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You searched for +publisher:"Vanderbilt University" +contributor:("Alfred L. George"). Showing records 1 – 10 of 10 total matches.

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Vanderbilt University

1. Armour, Eric Andrew. Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex.

Degree: PhD, Cell and Developmental Biology, 2013, Vanderbilt University

 Tuberous Sclerosis Complex (TSC) is a multi-organ hamartomatous disease caused by loss of function mutations in either the TSC1 or TSC2 genes. Despite involvement of… (more)

Subjects/Keywords: TSC; pluripotency; Tuberous Sclerosis; cilia; cystogenesis; mTOR

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APA (6th Edition):

Armour, E. A. (2013). Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14546

Chicago Manual of Style (16th Edition):

Armour, Eric Andrew. “Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/14546.

MLA Handbook (7th Edition):

Armour, Eric Andrew. “Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex.” 2013. Web. 15 Jan 2021.

Vancouver:

Armour EA. Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/14546.

Council of Science Editors:

Armour EA. Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/14546


Vanderbilt University

2. Murphy, Lisa Lynn. The Physiology and Pathophysiology of a Fetal Splice Variant of the Cardiac Sodium Channel.

Degree: PhD, Pharmacology, 2014, Vanderbilt University

 Mutations in SCN5A encoding the cardiac voltage-gated sodium channel (NaV1.5) can result in severe life-threatening cardiac arrhythmias such as long QT syndrome (LQTS). However, the… (more)

Subjects/Keywords: sodium channel; long QT syndrome; arrhythmias; ion channels

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APA (6th Edition):

Murphy, L. L. (2014). The Physiology and Pathophysiology of a Fetal Splice Variant of the Cardiac Sodium Channel. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11214

Chicago Manual of Style (16th Edition):

Murphy, Lisa Lynn. “The Physiology and Pathophysiology of a Fetal Splice Variant of the Cardiac Sodium Channel.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/11214.

MLA Handbook (7th Edition):

Murphy, Lisa Lynn. “The Physiology and Pathophysiology of a Fetal Splice Variant of the Cardiac Sodium Channel.” 2014. Web. 15 Jan 2021.

Vancouver:

Murphy LL. The Physiology and Pathophysiology of a Fetal Splice Variant of the Cardiac Sodium Channel. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/11214.

Council of Science Editors:

Murphy LL. The Physiology and Pathophysiology of a Fetal Splice Variant of the Cardiac Sodium Channel. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/11214


Vanderbilt University

3. Campbell, Courtney Michelle. Pharmacological Targeting of Gain-of-function KCNQ1 Mutations Predisposing to Atrial Fibrillation.

Degree: PhD, Pharmacology, 2013, Vanderbilt University

 Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in adults. The discovery of mutations in familial AF illustrated the contribution of specific genetic… (more)

Subjects/Keywords: atrial fibrillation; arrhythmia; personalized medicine; myocytes; cardiac; ion channels; potassium channels; pharmacology

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APA (6th Edition):

Campbell, C. M. (2013). Pharmacological Targeting of Gain-of-function KCNQ1 Mutations Predisposing to Atrial Fibrillation. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13258

Chicago Manual of Style (16th Edition):

Campbell, Courtney Michelle. “Pharmacological Targeting of Gain-of-function KCNQ1 Mutations Predisposing to Atrial Fibrillation.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/13258.

MLA Handbook (7th Edition):

Campbell, Courtney Michelle. “Pharmacological Targeting of Gain-of-function KCNQ1 Mutations Predisposing to Atrial Fibrillation.” 2013. Web. 15 Jan 2021.

Vancouver:

Campbell CM. Pharmacological Targeting of Gain-of-function KCNQ1 Mutations Predisposing to Atrial Fibrillation. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/13258.

