Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

You searched for subject:( Nuclear Proteins physiology 60). Showing records 1 – 30 of 43768 total matches.

[1] [2] [3] [4] [5] … [1459]

Search Limiters

Last 2 Years | English Only

Degrees

Levels

Languages

Country

▼ Search Limiters

1. Paik, Jason Chang. A nucleolar specificity factor for E2F1-induced cell death.

Degree: PhD, 2010, University of Alabama – Birmingham

The E2F family of transcription factors are important regulators of cell proliferation, and are often dysregulated in cancers. One member of the E2F family, E2F1,… (more)

Subjects/Keywords: Apoptosis<; br>; Chromosomal Proteins, Non-Histone  – physiology<; br>; E2F1 Transcription Factor  – physiology<; br>; Nuclear Proteins  – physiology<; br>; Transcription, Genetic<; br>; Transcriptional Activation

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Paik, J. C. (2010). A nucleolar specificity factor for E2F1-induced cell death. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1171

Chicago Manual of Style (16th Edition):

Paik, Jason Chang. “A nucleolar specificity factor for E2F1-induced cell death.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1171.

MLA Handbook (7th Edition):

Paik, Jason Chang. “A nucleolar specificity factor for E2F1-induced cell death.” 2010. Web. 18 Jan 2020.

Vancouver:

Paik JC. A nucleolar specificity factor for E2F1-induced cell death. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1171.

Council of Science Editors:

Paik JC. A nucleolar specificity factor for E2F1-induced cell death. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1171

2. Yu, Jei-Hwa. MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1.

Degree: PhD, 2008, University of Alabama – Birmingham

Papillomaviruses (PV) are prevalent pathogens that infect human or animal squamous epithelia. Its genome is a double strand circular DNA of approximately 7.9 kb. It… (more)

Subjects/Keywords: DNA Helicases  – metabolism <; br>; DNA-Binding Proteins  – metabolism <; br>; Human papillomavirus 11  – physiology <; br>; Mitogen-Activated Protein Kinases  – metabolism <; br>; Nuclear Localization Signals  – metabolism <; br>; Replication Origin <; br>; Viral Proteins  – metabolism

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Yu, J. (2008). MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,213

Chicago Manual of Style (16th Edition):

Yu, Jei-Hwa. “MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,213.

MLA Handbook (7th Edition):

Yu, Jei-Hwa. “MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1.” 2008. Web. 18 Jan 2020.

Vancouver:

Yu J. MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,213.

Council of Science Editors:

Yu J. MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,213

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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 January 18, 2020. 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. 18 Jan 2020.

Vancouver:

Meares GP. Directing Akt and GSK3[beta] : molecular insights into cell signaling and survival. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Jan 18]. 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. Mao,Weiming. The role of bHLH gene ash1 in the developing chick eye.

Degree: PhD, 2008, University of Alabama – Birmingham

Development of the vertebrate eye is controlled by a network of regulatory genes including those in the basic loop-helix-loop (bHLH) family. In this study, we… (more)

Subjects/Keywords: Amacrine Cells  – physiology<; br>; Avian Proteins  – metabolism<; br>; Basic Helix-Loop-Helix Transcription Factors  – metabolism<; br>; Gene Expression Regulation, Developmental  – physiology<; br>; Nerve Tissue Proteins  – genetics<; br>; Nuclear Reprogramming<; br>; Retina  – cytology<; br>; Retinal Neurons  – cytology Retinal Pigment Epithelium  – cytology<; br>; Stem Cells  – cytology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Mao,Weiming. (2008). The role of bHLH gene ash1 in the developing chick eye. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,527

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16th Edition):

Mao,Weiming. “The role of bHLH gene ash1 in the developing chick eye.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,527.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7th Edition):

Mao,Weiming. “The role of bHLH gene ash1 in the developing chick eye.” 2008. Web. 18 Jan 2020.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

Mao,Weiming. The role of bHLH gene ash1 in the developing chick eye. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,527.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

Mao,Weiming. The role of bHLH gene ash1 in the developing chick eye. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,527

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

5. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 January 18, 2020. 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. 18 Jan 2020.

Vancouver:

Matthews TA. Pathological modifications of tau induce toxicity and facilitate cell death. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Jan 18]. 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

6. Indran, Sabarish Vellatheri. Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions.

Degree: PhD, 2010, University of Alabama – Birmingham

Human cytomegalovirus, a ubiquitous human pathogen, establishes a persistent infection in the infected host. HCMV assembly takes place in the nucleus and cytoplasm of infected… (more)

Subjects/Keywords: Adaptor Proteins, Signal Transducing – physiology.<; br>; Cytomegalovirus<; br>; Cytoskeletal Proteins – physiology<; br>; Host-Pathogen Interactions.<; br>; Phosphoproteins – metabolism<; br>; Viral Matrix Proteins – metabolism.<; br>; Virus Assembly.<; br>; rab GTP-Binding Proteins – metabolism.

