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You searched for +publisher:"University of Alabama – Birmingham" +contributor:("Kirk, Kevin L. <br>"). Showing records 1 – 4 of 4 total matches.

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1. Grabski, Robert. Using RNA interference to study the function of the tethering protein p115 in ER-Golgi traffic.

Degree: PhD, 2008, University of Alabama – Birmingham

Metazoan cells are characterized with elaborate network of intracellular membranous compartments. These membranes allow the cell to spatially separate antagonistic processes and environments, and maintain… (more)

Subjects/Keywords: Carrier Proteins  – metabolism <; br>; Golgi Apparatus  – metabolism <; br>; Membrane Proteins  – metabolism <; br>; Protein Transport <; br>; RNA Interference

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

APA (6th Edition):

Grabski, R. (2008). Using RNA interference to study the function of the tethering protein p115 in ER-Golgi traffic. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,328

Chicago Manual of Style (16th Edition):

Grabski, Robert. “Using RNA interference to study the function of the tethering protein p115 in ER-Golgi traffic.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 16, 2019. http://contentdm.mhsl.uab.edu/u?/etd,328.

MLA Handbook (7th Edition):

Grabski, Robert. “Using RNA interference to study the function of the tethering protein p115 in ER-Golgi traffic.” 2008. Web. 16 Oct 2019.

Vancouver:

Grabski R. Using RNA interference to study the function of the tethering protein p115 in ER-Golgi traffic. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Oct 16]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,328.

Council of Science Editors:

Grabski R. Using RNA interference to study the function of the tethering protein p115 in ER-Golgi traffic. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,328

2. Jurkuvenaite, Asta. Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR).

Degree: PhD, 2008, University of Alabama – Birmingham

Cystic fibrosis (CF) is a genetic disease resulting from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel that functions at… (more)

Subjects/Keywords: Biotinylation. Cell Membrane  – metabolism<; br>; Cystic Fibrosis Transmembrane Conductance Regulator  – chemistry<; br>; Cystic Fibrosis Transmembrane Conductance Regulator  – metabolism<; br>; Mutation<; br>; Protein Structure, Tertiary

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APA (6th Edition):

Jurkuvenaite, A. (2008). Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR). (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,601

Chicago Manual of Style (16th Edition):

Jurkuvenaite, Asta. “Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR).” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 16, 2019. http://contentdm.mhsl.uab.edu/u?/etd,601.

MLA Handbook (7th Edition):

Jurkuvenaite, Asta. “Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR).” 2008. Web. 16 Oct 2019.

Vancouver:

Jurkuvenaite A. Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR). [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Oct 16]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,601.

Council of Science Editors:

Jurkuvenaite A. Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR). [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,601

3. Mathew, Seena S. Kainate receptor modulation of synaptic transmission in neocortex.

Degree: PhD, 2007, University of Alabama – Birmingham

The actions of the inhibitory neurotransmitter [gamma]-aminobutyric acid (GABA) are tightly regulated to ensure effective information processing as well as prevention of excess excitatory activity,… (more)

Subjects/Keywords: Excitatory Amino Acid Agonists  – pharmacology <; br>; gamma-Aminobutyric Acid  – metabolism <; br>; Kainic Acid  – pharmacology <; br>; Neocortex  – cytology <; br>; Presynaptic Terminals  – drug effects <; br>; Synapses  – drug effects

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APA (6th Edition):

Mathew, S. S. (2007). Kainate receptor modulation of synaptic transmission in neocortex. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,133

Chicago Manual of Style (16th Edition):

Mathew, Seena S. “Kainate receptor modulation of synaptic transmission in neocortex.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 16, 2019. http://contentdm.mhsl.uab.edu/u?/etd,133.

MLA Handbook (7th Edition):

Mathew, Seena S. “Kainate receptor modulation of synaptic transmission in neocortex.” 2007. Web. 16 Oct 2019.

Vancouver:

Mathew SS. Kainate receptor modulation of synaptic transmission in neocortex. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2019 Oct 16]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,133.

Council of Science Editors:

Mathew SS. Kainate receptor modulation of synaptic transmission in neocortex. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,133

4. Perez, Jessica. Regulation of vascular smooth muscle cell signaling and metabolism by platelet-derived growth factor.

Degree: PhD, 2010, University of Alabama – Birmingham

Growth factors are important inducers of vascular cell growth whose regulation is altered during the pathogenesis of atherosclerosis. An increase in growth factor and cytokine… (more)

Subjects/Keywords: Cell Proliferation  – drug effects<; br>; Glucose  – metabolism<; br>; Muscle, Smooth, Vascular  – cytology<; br>; Myocytes, Smooth Muscle  – cytology<; br>; Myocytes, Smooth Muscle  – drug effects<; br>; Phosphatidylinositol 3-Kinases  – antagonists & inhibitors<; br>; Platelet-Derived Growth Factor  – pharmacology<; br>

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

APA (6th Edition):

Perez, J. (2010). Regulation of vascular smooth muscle cell signaling and metabolism by platelet-derived growth factor. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,928

Chicago Manual of Style (16th Edition):

Perez, Jessica. “Regulation of vascular smooth muscle cell signaling and metabolism by platelet-derived growth factor.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 16, 2019. http://contentdm.mhsl.uab.edu/u?/etd,928.

MLA Handbook (7th Edition):

Perez, Jessica. “Regulation of vascular smooth muscle cell signaling and metabolism by platelet-derived growth factor.” 2010. Web. 16 Oct 2019.

Vancouver:

Perez J. Regulation of vascular smooth muscle cell signaling and metabolism by platelet-derived growth factor. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Oct 16]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,928.

Council of Science Editors:

Perez J. Regulation of vascular smooth muscle cell signaling and metabolism by platelet-derived growth factor. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,928

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