Council of Science Editors:

Campbell CM. Pharmacological Targeting of Gain-of-function KCNQ1 Mutations Predisposing to Atrial Fibrillation. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/13258


Vanderbilt University

4. Ciampa, Erin Julia. Investigating the function of KCNE4 in cardiac physiology.

Degree: PhD, Pharmacology, 2011, Vanderbilt University

 KCNE4 is a potassium channel modulating protein that can dramatically inhibit distinct potassium currents, but we lack a clear understanding its mechanism for doing so… (more)

Subjects/Keywords: electrophysiology; ion channel; KCNE4; calmodulin; cardiac repolarization

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APA (6th Edition):

Ciampa, E. J. (2011). Investigating the function of KCNE4 in cardiac physiology. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10729

Chicago Manual of Style (16th Edition):

Ciampa, Erin Julia. “Investigating the function of KCNE4 in cardiac physiology.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/10729.

MLA Handbook (7th Edition):

Ciampa, Erin Julia. “Investigating the function of KCNE4 in cardiac physiology.” 2011. Web. 15 Jan 2021.

Vancouver:

Ciampa EJ. Investigating the function of KCNE4 in cardiac physiology. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/10729.

Council of Science Editors:

Ciampa EJ. Investigating the function of KCNE4 in cardiac physiology. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/10729


Vanderbilt University

5. Jorge, Benjamin S. Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Epilepsy is a common neurological disease characterized by an enduring predisposition to generate seizures. Although multiple factors contribute to epilepsy, the majority of cases are… (more)

Subjects/Keywords: potassium channel; epileptic encephalopathy; mouse model; genetics; whole-exome sequencing; epilepsy

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APA (6th Edition):

Jorge, B. S. (2014). Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14387

Chicago Manual of Style (16th Edition):

Jorge, Benjamin S. “Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/14387.

MLA Handbook (7th Edition):

Jorge, Benjamin S. “Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility.” 2014. Web. 15 Jan 2021.

Vancouver:

Jorge BS. Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/14387.

Council of Science Editors:

Jorge BS. Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14387


Vanderbilt University

6. Bartlett, Christina Swan. Role of the prostaglandin E2 receptor EP1 in hypertensive end-organ damage.

Degree: PhD, Pharmacology, 2012, Vanderbilt University

 Hypertension is a prevalent disease affecting one in three adults in the United States. Approximately 25 % of the adult population is either not receiving… (more)

Subjects/Keywords: Prostaglandin; Receptor; Hypertension; Diabetes

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APA (6th Edition):

Bartlett, C. S. (2012). Role of the prostaglandin E2 receptor EP1 in hypertensive end-organ damage. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14916

Chicago Manual of Style (16th Edition):

Bartlett, Christina Swan. “Role of the prostaglandin E2 receptor EP1 in hypertensive end-organ damage.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/14916.

MLA Handbook (7th Edition):

Bartlett, Christina Swan. “Role of the prostaglandin E2 receptor EP1 in hypertensive end-organ damage.” 2012. Web. 15 Jan 2021.

Vancouver:

Bartlett CS. Role of the prostaglandin E2 receptor EP1 in hypertensive end-organ damage. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/14916.

Council of Science Editors:

Bartlett CS. Role of the prostaglandin E2 receptor EP1 in hypertensive end-organ damage. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/14916


Vanderbilt University

7. Huang, Xuan. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Epilepsy is a neurological disorder affecting almost one percent of the population, and genetic epilepsy are those caused by a presumed or unknown genetic factor(s).… (more)

Subjects/Keywords: GABA(A) receptors; GABRG2; genetic epilepsy; mutation; therapy

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APA (6th Edition):

Huang, X. (2014). Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14755

Chicago Manual of Style (16th Edition):

Huang, Xuan. “Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/14755.

MLA Handbook (7th Edition):

Huang, Xuan. “Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.” 2014. Web. 15 Jan 2021.

Vancouver:

Huang X. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/14755.

