Abstract

This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Type I cells of the carotid body (CB) are chemoreceptors that sense changes in blood pH, CO2, and O2. These cells respond to stimulation with a membrane depolarization that induces Ca2+ entry through voltage-dependent Ca2+ channels and the subsequent release of a neurotransmitter that activates the afferent fibers of the carotid sinus nerve. In the case of hypoxia, the cause of membrane depolarization seems to be the inhibition of K+ channels. Three different types of O2-sensitive K+ channels have been postulated to elicit such depolarization: a voltage-gated channel in rabbit type I cells and a large-conductance Ca2+ - dependent K+ channel (maxiK) and a TASK-like channel in rat type I cells.
The specific aim of this project will be to identify a putative membrane-bound hemoproteic sensor in type I cells of the carotid body (CB), and determine how this molecule interacts with O2-sensitive K+ channels to alter channel activity and confer hypoxic sensitivity to type I cells of the CB.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Exploratory Grants (P20)
Project #
2P20RR017675-06
Application #
7610429
Study Section
Special Emphasis Panel (ZRR1-RI-5 (01))
Project Start
2007-08-01
Project End
2008-07-31
Budget Start
2007-08-01
Budget End
2008-07-31
Support Year
6
Fiscal Year
2007
Total Cost
$71,550
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
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
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
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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