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You searched for +publisher:"University of Alabama – Birmingham" +contributor:("Lesort, Mathieu"). Showing records 1 – 8 of 8 total matches.

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1. Blaize, Marie Antionette. Degradation of the Huntington polyglutamine domain by the proteasome : implication to Huntington's disease.

Degree: MS, 2008, University of Alabama – Birmingham

Huntington’s disease (HD) is a progressive autosomal dominant neurodegenerative disorder. HD results from the genetic mutation that leads to an abnormally expanded polyglutamine (PolyQ) sequence… (more)

Subjects/Keywords: Huntington's chorea  – Genetic aspects <; br>; Peptides  – Antagonists <; br>; Protease inhibitors

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APA (6th Edition):

Blaize, M. A. (2008). Degradation of the Huntington polyglutamine domain by the proteasome : implication to Huntington's disease. (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,216

Chicago Manual of Style (16th Edition):

Blaize, Marie Antionette. “Degradation of the Huntington polyglutamine domain by the proteasome : implication to Huntington's disease.” 2008. Masters Thesis, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,216.

MLA Handbook (7th Edition):

Blaize, Marie Antionette. “Degradation of the Huntington polyglutamine domain by the proteasome : implication to Huntington's disease.” 2008. Web. 15 Sep 2019.

Vancouver:

Blaize MA. Degradation of the Huntington polyglutamine domain by the proteasome : implication to Huntington's disease. [Internet] [Masters thesis]. University of Alabama – Birmingham; 2008. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,216.

Council of Science Editors:

Blaize MA. Degradation of the Huntington polyglutamine domain by the proteasome : implication to Huntington's disease. [Masters Thesis]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,216

2. Taylor, Charles Alan. Examination Of Bafilomycin And Atp6v0c As Putative Mediators Of App Clearance In A Pre-Clinical Model Of Alzheimer's Disease.

Degree: MS, 2012, University of Alabama – Birmingham

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder and the most common form of dementia. Fundamental hallmarks of AD include progressive hippocampal neuron death, neurofibrillary… (more)

Subjects/Keywords: Macrolide antibiotics – Effectiveness.<; br>; Adenosine triphosphatase – Inhibitors.<; br>; Amyloid beta-protein precursor – Antagonists.<; br>; Alzheimer's disease – Treatment.<; br>; Alzheimer's disease – Genetic aspects.<; br>; Lysosomal storage diseases.<; br>; Chloroquine – Physiological effect.<; br>; Chloroquine – Antagonists.

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APA (6th Edition):

Taylor, C. A. (2012). Examination Of Bafilomycin And Atp6v0c As Putative Mediators Of App Clearance In A Pre-Clinical Model Of Alzheimer's Disease. (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1444

Chicago Manual of Style (16th Edition):

Taylor, Charles Alan. “Examination Of Bafilomycin And Atp6v0c As Putative Mediators Of App Clearance In A Pre-Clinical Model Of Alzheimer's Disease.” 2012. Masters Thesis, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1444.

MLA Handbook (7th Edition):

Taylor, Charles Alan. “Examination Of Bafilomycin And Atp6v0c As Putative Mediators Of App Clearance In A Pre-Clinical Model Of Alzheimer's Disease.” 2012. Web. 15 Sep 2019.

Vancouver:

Taylor CA. Examination Of Bafilomycin And Atp6v0c As Putative Mediators Of App Clearance In A Pre-Clinical Model Of Alzheimer's Disease. [Internet] [Masters thesis]. University of Alabama – Birmingham; 2012. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1444.

