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You searched for +publisher:"Vanderbilt University" +contributor:("Michael Aschner"). Showing records 1 – 14 of 14 total matches.

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Vanderbilt University

1. Chakraborty, Sudipta. Gene-Environment Interactions Between Manganese Toxicity and Early-Onset Parkinson's Disease Genes.

Degree: PhD, Neuroscience, 2015, Vanderbilt University

 Parkinson’s disease (PD) is a neurodegenerative, motor disorder that is characterized by selective dopaminergic cell loss in the substantia nigra pars compacta. About 10-20% of… (more)

Subjects/Keywords: Parkinsons disease; manganese; neurotoxicology; C. elegans; parkin; pink1; dj1; ferroportin; DMT1; oxidative stress

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APA (6th Edition):

Chakraborty, S. (2015). Gene-Environment Interactions Between Manganese Toxicity and Early-Onset Parkinson's Disease Genes. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10795

Chicago Manual of Style (16th Edition):

Chakraborty, Sudipta. “Gene-Environment Interactions Between Manganese Toxicity and Early-Onset Parkinson's Disease Genes.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/10795.

MLA Handbook (7th Edition):

Chakraborty, Sudipta. “Gene-Environment Interactions Between Manganese Toxicity and Early-Onset Parkinson's Disease Genes.” 2015. Web. 18 Jan 2021.

Vancouver:

Chakraborty S. Gene-Environment Interactions Between Manganese Toxicity and Early-Onset Parkinson's Disease Genes. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/10795.

Council of Science Editors:

Chakraborty S. Gene-Environment Interactions Between Manganese Toxicity and Early-Onset Parkinson's Disease Genes. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://hdl.handle.net/1803/10795


Vanderbilt University

2. Kwakye, Gunnar Francis. Development of a novel high throughput assay: impaired manganese transport kinetics and homeostasis in Huntington’s disease.

Degree: PhD, Neuroscience, 2011, Vanderbilt University

 Expansion in the glutamine encoding CAG triplet-repeat in the Huntingtin (HTT) gene causes Huntington’s disease (HD). The susceptibility, age of onset, and severity of HD… (more)

Subjects/Keywords: manganese; striatal cells; high throughput assay; metal transport; Huntingtons disease

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APA (6th Edition):

Kwakye, G. F. (2011). Development of a novel high throughput assay: impaired manganese transport kinetics and homeostasis in Huntington’s disease. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14123

Chicago Manual of Style (16th Edition):

Kwakye, Gunnar Francis. “Development of a novel high throughput assay: impaired manganese transport kinetics and homeostasis in Huntington’s disease.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/14123.

MLA Handbook (7th Edition):

Kwakye, Gunnar Francis. “Development of a novel high throughput assay: impaired manganese transport kinetics and homeostasis in Huntington’s disease.” 2011. Web. 18 Jan 2021.

Vancouver:

Kwakye GF. Development of a novel high throughput assay: impaired manganese transport kinetics and homeostasis in Huntington’s disease. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/14123.

Council of Science Editors:

Kwakye GF. Development of a novel high throughput assay: impaired manganese transport kinetics and homeostasis in Huntington’s disease. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/14123


Vanderbilt University

3. Nguyen, Thuy Tuong. Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging.

Degree: PhD, Pharmacology, 2016, Vanderbilt University

 Highly reactive acyclic levuglandin-like gamma-ketoaldehydes (gamma-KA, isoketals, or IsoKs) are formed as products of the isoprostane pathway of lipid peroxidation. IsoKs are known to covalently… (more)

Subjects/Keywords: isoketals; aging; Caenorhabditis elegans; sirtuins; isoprostanes

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APA (6th Edition):

Nguyen, T. T. (2016). Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14699

Chicago Manual of Style (16th Edition):

Nguyen, Thuy Tuong. “Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/14699.

MLA Handbook (7th Edition):

Nguyen, Thuy Tuong. “Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging.” 2016. Web. 18 Jan 2021.

Vancouver:

Nguyen TT. Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/14699.

Council of Science Editors:

Nguyen TT. Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/14699


Vanderbilt University

4. Ni, Mingwei. Acute response of primary glial cells to methylmercury exposure.

Degree: PhD, Pharmacology, 2011, Vanderbilt University

 Mercury accumulates in fish-eating populations. Glial cells have diverse functions including providing nutrition[1], maintaining CNS homeostasis, removing pathogens, inducing neuronal differentiation and mediating CNS immune… (more)

Subjects/Keywords: methylmercury; Nrf2; oxidative stress; glia

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APA (6th Edition):

Ni, M. (2011). Acute response of primary glial cells to methylmercury exposure. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14320

Chicago Manual of Style (16th Edition):

Ni, Mingwei. “Acute response of primary glial cells to methylmercury exposure.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/14320.