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Indran, S. V. (2010). Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1351

Chicago Manual of Style (16th Edition):

Indran, Sabarish Vellatheri. “Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1351.

MLA Handbook (7th Edition):

Indran, Sabarish Vellatheri. “Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions.” 2010. Web. 18 Jan 2020.

Vancouver:

Indran SV. Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1351.

Council of Science Editors:

Indran SV. Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1351

7. Harms, Paul William. Modulation of cell signaling by Tomoregulins in embryogenesis and cancer.

Degree: PhD, 2006, University of Alabama – Birmingham

Growth factor signals often regulate similar cellular processes both during embryogenesis and in adult homeostasis. Stringent control of these signals ensures proper embryonic development and… (more)

Subjects/Keywords: Homeodomain Proteins <; br>; Membrane Proteins  – metabolism <; br>; Neoplasm Proteins  – metabolism <; br>; Proteins <; br>; Signal Transduction  – physiology <; br>; Transcription Factors <; br>; Xenopus Proteins

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Harms, P. W. (2006). Modulation of cell signaling by Tomoregulins in embryogenesis and cancer. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,369

Chicago Manual of Style (16th Edition):

Harms, Paul William. “Modulation of cell signaling by Tomoregulins in embryogenesis and cancer.” 2006. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,369.

MLA Handbook (7th Edition):

Harms, Paul William. “Modulation of cell signaling by Tomoregulins in embryogenesis and cancer.” 2006. Web. 18 Jan 2020.

Vancouver:

Harms PW. Modulation of cell signaling by Tomoregulins in embryogenesis and cancer. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2006. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,369.

Council of Science Editors:

Harms PW. Modulation of cell signaling by Tomoregulins in embryogenesis and cancer. [Doctoral Dissertation]. University of Alabama – Birmingham; 2006. Available from: http://contentdm.mhsl.uab.edu/u?/etd,369

8. Kosek, David J. (David Jeffrey). Aging differences in mechanisms of human skeletal muscle hypertrophy.

Degree: PhD, 2007, University of Alabama – Birmingham

Sarcopenia, the age-associated loss of muscle mass, affects all individuals to varying degrees as years advance, and leads to decreases in strength, power and agility… (more)

Subjects/Keywords: Aging  – physiology<; br>; Dystrophin-Associated Proteins  – physiology<; br>; Exercise  – physiology<; br>; Muscle Development  – physiology<; br>; Muscle, Skeletal  – cytology<; br>; Physical Fitness  – physiology<; br>; Satellite Cells, Skeletal Muscle  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Kosek, D. J. (. J. (2007). Aging differences in mechanisms of human skeletal muscle hypertrophy. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,603

Chicago Manual of Style (16th Edition):

Kosek, David J (David Jeffrey). “Aging differences in mechanisms of human skeletal muscle hypertrophy.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,603.

MLA Handbook (7th Edition):

Kosek, David J (David Jeffrey). “Aging differences in mechanisms of human skeletal muscle hypertrophy.” 2007. Web. 18 Jan 2020.

Vancouver:

Kosek DJ(J. Aging differences in mechanisms of human skeletal muscle hypertrophy. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,603.

Council of Science Editors:

Kosek DJ(J. Aging differences in mechanisms of human skeletal muscle hypertrophy. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,603

9. Ontiveros, Steven J. Intracellular trafficking of the hantaviral nucleocapsid protein and its function in modulation of immune signaling.

Degree: PhD, 2009, University of Alabama – Birmingham

Old World and New World hantaviruses, family Bunyaviridae, mature intracellularly within cellular compartments. Although it is generally accepted they assemble and bud in the Golgi… (more)

Subjects/Keywords: Apoptosis<; br>; Capsid Proteins  – physiology<; br>; Hantaan virus  – pathogenicity<; br>; Hantavirus  – pathogenicity<; br>; Signal Transduction<; br>; Viral Core Proteins  – physiology<; br>; Virulence Factors  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Ontiveros, S. J. (2009). Intracellular trafficking of the hantaviral nucleocapsid protein and its function in modulation of immune signaling. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,687

Chicago Manual of Style (16th Edition):

Ontiveros, Steven J. “Intracellular trafficking of the hantaviral nucleocapsid protein and its function in modulation of immune signaling.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,687.

MLA Handbook (7th Edition):

Ontiveros, Steven J. “Intracellular trafficking of the hantaviral nucleocapsid protein and its function in modulation of immune signaling.” 2009. Web. 18 Jan 2020.

Vancouver:

Ontiveros SJ. Intracellular trafficking of the hantaviral nucleocapsid protein and its function in modulation of immune signaling. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,687.

