Abstract

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The human protein DJ-1 has been implicated both in hereditary Parkinsonism and in certain cancers and appears to play a critical role in protecting cells from the damaging effects of oxidative stress. Oxidative stress has been linked to the molecular pathogenesis of several diseases, and may play a key role in the etiology of Parkinson's disease. The biochemical mechanism by which DJ-1 protects cells is unknown, however it is specifically modified by reactive oxygen species (ROS) by formation of cysteine sulfinic acid. This oxidation of DJ-1 activates a chaperone function that suppresses the cytotoxic aggregation of alpha-synuclein, alters the protein binding partners for DJ-1, and may increase the pool of DJ-1 that is localized to the mitochondria.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Exploratory Grants (P20)
Project #
5P20RR017675-05
Application #
7381841
Study Section
Special Emphasis Panel (ZRR1-RI-A (02))
Project Start
2006-07-01
Project End
2007-06-30
Budget Start
2006-07-01
Budget End
2007-06-30
Support Year
5
Fiscal Year
2006
Total Cost
$173,255
Indirect Cost

  Institution

Name
University of Nebraska Lincoln
Department
Biochemistry
Type
Schools of Earth Sciences/Natur
DUNS #
555456995
City
Lincoln
State
NE
Country
United States
Zip Code
68588

  Publications

Garza-Lombó, Carla; Schroder, Annika; Reyes-Reyes, Elsa M et al. (2018) mTOR/AMPK signaling in the brain: Cell metabolism, proteostasis and survival. Curr Opin Toxicol 8:102-110
Rose, Jordan; Brian, Christian; Woods, Jade et al. (2017) Mitochondrial dysfunction in glial cells: Implications for neuronal homeostasis and survival. Toxicology 391:109-115
Boone, Cory H T; Grove, Ryan A; Adamcova, Dana et al. (2017) Oxidative stress, metabolomics profiling, and mechanism of local anesthetic induced cell death in yeast. Redox Biol 12:139-149
Markley, John L; Brüschweiler, Rafael; Edison, Arthur S et al. (2017) The future of NMR-based metabolomics. Curr Opin Biotechnol 43:34-40
Duszenko, Nikolas; Buan, Nicole R (2017) Physiological Evidence for Isopotential Tunneling in the Electron Transport Chain of Methane-Producing Archaea. Appl Environ Microbiol 83:
Anandhan, Annadurai; Jacome, Maria S; Lei, Shulei et al. (2017) Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism. Brain Res Bull 133:12-30
Marshall, Darrell D; Powers, Robert (2017) Beyond the paradigm: Combining mass spectrometry and nuclear magnetic resonance for metabolomics. Prog Nucl Magn Reson Spectrosc 100:1-16
Anandhan, Annadurai; Lei, Shulei; Levytskyy, Roman et al. (2017) Glucose Metabolism and AMPK Signaling Regulate Dopaminergic Cell Death Induced by Gene (?-Synuclein)-Environment (Paraquat) Interactions. Mol Neurobiol 54:3825-3842
Gebregiworgis, Teklab; Nielsen, Helle H; Massilamany, Chandirasegaran et al. (2016) A Urinary Metabolic Signature for Multiple Sclerosis and Neuromyelitis Optica. J Proteome Res 15:659-66
Navarro-Yepes, Juliana; Anandhan, Annadurai; Bradley, Erin et al. (2016) Inhibition of Protein Ubiquitination by Paraquat and 1-Methyl-4-Phenylpyridinium Impairs Ubiquitin-Dependent Protein Degradation Pathways. Mol Neurobiol 53:5229-51

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