MLA Handbook (7th Edition):

Ni, Mingwei. “Acute response of primary glial cells to methylmercury exposure.” 2011. Web. 18 Jan 2021.

Vancouver:

Ni M. Acute response of primary glial cells to methylmercury exposure. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/14320.

Council of Science Editors:

Ni M. Acute response of primary glial cells to methylmercury exposure. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/14320


Vanderbilt University

5. Meredith, Martha Elizabeth. Multiple roles for Ascorbic Acid in the Brain: Transporter Regulation, Neurotransmitter Synthesis, and Brain Endothelial Cell Stability.

Degree: PhD, Molecular Physiology and Biophysics, 2014, Vanderbilt University

 The roles for ascorbic acid (ASC) in regulation of its transporter, in neurotransmitter synthesis, and in brain endothelial cell barrier permeability were investigated in the… (more)

Subjects/Keywords: permeability; neurotransmitter; oxidative stress; SVCT2; ascorbic acid; diabetes; blood brain barrier

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APA (6th Edition):

Meredith, M. E. (2014). Multiple roles for Ascorbic Acid in the Brain: Transporter Regulation, Neurotransmitter Synthesis, and Brain Endothelial Cell Stability. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11317

Chicago Manual of Style (16th Edition):

Meredith, Martha Elizabeth. “Multiple roles for Ascorbic Acid in the Brain: Transporter Regulation, Neurotransmitter Synthesis, and Brain Endothelial Cell Stability.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/11317.

MLA Handbook (7th Edition):

Meredith, Martha Elizabeth. “Multiple roles for Ascorbic Acid in the Brain: Transporter Regulation, Neurotransmitter Synthesis, and Brain Endothelial Cell Stability.” 2014. Web. 18 Jan 2021.

Vancouver:

Meredith ME. Multiple roles for Ascorbic Acid in the Brain: Transporter Regulation, Neurotransmitter Synthesis, and Brain Endothelial Cell Stability. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/11317.

Council of Science Editors:

Meredith ME. Multiple roles for Ascorbic Acid in the Brain: Transporter Regulation, Neurotransmitter Synthesis, and Brain Endothelial Cell Stability. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/11317


Vanderbilt University

6. Tidball, Andrew Martin. A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 The essential micronutrient manganese is enriched in brain, especially the basal ganglia. We sought to identify neuronal signaling pathways responsive to neurologically relevant manganese levels,… (more)

Subjects/Keywords: manganese; induced-pluripotent stem cells; ATM; p53; cell signaling; cytotoxicity; genomic instability; Huntingtons disease

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APA (6th Edition):

Tidball, A. M. (2014). A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14230

Chicago Manual of Style (16th Edition):

Tidball, Andrew Martin. “A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/14230.

MLA Handbook (7th Edition):

Tidball, Andrew Martin. “A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling.” 2014. Web. 18 Jan 2021.

Vancouver:

Tidball AM. A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/14230.

Council of Science Editors:

Tidball AM. A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14230


Vanderbilt University

7. Bichell, Terry Jo Vetters. Reduced Striatal Mn-accumulation in Huntington’s Disease Mouse Model Causes Reversible Alterations in Mn-dependent Enzyme Pathways.

Degree: PhD, Neuroscience, 2016, Vanderbilt University

 Huntington’s disease (HD) is caused by an increase in CAG repeats in exon 1 of the huntingtin gene (HTT), which results in a polyglutamine expansion… (more)

Subjects/Keywords: manganese; Huntingtons disease; arginase; gene environment interactions; neurodegeneration; mouse models; striatum; urea cycle

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APA (6th Edition):

Bichell, T. J. V. (2016). Reduced Striatal Mn-accumulation in Huntington’s Disease Mouse Model Causes Reversible Alterations in Mn-dependent Enzyme Pathways. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/15162

Chicago Manual of Style (16th Edition):

Bichell, Terry Jo Vetters. “Reduced Striatal Mn-accumulation in Huntington’s Disease Mouse Model Causes Reversible Alterations in Mn-dependent Enzyme Pathways.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/15162.

MLA Handbook (7th Edition):

Bichell, Terry Jo Vetters. “Reduced Striatal Mn-accumulation in Huntington’s Disease Mouse Model Causes Reversible Alterations in Mn-dependent Enzyme Pathways.” 2016. Web. 18 Jan 2021.