Council of Science Editors:

Ontiveros SJ. Intracellular trafficking of the hantaviral nucleocapsid protein and its function in modulation of immune signaling. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,687

10. Lai, Yun-Ju. Role of TRIP6 in LPA-induced cell migration.

Degree: PhD, 2007, University of Alabama – Birmingham

The LIM domain-containing Thyroid Receptor-Interacting Protein 6 (TRIP6) is a zyxin family member that has been implicated in actin dynamics and cell motility. In this… (more)

Subjects/Keywords: Adaptor Proteins, Signal Transducing<; br>; Carrier Proteins  – physiology<; br>; Cell Movement<; br>; Feedback, Biochemical<; br>; Lysophospholipids<; br>; Protein-Tyrosine Kinases  – physiology<; br>; Receptors, G-Protein-Coupled  – metabolism<; br>; Transcription Factors

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Lai, Y. (2007). Role of TRIP6 in LPA-induced cell migration. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,453

Chicago Manual of Style (16th Edition):

Lai, Yun-Ju. “Role of TRIP6 in LPA-induced cell migration.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,453.

MLA Handbook (7th Edition):

Lai, Yun-Ju. “Role of TRIP6 in LPA-induced cell migration.” 2007. Web. 18 Jan 2020.

Vancouver:

Lai Y. Role of TRIP6 in LPA-induced cell migration. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,453.

Council of Science Editors:

Lai Y. Role of TRIP6 in LPA-induced cell migration. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,453

11. Krzyzaniak, Magdalena Anna. Role of the gM/gN glycoprotein complex in the final assembly and egress of the human cytomegalovirus (HCMV).

Degree: PhD, 2008, University of Alabama – Birmingham

HCMV consists of a dsDNA genome enclosed by, an icosahedral capsid surrounded by a layer of tegument proteins; the virion structure is enclosed in a… (more)

Subjects/Keywords: Cytomegalovirus  – physiology <; br>; Glycoproteins  – metabolism <; br>; Protein Sorting Signals <; br>; Viral Envelope Proteins  – metabolism <; br>; Virus Assembly <; br>; Virus Replication

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Krzyzaniak, M. A. (2008). Role of the gM/gN glycoprotein complex in the final assembly and egress of the human cytomegalovirus (HCMV). (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,231

Chicago Manual of Style (16th Edition):

Krzyzaniak, Magdalena Anna. “Role of the gM/gN glycoprotein complex in the final assembly and egress of the human cytomegalovirus (HCMV).” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,231.

MLA Handbook (7th Edition):

Krzyzaniak, Magdalena Anna. “Role of the gM/gN glycoprotein complex in the final assembly and egress of the human cytomegalovirus (HCMV).” 2008. Web. 18 Jan 2020.

Vancouver:

Krzyzaniak MA. Role of the gM/gN glycoprotein complex in the final assembly and egress of the human cytomegalovirus (HCMV). [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,231.

Council of Science Editors:

Krzyzaniak MA. Role of the gM/gN glycoprotein complex in the final assembly and egress of the human cytomegalovirus (HCMV). [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,231

12. Smith, Rebecca Burt. Axonal trafficking of BMP signals in Drosophila motoneurons.

Degree: PhD, 2009, University of Alabama – Birmingham

The Drosophila Bone Morphogenetic Protein (BMP) Glass bottom boat (Gbb) is a ligand for the BMP type II receptor, Wishful thinking (Wit). Mutations in either… (more)

Subjects/Keywords: Axonal Transport<; br>; Bone Morphogenetic Proteins  – genetics<; br>; Drosophila  – genetics<; br>; Motor Neurons<; br>; Neuronal Plasticity<; br>; Synapses  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Smith, R. B. (2009). Axonal trafficking of BMP signals in Drosophila motoneurons. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,930

Chicago Manual of Style (16th Edition):

Smith, Rebecca Burt. “Axonal trafficking of BMP signals in Drosophila motoneurons.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,930.

MLA Handbook (7th Edition):

Smith, Rebecca Burt. “Axonal trafficking of BMP signals in Drosophila motoneurons.” 2009. Web. 18 Jan 2020.

Vancouver:

Smith RB. Axonal trafficking of BMP signals in Drosophila motoneurons. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,930.

Council of Science Editors:

Smith RB. Axonal trafficking of BMP signals in Drosophila motoneurons. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,930

13. Dolan, Philip J. The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau.

Degree: PhD, 2010, University of Alabama – Birmingham

Alzheimer Disease (AD) is pathologically characterized by the appearance of senile plaques composed of β-amyloid (Aβ) and neurofibrillary tangles composed of the microtubule-associated protein tau.… (more)

Subjects/Keywords: Alzheimer Disease  – enzymology<; br>; Autophagy<; br>; Caspases  – metabolism<; br>; Protein Kinases  – metabolism<; br>; Signal Transduction<; br>; tau Proteins  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Dolan, P. J. (2010). The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1090

Chicago Manual of Style (16th Edition):

Dolan, Philip J. “The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1090.

MLA Handbook (7th Edition):

Dolan, Philip J. “The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau.” 2010. Web. 18 Jan 2020.