Council of Science Editors:

Huang X. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14755


Vanderbilt University

8. Tang, Xin. Modulation of GABAA receptor function by PKA and PKC protein phosphorylation.

Degree: PhD, Neuroscience, 2010, Vanderbilt University

 We studied the modulation of ¦Á4¦Â3¦Ã2L and ¦Á4¦Â3¦Ä GABAA receptor currents by two protein kinases, PKA and PKC. Although modulation of synaptic ¦Á1¦Â¦Ã2 GABAA receptor… (more)

Subjects/Keywords: PKC; GABAA receptor; phosphorylation; PKA

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APA (6th Edition):

Tang, X. (2010). Modulation of GABAA receptor function by PKA and PKC protein phosphorylation. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11843

Chicago Manual of Style (16th Edition):

Tang, Xin. “Modulation of GABAA receptor function by PKA and PKC protein phosphorylation.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/11843.

MLA Handbook (7th Edition):

Tang, Xin. “Modulation of GABAA receptor function by PKA and PKC protein phosphorylation.” 2010. Web. 15 Jan 2021.

Vancouver:

Tang X. Modulation of GABAA receptor function by PKA and PKC protein phosphorylation. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/11843.

Council of Science Editors:

Tang X. Modulation of GABAA receptor function by PKA and PKC protein phosphorylation. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11843


Vanderbilt University

9. Xu, Ming. Molecular mechanisms of ADAR2 localization and substrate specificity.

Degree: PhD, Pharmacology, 2006, Vanderbilt University

 ADAR2-mediated adenosine-to-inosine (A-to-I) RNA editing can affect the coding potential, splicing pattern, stability, and localization of the targeted RNA transcripts. ADAR2 contains two double-stranded RNA… (more)

Subjects/Keywords: Double-stranded RNA; dsRNA; specific recognition; nucleolar localization; RNA editing; Adenosine deaminase

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APA (6th Edition):

Xu, M. (2006). Molecular mechanisms of ADAR2 localization and substrate specificity. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11271

Chicago Manual of Style (16th Edition):

Xu, Ming. “Molecular mechanisms of ADAR2 localization and substrate specificity.” 2006. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/11271.

MLA Handbook (7th Edition):

Xu, Ming. “Molecular mechanisms of ADAR2 localization and substrate specificity.” 2006. Web. 15 Jan 2021.

Vancouver:

Xu M. Molecular mechanisms of ADAR2 localization and substrate specificity. [Internet] [Doctoral dissertation]. Vanderbilt University; 2006. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/11271.

Council of Science Editors:

Xu M. Molecular mechanisms of ADAR2 localization and substrate specificity. [Doctoral Dissertation]. Vanderbilt University; 2006. Available from: http://hdl.handle.net/1803/11271


Vanderbilt University

10. Misra, Sunita N. Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy.

Degree: PhD, Pharmacology, 2008, Vanderbilt University

 Investigating genetic forms of epilepsy allows for improved understanding of epilepsy pathophysiology in general. Mutations in voltage-gated sodium channels are a frequent cause of genetic… (more)

Subjects/Keywords: Sodium channels  – Pathophysiology; electrophysiology; epilepsy; Epilepsy  – Genetic aspects; Epilepsy  – Molecular aspects

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APA (6th Edition):

Misra, S. N. (2008). Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12753

Chicago Manual of Style (16th Edition):

Misra, Sunita N. “Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy.” 2008. Doctoral Dissertation, Vanderbilt University. Accessed January 15, 2021. http://hdl.handle.net/1803/12753.

MLA Handbook (7th Edition):

Misra, Sunita N. “Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy.” 2008. Web. 15 Jan 2021.

Vancouver:

Misra SN. Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy. [Internet] [Doctoral dissertation]. Vanderbilt University; 2008. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1803/12753.

Council of Science Editors:

Misra SN. Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy. [Doctoral Dissertation]. Vanderbilt University; 2008. Available from: http://hdl.handle.net/1803/12753

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