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Complex I protein NDUFS2 is vital for growth, ROS generation, membrane integrity, apoptosis, and mitochondrial energetics.

Mitochondrion

Bandara AB, Drake JC, James CC, Smyth JW, Brown DA.
PMID: 33744462
Mitochondrion. 2021 May;58:160-168. doi: 10.1016/j.mito.2021.03.003. Epub 2021 Mar 18.

Complex I is the largest and most intricate of the protein complexes of mitochondrial electron transport chain (ETC). This L-shaped enzyme consists of a peripheral hydrophilic matrix domain and a membrane-bound orthogonal hydrophobic domain. The interfacial region between these...

Cite
Bandara AB, Drake JC, James CC, et al. Complex I protein NDUFS2 is vital for growth, ROS generation, membrane integrity, apoptosis, and mitochondrial energetics. Mitochondrion. 2021;58:160-168doi: 10.1016/j.mito.2021.03.003.
Bandara, A. B., Drake, J. C., James, C. C., Smyth, J. W., & Brown, D. A. (2021). Complex I protein NDUFS2 is vital for growth, ROS generation, membrane integrity, apoptosis, and mitochondrial energetics. Mitochondrion, 58160-168. https://doi.org/10.1016/j.mito.2021.03.003
Bandara, Aloka B, et al. "Complex I protein NDUFS2 is vital for growth, ROS generation, membrane integrity, apoptosis, and mitochondrial energetics." Mitochondrion vol. 58 (2021): 160-168. doi: https://doi.org/10.1016/j.mito.2021.03.003
Bandara AB, Drake JC, James CC, Smyth JW, Brown DA. Complex I protein NDUFS2 is vital for growth, ROS generation, membrane integrity, apoptosis, and mitochondrial energetics. Mitochondrion. 2021 May;58:160-168. doi: 10.1016/j.mito.2021.03.003. Epub 2021 Mar 18. PMID: 33744462; PMCID: PMC8113094.
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Translating Translation to Mechanisms of Cardiac Hypertrophy.

Journal of cardiovascular development and disease

Zeitz MJ, Smyth JW.
PMID: 32164190
J Cardiovasc Dev Dis. 2020 Mar 10;7(1). doi: 10.3390/jcdd7010009.

Cardiac hypertrophy in response to chronic pathological stress is a common feature occurring with many forms of heart disease. This pathological hypertrophic growth increases the risk for arrhythmias and subsequent heart failure. While several factors promoting cardiac hypertrophy are...

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Zeitz MJ, Smyth JW. Translating Translation to Mechanisms of Cardiac Hypertrophy. J Cardiovasc Dev Dis. 2020;7(1)doi: 10.3390/jcdd7010009.
Zeitz, M. J., & Smyth, J. W. (2020). Translating Translation to Mechanisms of Cardiac Hypertrophy. Journal of cardiovascular development and disease, 7(1), . https://doi.org/10.3390/jcdd7010009
Zeitz, Michael J, and Smyth, James W. "Translating Translation to Mechanisms of Cardiac Hypertrophy." Journal of cardiovascular development and disease vol. 7,1 (2020). doi: https://doi.org/10.3390/jcdd7010009
Zeitz MJ, Smyth JW. Translating Translation to Mechanisms of Cardiac Hypertrophy. J Cardiovasc Dev Dis. 2020 Mar 10;7(1). doi: 10.3390/jcdd7010009. PMID: 32164190; PMCID: PMC7151157.
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Altered translation initiation of .

Molecular biology of the cell

James CC, Zeitz MJ, Calhoun PJ, Lamouille S, Smyth JW.
PMID: 29467255
Mol Biol Cell. 2018 Apr 01;29(7):797-808. doi: 10.1091/mbc.E17-06-0406.

Epithelial-mesenchymal transition (EMT) is activated during development, wound healing, and pathologies including fibrosis and cancer metastasis. Hallmarks of EMT are remodeling of intercellular junctions and adhesion proteins, including gap junctions. The

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James CC, Zeitz MJ, Calhoun PJ, et al. Altered translation initiation of . Mol Biol Cell. 2018;29(7):797-808doi: 10.1091/mbc.E17-06-0406.
James, C. C., Zeitz, M. J., Calhoun, P. J., Lamouille, S., & Smyth, J. W. (2018). Altered translation initiation of . Molecular biology of the cell, 29(7), 797-808. https://doi.org/10.1091/mbc.E17-06-0406
James, Carissa C, et al. "Altered translation initiation of ." Molecular biology of the cell vol. 29,7 (2018): 797-808. doi: https://doi.org/10.1091/mbc.E17-06-0406
James CC, Zeitz MJ, Calhoun PJ, Lamouille S, Smyth JW. Altered translation initiation of . Mol Biol Cell. 2018 Apr 01;29(7):797-808. doi: 10.1091/mbc.E17-06-0406. PMID: 29467255; PMCID: PMC5905293.
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Showing 1 to 3 of 3 entries