Vancouver:

Dolan PJ. The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1090.

Council of Science Editors:

Dolan PJ. The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1090

14. Joo, Heui Yun. Understanding the regulatory mechanisms of UBP-M and H2A deubiquitination in chromatin and cellular functions.

Degree: PhD, 2009, University of Alabama – Birmingham

Posttranslational modifications of histones regulate important chromatin and cellular functions. Among them, ubiquitination of histone H2A is correlated to transcriptional repression, such as HOX gene… (more)

Subjects/Keywords: Chromatin  – physiology<; br>; Endopeptidases  – metabolism<; br>; Histones  – metabolism<; br>; Ubiquitin Thiolesterase  – metabolism<; br>; Xenopus Proteins  – metabolism<; br>; Xenopus laevis  – embryology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Joo, H. Y. (2009). Understanding the regulatory mechanisms of UBP-M and H2A deubiquitination in chromatin and cellular functions. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1101

Chicago Manual of Style (16th Edition):

Joo, Heui Yun. “Understanding the regulatory mechanisms of UBP-M and H2A deubiquitination in chromatin and cellular functions.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1101.

MLA Handbook (7th Edition):

Joo, Heui Yun. “Understanding the regulatory mechanisms of UBP-M and H2A deubiquitination in chromatin and cellular functions.” 2009. Web. 18 Jan 2020.

Vancouver:

Joo HY. Understanding the regulatory mechanisms of UBP-M and H2A deubiquitination in chromatin and cellular functions. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1101.

Council of Science Editors:

Joo HY. Understanding the regulatory mechanisms of UBP-M and H2A deubiquitination in chromatin and cellular functions. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1101

15. Yang, Youfeng. The Role Of Map Kinase Cascade In Msp Signaling Response.

Degree: PhD, 2010, University of Alabama – Birmingham

The MSP domain is an evolutionarily conserved immunoglobulin-like structure of about 120 amino acids (Miller et al., 2001). A P56S missense mutation in the MSP… (more)

Subjects/Keywords: Caenorhabditis elegans – metabolism.<; br>; Helminth Proteins – physiology.<; br>; MAP Kinase Signaling System – physiology.<; br>; Mitogen-Activated Protein Kinases – metabolism.<; br>; Oocytes – physiology<; br>; Reactive Oxygen Species – metabolism<; br>; Signal Transduction – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Yang, Y. (2010). The Role Of Map Kinase Cascade In Msp Signaling Response. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1399

Chicago Manual of Style (16th Edition):

Yang, Youfeng. “The Role Of Map Kinase Cascade In Msp Signaling Response.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1399.

MLA Handbook (7th Edition):

Yang, Youfeng. “The Role Of Map Kinase Cascade In Msp Signaling Response.” 2010. Web. 18 Jan 2020.

Vancouver:

Yang Y. The Role Of Map Kinase Cascade In Msp Signaling Response. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1399.

Council of Science Editors:

Yang Y. The Role Of Map Kinase Cascade In Msp Signaling Response. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1399

16. Masyukova, Svetlana V. Analysis of NPHP complex genetic interactions associated with human cilia disorders.

Degree: PhD, 2011, University of Alabama – Birmingham

Primary cilia are antenna-like organelles that extend from the surface of almost all mammalian cell types. They regulate many signaling pathways and sense physical and… (more)

Subjects/Keywords: Caenorhabditis elegans Proteins – metabolism.<; br>; Cilia – metabolism.<; br>; Membrane Proteins – metabolism<; br>; Mutation, Missense – physiology.<; br>; Proteins – genetics<; br>; Proteins – metabolism

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Masyukova, S. V. (2011). Analysis of NPHP complex genetic interactions associated with human cilia disorders. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1352

Chicago Manual of Style (16th Edition):

Masyukova, Svetlana V. “Analysis of NPHP complex genetic interactions associated with human cilia disorders.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1352.

MLA Handbook (7th Edition):

Masyukova, Svetlana V. “Analysis of NPHP complex genetic interactions associated with human cilia disorders.” 2011. Web. 18 Jan 2020.

Vancouver:

Masyukova SV. Analysis of NPHP complex genetic interactions associated with human cilia disorders. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1352.

Council of Science Editors:

Masyukova SV. Analysis of NPHP complex genetic interactions associated with human cilia disorders. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1352

17. Baker, Brandi J. Oncostatin M-induced gene expression and regulation in astrocytes and microglia.

Degree: PhD, 2009, University of Alabama – Birmingham

Astrocytes and microglia are specialized glial cells of the Central Nervous System (CNS) that modulate neural activity and regulate immunological and inflammatory events. These cells… (more)

Subjects/Keywords: Astrocytes  – physiology<; br>; Central Nervous System  – immunology<; br>; Central Nervous System Diseases  – immunology<; br>; Gene Expression Regulation  – physiology<; br>; Microglia  – physiology<; br>; Oncostatin M  – physiology<; br>; Suppressor of Cytokine Signaling Proteins  – biosynthesis<; br>; Suppressor of Cytokine Signaling Proteins  – metabolism

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Baker, B. J. (2009). Oncostatin M-induced gene expression and regulation in astrocytes and microglia. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,560

Chicago Manual of Style (16th Edition):

Baker, Brandi J. “Oncostatin M-induced gene expression and regulation in astrocytes and microglia.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,560.