Council of Science Editors:

Taylor CA. Examination Of Bafilomycin And Atp6v0c As Putative Mediators Of App Clearance In A Pre-Clinical Model Of Alzheimer's Disease. [Masters Thesis]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1444

3. Meares, Gordon P. Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival.

Degree: PhD, 2007, University of Alabama – Birmingham

Proper regulation of survival signaling is critical for all organisms. One important signaling cascade involved in the coordinated effort to control signals influencing cell fate… (more)

Subjects/Keywords: Apoptosis  – physiology <; br>; Cell Nucleus  – metabolism <; br>; Glycogen Synthase Kinase 3  – metabolism <; br>; HSP90 Heat-Shock Proteins  – physiology <; br>; Insulin  – physiology <; br>; Insulin-Like Growth Factor I  – physiology <; br>; Nuclear Localization Signals <; br>; Signal Transduction  – physiology

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APA (6th Edition):

Meares, G. P. (2007). Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,134

Chicago Manual of Style (16th Edition):

Meares, Gordon P. “Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,134.

MLA Handbook (7th Edition):

Meares, Gordon P. “Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival.” 2007. Web. 15 Sep 2019.

Vancouver:

Meares GP. Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,134.

Council of Science Editors:

Meares GP. Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,134

4. Reyes, Reno Cervo. The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes.

Degree: PhD, 2009, University of Alabama – Birmingham

Astrocytes, a type of glial cell in the central nervous system, are recognized for their support roles to neurons. They supply neurons with metabolites, maintain… (more)

Subjects/Keywords: Astrocytes  – metabolism<; br>; Astrocytes  – ultrastructure<; br>; Calcium  – metabolism<; br>; Exocytosis  – physiology<; br>; Glutamic Acid  – metabolism<; br>; Mitochondria  – physiology<; br>; Visual Cortex  – cytology

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APA (6th Edition):

Reyes, R. C. (2009). The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,688

Chicago Manual of Style (16th Edition):

Reyes, Reno Cervo. “The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,688.

MLA Handbook (7th Edition):

Reyes, Reno Cervo. “The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes.” 2009. Web. 15 Sep 2019.

Vancouver:

Reyes RC. The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,688.

Council of Science Editors:

Reyes RC. The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,688

5. Beagle, Brandon Richard. Canonical Wnt signaling by the proteolytic processing of LRP6.

Degree: PhD, 2010, University of Alabama – Birmingham

Low density Lipoprotein receptor Related 6 (LRP6) functions as an essential coreceptor for Wnt/β-catenin signaling as pathway activation, reflected by cytosolic β- catenin stabilization and… (more)

Subjects/Keywords: beta Catenin  – metabolism<; br>; Glycogen Synthase Kinase 3  – metabolism<; br>; LDL-Receptor Related Proteins  – metabolism<; br>; Lymphoid Enhancer-Binding Factor 1  – metabolism<; br>; Repressor Proteins  – metabolism<; br>; Transcription Factors  – metabolism<; br>; Wnt Proteins  – metabolism

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APA (6th Edition):

Beagle, B. R. (2010). Canonical Wnt signaling by the proteolytic processing of LRP6. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,857

Chicago Manual of Style (16th Edition):

Beagle, Brandon Richard. “Canonical Wnt signaling by the proteolytic processing of LRP6.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,857.

MLA Handbook (7th Edition):

Beagle, Brandon Richard. “Canonical Wnt signaling by the proteolytic processing of LRP6.” 2010. Web. 15 Sep 2019.

Vancouver:

Beagle BR. Canonical Wnt signaling by the proteolytic processing of LRP6. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,857.

Council of Science Editors:

Beagle BR. Canonical Wnt signaling by the proteolytic processing of LRP6. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,857

6. Ding, Huiping. Regulation of tau functions by posttranslational modifications of tau and histone deacetylase 6.

Degree: PhD, 2008, University of Alabama – Birmingham

Alzheimer’s disease (AD), the most common neurodegenerative disease, is pathologically characterized by senile plaques composed of amyloid [beta] peptide and neurofibrillary tangles composed of hyperphosphorylated… (more)

Subjects/Keywords: Alzheimer Disease  – metabolism<; br>; Brain  – metabolism<; br>; Caspases  – metabolism<; br>; Histone Deacetylases  – metabolism<; br>; Microtubules  – metabolism<; br>; Neurons  – metabolism<; br>; tau Proteins  – metabolism

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APA (6th Edition):

Ding, H. (2008). Regulation of tau functions by posttranslational modifications of tau and histone deacetylase 6. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,439

Chicago Manual of Style (16th Edition):

Ding, Huiping. “Regulation of tau functions by posttranslational modifications of tau and histone deacetylase 6.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,439.