Vancouver:

Bichell TJV. Reduced Striatal Mn-accumulation in Huntington’s Disease Mouse Model Causes Reversible Alterations in Mn-dependent Enzyme Pathways. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/15162.

Council of Science Editors:

Bichell TJV. Reduced Striatal Mn-accumulation in Huntington’s Disease Mouse Model Causes Reversible Alterations in Mn-dependent Enzyme Pathways. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/15162


Vanderbilt University

8. Kumar, Kevin Krishan. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Manganese (Mn) is both an essential biological cofactor and neurotoxicant. Disruption of Mn biology in the basal ganglia has been implicated in the pathogenesis of… (more)

Subjects/Keywords: High Throughput Screening; Manganese; Neurodegenerative diseases; Human Induced Pluripotent Stem Cells; Metabolomics

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APA (6th Edition):

Kumar, K. K. (2014). Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14021

Chicago Manual of Style (16th Edition):

Kumar, Kevin Krishan. “Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/14021.

MLA Handbook (7th Edition):

Kumar, Kevin Krishan. “Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.” 2014. Web. 18 Jan 2021.

Vancouver:

Kumar KK. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/14021.

Council of Science Editors:

Kumar KK. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14021


Vanderbilt University

9. Buckman, Laura Beth. Studies on the Development and Consequences of Neuroinflammation in Obesity.

Degree: PhD, Molecular Physiology and Biophysics, 2014, Vanderbilt University

 In the past decade, evidence has emerged that obesity induces a neuroinflammatory response in the hypothalamus, a part of the brain that contains neuronal circuitry… (more)

Subjects/Keywords: neuroinflammation; diet-induced obesity; CNS; obesity; microglia; astrocytes; high-fat diet

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APA (6th Edition):

Buckman, L. B. (2014). Studies on the Development and Consequences of Neuroinflammation in Obesity. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12699

Chicago Manual of Style (16th Edition):

Buckman, Laura Beth. “Studies on the Development and Consequences of Neuroinflammation in Obesity.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/12699.

MLA Handbook (7th Edition):

Buckman, Laura Beth. “Studies on the Development and Consequences of Neuroinflammation in Obesity.” 2014. Web. 18 Jan 2021.

Vancouver:

Buckman LB. Studies on the Development and Consequences of Neuroinflammation in Obesity. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/12699.

Council of Science Editors:

Buckman LB. Studies on the Development and Consequences of Neuroinflammation in Obesity. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/12699


Vanderbilt University

10. Madison, Jennifer Lea. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.

Degree: PhD, Pharmacology, 2011, Vanderbilt University

 Huntington’s disease is a fatal autosomal dominant neurodegenerative disease caused by an expansion of CAG repeats in the DNA of the Huntingtin gene. The length… (more)

Subjects/Keywords: neuron morphology; YAC128; manganese; Huntington's disease; medium spiny neuron; neurochemistry

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APA (6th Edition):

Madison, J. L. (2011). Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12672

Chicago Manual of Style (16th Edition):

Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/12672.

MLA Handbook (7th Edition):

Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Web. 18 Jan 2021.

Vancouver:

Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/12672.

Council of Science Editors:

Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/12672


Vanderbilt University

11. Williams, Brooke Blairanne. A novel gene-environment interaction: the Huntington mutation suppresses manganese accumulation and toxicity.

Degree: PhD, Neuroscience, 2010, Vanderbilt University

 ABSTRACT Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder predominantly afflicting the striatum. It is clear that an expansion of a glutamine encoding CAG… (more)

Subjects/Keywords: metals; manganese; Huntington's disease; neurodegeneration; STHdh

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APA (6th Edition):

Williams, B. B. (2010). A novel gene-environment interaction: the Huntington mutation suppresses manganese accumulation and toxicity. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11692

Chicago Manual of Style (16th Edition):

Williams, Brooke Blairanne. “A novel gene-environment interaction: the Huntington mutation suppresses manganese accumulation and toxicity.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/11692.

MLA Handbook (7th Edition):

Williams, Brooke Blairanne. “A novel gene-environment interaction: the Huntington mutation suppresses manganese accumulation and toxicity.” 2010. Web. 18 Jan 2021.

Vancouver:

Williams BB. A novel gene-environment interaction: the Huntington mutation suppresses manganese accumulation and toxicity. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/11692.