MLA Handbook (7th Edition):

Baker, Brandi J. “Oncostatin M-induced gene expression and regulation in astrocytes and microglia.” 2009. Web. 18 Jan 2020.

Vancouver:

Baker BJ. Oncostatin M-induced gene expression and regulation in astrocytes and microglia. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,560.

Council of Science Editors:

Baker BJ. Oncostatin M-induced gene expression and regulation in astrocytes and microglia. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,560

18. Murakami, Miho. Fiber modification of adenoviral vectors for cancer gene therapy.

Degree: PhD, 2010, University of Alabama – Birmingham

Cancer still remains a major public health concern despite improvements in primary prevention, early detection and advanced treatments. Cancer gene therapy using human adenovirus serotype… (more)

Subjects/Keywords: Adenoviruses, Human<; br>; Capsid Proteins<; br>; Gene Therapy  – methods<; br>; Genetic Vectors<; br>; Prostatic Neoplasms  – genetics<; br>; Recombinant Fusion Proteins  – metabolism<; br>; Transduction, Genetic<; br>; Viral Tropism  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Murakami, M. (2010). Fiber modification of adenoviral vectors for cancer gene therapy. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1166

Chicago Manual of Style (16th Edition):

Murakami, Miho. “Fiber modification of adenoviral vectors for cancer gene therapy.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1166.

MLA Handbook (7th Edition):

Murakami, Miho. “Fiber modification of adenoviral vectors for cancer gene therapy.” 2010. Web. 18 Jan 2020.

Vancouver:

Murakami M. Fiber modification of adenoviral vectors for cancer gene therapy. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1166.

Council of Science Editors:

Murakami M. Fiber modification of adenoviral vectors for cancer gene therapy. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1166

19. Cheetham, Chad Christopher. Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models.

Degree: PhD, 2011, University of Alabama – Birmingham

DYT1 dystonia is an inherited movement disorder caused by a trinucleotide deletion (DeltaGAG) in the DYT1 (TOR1A) gene, which codes for the torsinA protein. Dr.… (more)

Subjects/Keywords: Adrenergic Neurons – physiology.<; br>; Adrenergic Uptake Inhibitors – pharmacology.<; br>; Antidepressive Agents – pharmacology<; br>; Antidepressive Agents, Tricyclic – pharmacology.<; br>; Arrestins – physiology.<; br>; Desipramine – pharmacology.<; br>; Microfilament Proteins – physiology.<; br>; Mitogen-Activated Protein Kinase 1 – biosynthesis.<; br>; Mitogen-Activated Protein Kinase 3 – biosynthesis.<; br>; Nerve Tissue Proteins – physiology<; br>; Receptors, Adrenergic, alpha-2 – physiology.

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Cheetham, C. C. (2011). Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1433

Chicago Manual of Style (16th Edition):

Cheetham, Chad Christopher. “Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1433.

MLA Handbook (7th Edition):

Cheetham, Chad Christopher. “Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models.” 2011. Web. 18 Jan 2020.

Vancouver:

Cheetham CC. Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1433.

Council of Science Editors:

Cheetham CC. Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1433

20. Parks, Brian W. Modulation of lipoprotein metabolism and atherosclerosis by the G protein-coupled receptor, G2A.

Degree: PhD, 2008, University of Alabama – Birmingham

The G protein-coupled receptor, G2A, is expressed by multiple cell-types involved in atherosclerosis and is activated by structurally related lysophospholipids generated during low-density lipoprotein (LDL)… (more)

Subjects/Keywords: Apolipoproteins E  – metabolism<; br>; Arteriosclerosis<; br>; Bone Marrow Cells  – metabolism<; br>; Cell Cycle Proteins<; br>; Hypercholesterolemia  – metabolism<; br>; Lysophosphatidylcholines  – metabolism<; br>; Macrophages  – physiology<; br>; Receptors, G-Protein-Coupled<; br>; Receptors, LDL

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Parks, B. W. (2008). Modulation of lipoprotein metabolism and atherosclerosis by the G protein-coupled receptor, G2A. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,768

Chicago Manual of Style (16th Edition):

Parks, Brian W. “Modulation of lipoprotein metabolism and atherosclerosis by the G protein-coupled receptor, G2A.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,768.

MLA Handbook (7th Edition):

Parks, Brian W. “Modulation of lipoprotein metabolism and atherosclerosis by the G protein-coupled receptor, G2A.” 2008. Web. 18 Jan 2020.

Vancouver:

Parks BW. Modulation of lipoprotein metabolism and atherosclerosis by the G protein-coupled receptor, G2A. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,768.