MLA Handbook (7th Edition):

Ding, Huiping. “Regulation of tau functions by posttranslational modifications of tau and histone deacetylase 6.” 2008. Web. 15 Sep 2019.

Vancouver:

Ding H. Regulation of tau functions by posttranslational modifications of tau and histone deacetylase 6. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,439.

Council of Science Editors:

Ding H. Regulation of tau functions by posttranslational modifications of tau and histone deacetylase 6. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,439

7. Matthews, Tori A. Pathological modifications of tau induce toxicity and facilitate cell death.

Degree: PhD, 2009, University of Alabama – Birmingham

lzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by two major pathophysiological hallmarks, beta-amyloid (A[Beta]) plaques and tau tangles. In AD and other tau… (more)

Subjects/Keywords: Caspases  – metabolism<; br>; Cell Death  – physiology<; br>; Microtubules  – metabolism<; br>; tau Proteins  – physiology

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APA (6th Edition):

Matthews, T. A. (2009). Pathological modifications of tau induce toxicity and facilitate cell death. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,607

Chicago Manual of Style (16th Edition):

Matthews, Tori A. “Pathological modifications of tau induce toxicity and facilitate cell death.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,607.

MLA Handbook (7th Edition):

Matthews, Tori A. “Pathological modifications of tau induce toxicity and facilitate cell death.” 2009. Web. 15 Sep 2019.

Vancouver:

Matthews TA. Pathological modifications of tau induce toxicity and facilitate cell death. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,607.

Council of Science Editors:

Matthews TA. Pathological modifications of tau induce toxicity and facilitate cell death. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,607

8. King, Adrienne Lester. Chronic alcohol consumption promotes opening of the mitochondrial permeability transition pore and increases mitochondrial injury in liver.

Degree: PhD, 2010, University of Alabama – Birmingham

Alcoholic liver disease is a serious public health concern. In particular, the mitochondrion is a specific target of ethanol toxicity and much of the damage… (more)

Subjects/Keywords: Alcohols  – pharmacology<; br>; Calcium  – metabolism<; br>; Cyclophilins  – metabolism<; br>; Ethanol  – adverse effects<; br>; Fatty Liver  – chemically induced<; br>; Liver  – drug effects<; br>; Mitochondria  – pathology<; br>; Mitochondrial Membrane Transport Proteins  – metabolism<; br>; Oxidative Stress

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

King, A. L. (2010). Chronic alcohol consumption promotes opening of the mitochondrial permeability transition pore and increases mitochondrial injury in liver. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,842

Chicago Manual of Style (16th Edition):

King, Adrienne Lester. “Chronic alcohol consumption promotes opening of the mitochondrial permeability transition pore and increases mitochondrial injury in liver.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed September 15, 2019. http://contentdm.mhsl.uab.edu/u?/etd,842.

MLA Handbook (7th Edition):

King, Adrienne Lester. “Chronic alcohol consumption promotes opening of the mitochondrial permeability transition pore and increases mitochondrial injury in liver.” 2010. Web. 15 Sep 2019.

Vancouver:

King AL. Chronic alcohol consumption promotes opening of the mitochondrial permeability transition pore and increases mitochondrial injury in liver. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Sep 15]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,842.

Council of Science Editors:

King AL. Chronic alcohol consumption promotes opening of the mitochondrial permeability transition pore and increases mitochondrial injury in liver. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,842

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