Council of Science Editors:

Williams BB. A novel gene-environment interaction: the Huntington mutation suppresses manganese accumulation and toxicity. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11692


Vanderbilt University

12. Helmcke, Kirsten Jeanne. Caenorhabditis elegans as a model to study molecular mechanisms of methylmercury toxicity.

Degree: PhD, Pharmacology, 2010, Vanderbilt University

 Methylmercury (MeHg), a known neurotoxicant, is found in seafood, leading to regular exposure of humans to this compound. Many of the molecular targets and detoxifying… (more)

Subjects/Keywords: Caenorhabditis elegans; methylmercury; toxicity

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APA (6th Edition):

Helmcke, K. J. (2010). Caenorhabditis elegans as a model to study molecular mechanisms of methylmercury toxicity. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10424

Chicago Manual of Style (16th Edition):

Helmcke, Kirsten Jeanne. “Caenorhabditis elegans as a model to study molecular mechanisms of methylmercury toxicity.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/10424.

MLA Handbook (7th Edition):

Helmcke, Kirsten Jeanne. “Caenorhabditis elegans as a model to study molecular mechanisms of methylmercury toxicity.” 2010. Web. 18 Jan 2021.

Vancouver:

Helmcke KJ. Caenorhabditis elegans as a model to study molecular mechanisms of methylmercury toxicity. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/10424.

Council of Science Editors:

Helmcke KJ. Caenorhabditis elegans as a model to study molecular mechanisms of methylmercury toxicity. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/10424


Vanderbilt University

13. Neill, Meaghan Anne. Nitrogen Metabolism: Enzyme Expression and Protein Interactions in the Urea and Nitric Oxide Cycles.

Degree: PhD, Human Genetics, 2010, Vanderbilt University

 The urea cycle enzymes play an important role in the processing of nitrogen to urea and in producing endogenous nitric oxide by the citrulline-nitric oxide… (more)

Subjects/Keywords: mRNA expression; protein interactions; nitric oxide cycle; urea cycle; protein expression; nitrogen metabolism

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APA (6th Edition):

Neill, M. A. (2010). Nitrogen Metabolism: Enzyme Expression and Protein Interactions in the Urea and Nitric Oxide Cycles. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11764

Chicago Manual of Style (16th Edition):

Neill, Meaghan Anne. “Nitrogen Metabolism: Enzyme Expression and Protein Interactions in the Urea and Nitric Oxide Cycles.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/11764.

MLA Handbook (7th Edition):

Neill, Meaghan Anne. “Nitrogen Metabolism: Enzyme Expression and Protein Interactions in the Urea and Nitric Oxide Cycles.” 2010. Web. 18 Jan 2021.

Vancouver:

Neill MA. Nitrogen Metabolism: Enzyme Expression and Protein Interactions in the Urea and Nitric Oxide Cycles. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/11764.

Council of Science Editors:

Neill MA. Nitrogen Metabolism: Enzyme Expression and Protein Interactions in the Urea and Nitric Oxide Cycles. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11764


Vanderbilt University

14. Brown, Molly Nicole. GABA synthesis in developing hippocampus: SNAT1 surfaces as a dynamic regulator of inhibitory synaptic transmission.

Degree: PhD, Pharmacology, 2010, Vanderbilt University

 GABA functions as the primary inhibitory neurotransmitter in the mammalian brain. In hippocampus, GABA serves multiple roles during development and throughout adulthood, which include: 1)… (more)

Subjects/Keywords: SNAT1; System A; GABA; glutamine; hippocampus; development

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APA (6th Edition):

Brown, M. N. (2010). GABA synthesis in developing hippocampus: SNAT1 surfaces as a dynamic regulator of inhibitory synaptic transmission. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11698

Chicago Manual of Style (16th Edition):

Brown, Molly Nicole. “GABA synthesis in developing hippocampus: SNAT1 surfaces as a dynamic regulator of inhibitory synaptic transmission.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2021. http://hdl.handle.net/1803/11698.

MLA Handbook (7th Edition):

Brown, Molly Nicole. “GABA synthesis in developing hippocampus: SNAT1 surfaces as a dynamic regulator of inhibitory synaptic transmission.” 2010. Web. 18 Jan 2021.

Vancouver:

Brown MN. GABA synthesis in developing hippocampus: SNAT1 surfaces as a dynamic regulator of inhibitory synaptic transmission. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1803/11698.

Council of Science Editors:

Brown MN. GABA synthesis in developing hippocampus: SNAT1 surfaces as a dynamic regulator of inhibitory synaptic transmission. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11698

.