Council of Science Editors:

Parks BW. Modulation of lipoprotein metabolism and atherosclerosis by the G protein-coupled receptor, G2A. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,768

21. Nash, Kevin T. (Kevin Tyler). KISS1 metastasis suppressor secretion is required for metastasis suppression.

Degree: PhD, 2006, University of Alabama – Birmingham

Failure to reduce the number of cancer deaths over the last 50 years is due to the inability to selectively target metastatic disease. Recently, the… (more)

Subjects/Keywords: Gene Expression Regulation, Neoplastic <; br>; Melanoma  – metabolism <; br>; Melanoma  – secretion <; br>; Neoplasm Metastasis  – prevention & control <; br>; Proteins  – physiology <; br>; Receptors, G-Protein-Coupled  – metabolism <; br>; Tumor Suppressor Proteins  – secretion

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Nash, K. T. (. T. (2006). KISS1 metastasis suppressor secretion is required for metastasis suppression. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,380

Chicago Manual of Style (16th Edition):

Nash, Kevin T (Kevin Tyler). “KISS1 metastasis suppressor secretion is required for metastasis suppression.” 2006. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,380.

MLA Handbook (7th Edition):

Nash, Kevin T (Kevin Tyler). “KISS1 metastasis suppressor secretion is required for metastasis suppression.” 2006. Web. 18 Jan 2020.

Vancouver:

Nash KT(T. KISS1 metastasis suppressor secretion is required for metastasis suppression. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2006. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,380.

Council of Science Editors:

Nash KT(T. KISS1 metastasis suppressor secretion is required for metastasis suppression. [Doctoral Dissertation]. University of Alabama – Birmingham; 2006. Available from: http://contentdm.mhsl.uab.edu/u?/etd,380

22. Harouaka, Djamila. Investigation of residues of the vesicular stomatitis virus nucleocapsid protein that affect transcription and RNA replication.

Degree: PhD, 2010, University of Alabama – Birmingham

The template for transcription and RNA replication for vesicular stomatitis virus (VSV) and other negative-strand RNA viruses is a ribonucleoprotein (RNP) complex consisting of the… (more)

Subjects/Keywords: Nucleocapsid Proteins  – chemistry<; br>; Nucleocapsid Proteins  – genetics<; br>; Reverse Transcription  – genetics<; br>; RNA, Viral  – genetics<; br>; Vesiculovirus  – genetics<; br>; Vesiculovirus  – physiology<; br>; Virus Replication – genetics

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Harouaka, D. (2010). Investigation of residues of the vesicular stomatitis virus nucleocapsid protein that affect transcription and RNA replication. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,848

Chicago Manual of Style (16th Edition):

Harouaka, Djamila. “Investigation of residues of the vesicular stomatitis virus nucleocapsid protein that affect transcription and RNA replication.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,848.

MLA Handbook (7th Edition):

Harouaka, Djamila. “Investigation of residues of the vesicular stomatitis virus nucleocapsid protein that affect transcription and RNA replication.” 2010. Web. 18 Jan 2020.

Vancouver:

Harouaka D. Investigation of residues of the vesicular stomatitis virus nucleocapsid protein that affect transcription and RNA replication. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,848.

Council of Science Editors:

Harouaka D. Investigation of residues of the vesicular stomatitis virus nucleocapsid protein that affect transcription and RNA replication. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,848

23. Balasubramani, Anand. Evolutionarily Conserved Cis-Acting Elements Regulate Lineage-Specific Expression Of Ifng.

Degree: PhD, 2010, University of Alabama – Birmingham

The ability to differentially manipulate available genetic information in order to generate diverse cellular identities represents an innovation of complex multicellular eukaryotic organisms. Cis-acting modules… (more)

Subjects/Keywords: DNA Replication – physiology.<; br>; Drosophila – metabolism.<; br>; Drosophila Proteins – metabolism.<; br>; GTP Phosphohydrolases – metabolism.<; br>; Microfilament Proteins – metabolism.<; br>; Multiprotein Complexes – metabolism.<; br>; Origin Recognition Complex – metabolism.

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Balasubramani, A. (2010). Evolutionarily Conserved Cis-Acting Elements Regulate Lineage-Specific Expression Of Ifng. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1428

Chicago Manual of Style (16th Edition):

Balasubramani, Anand. “Evolutionarily Conserved Cis-Acting Elements Regulate Lineage-Specific Expression Of Ifng.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1428.

MLA Handbook (7th Edition):

Balasubramani, Anand. “Evolutionarily Conserved Cis-Acting Elements Regulate Lineage-Specific Expression Of Ifng.” 2010. Web. 18 Jan 2020.

Vancouver:

Balasubramani A. Evolutionarily Conserved Cis-Acting Elements Regulate Lineage-Specific Expression Of Ifng. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1428.

