positioning in a number of diverse cell types. However, the functional role of GCN5L1 in the heart is currently unknow
Autor:
Edward J. Wentzler, Katsuhiko Funai, Anthony R.P. Verkerke, P. Darrell Neufer, Lisandra E. de Castro Brás, Jordan M. Johnson, Chanel B. Coleman, Kimberly A. Kew, Patrick J. Ferrara
Publikováno v:
Journal of Molecular and Cellular Cardiology. 121:94-102
Barth Syndrome (BTHS) is an X-linked recessive disorder characterized by cardiomyopathy and muscle weakness. The underlying cause of BTHS is a mutation in the tafazzin (TAZ) gene, a key enzyme of cardiolipin biosynthesis. The lack of CL arising from
Autor:
Bruno D. Stuyvers, Rebecca E. Daniels, John J. McGuire, Vincenzo Sorrentino, Elizabeth W. Chia, Kazi T. Haq, Masahito Miura, Lawson Miller
Publikováno v:
Journal of Molecular and Cellular Cardiology. 104:31-42
Background Three distinct Ca 2 + release channels were identified in dog P-cells: the ryanodine receptor subtype 2 ( RyR2 ) was detected throughout the cell, while the ryanodine receptor subtype 3 ( RyR3 ) and inositol phosphate sensitive Ca 2 + rele
Publikováno v:
Journal of Molecular and Cellular Cardiology. 99:65-75
The mammalian Na+/H+ exchanger isoform 1 (NHE1) is a ubiquitous plasma membrane protein that is a key regulator of intracellular pH in isolated cardiomyocytes. A 500 amino acid membrane domain removes protons and is regulated by a 315 amino acid cyto
Autor:
Jie Liu, Hiroyuki Kawagishi, Ilsa I. Rovira, Toren Finkel, Tomoko Yamazaki, Michael J. Wolfgang, Zu Xi Yu, Mitsunori Nomura, Yoh suke Mukouyama, Ye Yan, Chengyu Liu
Publikováno v:
J Mol Cell Cardiol
Atherosclerosis is a chronic disorder of the vessel wall. One key regulator of disease progression is lipid handling in macrophages. However, the role of macrophage mitochondrial-dependent fatty acid β-oxidation (FAO) in atherosclerosis is not well
Autor:
Jaewon Lee, Ho Jae Lee, Hyun-Jai Cho, In-Ho Chae, Jin Hur, Jung-Kyu Han, Young-Bae Park, Saet-Byeol Choi, Byung Hee Oh, Hyo-Soo Kim, Seok-Jin Koh, Back-Kyung Kim, Joo-Yun Won, Youngchul Shin, Injoo Hwang, Jeehoon Kang
Publikováno v:
Journal of Molecular and Cellular Cardiology. 97:266-277
Background Peroxisome proliferator-activated receptor (PPAR)-δ is a nuclear receptor regulating cell metabolism. The role of PPAR-δ in late endothelial progenitor cells (EPCs) has not been fully elucidated. We aim to understand the effects of PPAR-
Autor:
Leonardo J. Leon, Åsa B. Gustafsson
Publikováno v:
Journal of Molecular and Cellular Cardiology. 95:78-85
Aging is a predominant risk factor for developing cardiovascular disease. Therefore, the cellular processes that contributes to aging are attractive targets for therapeutic interventions that can delay or prevent the development of age-related diseas
Autor:
Hui-Young Lee, Monica Palmeri, Xiaohong Wu, Raymond R. Russell, Lawrence H. Young, Peter S. Rabinovitch, Dake Qi, Xiaoyue Hu, Vlad G. Zaha, Kevin N. Su, Gerald I. Shulman
Publikováno v:
Journal of Molecular and Cellular Cardiology. 91:104-113
AMP-activated kinase (AMPK) is a stress responsive kinase that regulates cellular metabolism and protects against cardiomyocyte injury during ischemia-reperfusion (IR). Mitochondria play an important role in cell survival, but the specific actions of
Autor:
Yeong-Renn Chen, Patrick T. Kang, Daniel J. Luther, J. Gary Meszaros, Vahagn Ohanyan, William M. Chilian, Chwen-Lih Chen
Publikováno v:
Journal of Molecular and Cellular Cardiology. 88:14-28
During heightened cardiac work, O2 consumption by the heart benefits energy production via mitochondria. However, some electrons leak from the respiratory chain and yield superoxide, which is rapidly metabolized into H2O2 by SOD2. To understand the s