BethAnn McLaughlin

Neurology Vanderbilt University, Nashville, TN 
Cell Death, Ischemia, Neuroprotection, Stroke, Parkinsons Disease
"BethAnn McLaughlin"
Mean distance: 14.19 (cluster 11)
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Klionsky DJ, Abdel-Aziz AK, Abdelfatah S, et al. (2021) Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition). Autophagy. 1-382
Musiek ES, Brooks JD, Joo M, et al. (2019) Correction: Electrophilic cyclopentenone neuroprostanes are anti-inflammatory mediators formed from the peroxidation of the ω -3 polyunsaturated fatty acid docosahexaenoic acid. The Journal of Biological Chemistry. 294: 6657
Lizama BN, Palubinsky AM, Raveendran VA, et al. (2018) Neuronal Preconditioning Requires the Mitophagic Activity of C-terminus of HSC70-Interacting Protein. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience
Connolly NMC, Theurey P, Adam-Vizi V, et al. (2017) Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases. Cell Death and Differentiation
Lizama BN, Palubinsky AM, McLaughlin B. (2017) Alterations in the E3 ligases Parkin and CHIP result in unique metabolic signaling defects and mitochondrial quality control issues. Neurochemistry International
Lizama-Manibusan BN, Klein S, McKenzie JR, et al. (2016) Analysis of a Nitroreductase-based Hypoxia Sensor in Primary Neuronal Cultures. Acs Chemical Neuroscience
Palubinsky AM, Stankowski JN, Kale AC, et al. (2015) CHIP Is an Essential Determinant of Neuronal Mitochondrial Stress Signaling. Antioxidants & Redox Signaling
Naik M, Humnabadkar V, Tantry SJ, et al. (2014) 4-aminoquinolone piperidine amides: noncovalent inhibitors of DprE1 with long residence time and potent antimycobacterial activity. Journal of Medicinal Chemistry. 57: 5419-34
Lizama-Manibusan B, McLaughlin B. (2013) Redox modification of proteins as essential mediators of CNS autophagy and mitophagy. Febs Letters. 587: 2291-8
Grelli KN, Palubinsky AM, Kale AC, et al. (2013) Alteration of isocitrate dehydrogenase following acute ischemic injury as a means to improve cellular energetic status in neuroadaptation. Cns & Neurological Disorders Drug Targets. 12: 849-60
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