Council of Science Editors:

Balasubramani A. Evolutionarily Conserved Cis-Acting Elements Regulate Lineage-Specific Expression Of Ifng. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1428

24. Genovese, Nicholas J. The mechanism of human papillomavirus E7 protein mediated S-phase reentry in the squamous epithelium.

Degree: PhD, 2010, University of Alabama – Birmingham

Though human papillomavirus infection of the human epidermis is epidemiologically widespread and typically benign, manipulation of the cell cycle within host tissues during infections can… (more)

Subjects/Keywords: Cell Cycle<; br>; Cell Transformation, Viral<; br>; Human papillomavirus 16  – metabolism<; br>; Keratinocytes<; br>; Oncogene Proteins, Viral  – metabolism<; br>; Papillomaviridae  – physiology<; br>; Papillomavirus E7 Proteins  – metabolism<; br>; Receptors, Estrogen  – metabolism<; br>; Retinoblastoma-Like Protein p130  – metabolism<; br>; S Phase

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Genovese, N. J. (2010). The mechanism of human papillomavirus E7 protein mediated S-phase reentry in the squamous epithelium. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1158

Chicago Manual of Style (16th Edition):

Genovese, Nicholas J. “The mechanism of human papillomavirus E7 protein mediated S-phase reentry in the squamous epithelium.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1158.

MLA Handbook (7th Edition):

Genovese, Nicholas J. “The mechanism of human papillomavirus E7 protein mediated S-phase reentry in the squamous epithelium.” 2010. Web. 18 Jan 2020.

Vancouver:

Genovese NJ. The mechanism of human papillomavirus E7 protein mediated S-phase reentry in the squamous epithelium. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1158.

Council of Science Editors:

Genovese NJ. The mechanism of human papillomavirus E7 protein mediated S-phase reentry in the squamous epithelium. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1158

25. Thal, Melissa Ann. Characterization of the induction and regulation of early B cell development.

Degree: PhD, 2009, University of Alabama – Birmingham

Hematopoiesis is a highly regulated process directed by the microenvironment or niche in the bone marrow and the transcription factors those signals activate. Gene knockout… (more)

Subjects/Keywords: B-Lymphocytes  – cytology<; br>; Down-Regulation<; br>; Inhibitor of Differentiation Protein 2  – genetics<; br>; Inhibitor of Differentiation Proteins  – genetics<; br>; Receptors, Interleukin-7  – deficiency<; br>; TCF Transcription Factors  – physiology<; br>; Trans-Activators  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Thal, M. A. (2009). Characterization of the induction and regulation of early B cell development. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,578

Chicago Manual of Style (16th Edition):

Thal, Melissa Ann. “Characterization of the induction and regulation of early B cell development.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,578.

MLA Handbook (7th Edition):

Thal, Melissa Ann. “Characterization of the induction and regulation of early B cell development.” 2009. Web. 18 Jan 2020.

Vancouver:

Thal MA. Characterization of the induction and regulation of early B cell development. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,578.

Council of Science Editors:

Thal MA. Characterization of the induction and regulation of early B cell development. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,578

26. Deshane, Jessy S. Regulation of HO-1 and its role in angiogenesis.

Degree: PhD, 2007, University of Alabama – Birmingham

Ischemic tissue and organ dysfunction occur in a variety of cardiovascular diseases. The hypoxic environment created during ischemic injury activates cytoprotective genes, of which heme… (more)

Subjects/Keywords: Angiogenic Proteins  – physiology<; br>; Endothelial Cells  – enzymology<; br>; Endothelial Cells  – physiology<; br>; Endothelium, Vascular<; br>; Heme Oxygenase-1  – genetics<; br>; Heme Oxygenase-1  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Deshane, J. S. (2007). Regulation of HO-1 and its role in angiogenesis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,437

Chicago Manual of Style (16th Edition):

Deshane, Jessy S. “Regulation of HO-1 and its role in angiogenesis.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,437.

MLA Handbook (7th Edition):

Deshane, Jessy S. “Regulation of HO-1 and its role in angiogenesis.” 2007. Web. 18 Jan 2020.

Vancouver:

Deshane JS. Regulation of HO-1 and its role in angiogenesis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,437.

Council of Science Editors:

Deshane JS. Regulation of HO-1 and its role in angiogenesis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,437

27. Qian, Yingjuan, Ph.D. The role of DEC1 in P53-dependent cellular senescence.

Degree: PhD, 2008, University of Alabama – Birmingham

The p53 tumor suppressor is the most commonly mutated gene in human cancers. As a transcription factor, p53 exerts its tumor suppressor function through the… (more)

Subjects/Keywords: Basic Helix-Loop-Helix Transcription Factors  – genetics<; br>; Basic Helix-Loop-Helix Transcription Factors  – physiology<; br>; Cell Aging  – physiology<; br>; DNA Damage<; br>; Tumor Suppressor Protein p53  – physiology<; br>; Tumor Suppressor Proteins  – genetics

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Qian, Yingjuan, P. D. (2008). The role of DEC1 in P53-dependent cellular senescence. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,462

Chicago Manual of Style (16th Edition):

Qian, Yingjuan, Ph D. “The role of DEC1 in P53-dependent cellular senescence.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,462.

MLA Handbook (7th Edition):

Qian, Yingjuan, Ph D. “The role of DEC1 in P53-dependent cellular senescence.” 2008. Web. 18 Jan 2020.

Vancouver:

Qian, Yingjuan PD. The role of DEC1 in P53-dependent cellular senescence. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,462.

Council of Science Editors:

Qian, Yingjuan PD. The role of DEC1 in P53-dependent cellular senescence. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,462

28. Maitra, Sushmit. The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase.

Degree: PhD, 2008, University of Alabama – Birmingham

Regulated mRNA decay is a highly important process for the tight control of gene expression. Inherently unstable mRNAs contain AU-rich elements (AREs) in the 3’… (more)

Subjects/Keywords: Intracellular Signaling Peptides and Proteins  – metabolism <; br>; Protein-Serine-Threonine Kinases  – metabolism <; br>; RNA, Messenger  – metabolism <; br>; RNA Stability  – physiology <; br>; RNA-Binding Proteins  – metabolism <; br>; TATA-Binding Protein Associated Factors  – metabolism

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Maitra, S. (2008). The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,379

Chicago Manual of Style (16th Edition):

Maitra, Sushmit. “The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,379.

MLA Handbook (7th Edition):

Maitra, Sushmit. “The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase.” 2008. Web. 18 Jan 2020.

Vancouver:

Maitra S. The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,379.

Council of Science Editors:

Maitra S. The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,379

29. Kallmeyer, Adam K. (Adam Keith). Regulatory mechanisms of eukaryotic translation termination.

Degree: PhD, 2007, University of Alabama – Birmingham

Translation is separated into three distinct steps: initiation, elongation, and termination. Termination is mediated by a heterodimer of eRF1 and eRF3. eRF1 (encoded by the… (more)

Subjects/Keywords: Casein Kinase II  – metabolism<; br>; Peptide Termination Factors  – metabolism<; br>; Protein Biosynthesis  – physiology<; br>; Recombinant Fusion Proteins<; br>; Saccharomyces cerevisiae  – genetics<; br>; Saccharomyces cerevisiae Proteins  – metabolism

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Kallmeyer, A. K. (. K. (2007). Regulatory mechanisms of eukaryotic translation termination. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,450

Chicago Manual of Style (16th Edition):

Kallmeyer, Adam K (Adam Keith). “Regulatory mechanisms of eukaryotic translation termination.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,450.

MLA Handbook (7th Edition):

Kallmeyer, Adam K (Adam Keith). “Regulatory mechanisms of eukaryotic translation termination.” 2007. Web. 18 Jan 2020.

Vancouver:

Kallmeyer AK(K. Regulatory mechanisms of eukaryotic translation termination. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,450.

Council of Science Editors:

Kallmeyer AK(K. Regulatory mechanisms of eukaryotic translation termination. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,450

30. Marion, William R. (William Robert). Bacteriophage P22 scaffolding protein : functions and mechanisms in procapsid assembly.

Degree: MS, 2007, University of Alabama – Birmingham

Bacteriophage P22 scaffolding protein is responsible for controlling the assembly of 420 monomeric coat protein subunits into a spherical, T=7 procapsid lattice. The precise mechanism… (more)

Subjects/Keywords: Bacteriophage P22  – growth & development<; br>; Bacteriophage P22  – chemistry<; br>; Bacteriophage P22  – genetics<; br>; Capsid Proteins  – chemistry<; br>; Models, Molecular<; br>; Viral Structural Proteins  – physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Marion, W. R. (. R. (2007). Bacteriophage P22 scaffolding protein : functions and mechanisms in procapsid assembly. (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,455

Chicago Manual of Style (16th Edition):

Marion, William R (William Robert). “Bacteriophage P22 scaffolding protein : functions and mechanisms in procapsid assembly.” 2007. Masters Thesis, University of Alabama – Birmingham. Accessed January 18, 2020. http://contentdm.mhsl.uab.edu/u?/etd,455.

MLA Handbook (7th Edition):

Marion, William R (William Robert). “Bacteriophage P22 scaffolding protein : functions and mechanisms in procapsid assembly.” 2007. Web. 18 Jan 2020.

Vancouver:

Marion WR(R. Bacteriophage P22 scaffolding protein : functions and mechanisms in procapsid assembly. [Internet] [Masters thesis]. University of Alabama – Birmingham; 2007. [cited 2020 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,455.

Council of Science Editors:

Marion WR(R. Bacteriophage P22 scaffolding protein : functions and mechanisms in procapsid assembly. [Masters Thesis]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,455

[1] [2] [3] [4] [5] … [1459]

.