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You searched for subject:( Neoplasm Proteins biosynthesis 60). Showing records 1 – 30 of 15028 total matches.

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1. Khotskaya, Yekaterina B. Role of syndecan-1 as key regulator of multiple myeloma pathogenesis.

Degree: PhD, 2009, University of Alabama – Birmingham

Syndecan-1 (CD138), a transmembrane heparan sulfate-bearing proteoglycan, is expressed at high levels on most myeloma cells and is shed into the microenvironment. In patients, high… (more)

Subjects/Keywords: Gene Expression Regulation, Neoplastic<; br>; Melanoma  – metabolism<; br>; Neoplasm Proteins  – biosynthesis<; br>; Neovascularization, Pathologic  – metabolism<; br>; Syndecan-1  – biosynthesis

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APA (6th Edition):

Khotskaya, Y. B. (2009). Role of syndecan-1 as key regulator of multiple myeloma pathogenesis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,766

Chicago Manual of Style (16th Edition):

Khotskaya, Yekaterina B. “Role of syndecan-1 as key regulator of multiple myeloma pathogenesis.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,766.

MLA Handbook (7th Edition):

Khotskaya, Yekaterina B. “Role of syndecan-1 as key regulator of multiple myeloma pathogenesis.” 2009. Web. 22 Feb 2020.

Vancouver:

Khotskaya YB. Role of syndecan-1 as key regulator of multiple myeloma pathogenesis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,766.

Council of Science Editors:

Khotskaya YB. Role of syndecan-1 as key regulator of multiple myeloma pathogenesis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,766

2. Spratling, Patsy M. Cardiovascular Disease Knowledge And Risk Perception Among Women With Recent Preeclampsia: Interventional Education In Disease Management And Prevention.

Degree: PhD, 2012, University of Alabama – Birmingham

There is a growing body of evidence linking preeclampsia to future development of cardiovascular disease (CVD). Although CVD is well-known as the leading cause of… (more)

Subjects/Keywords: Breast Neoplasms<; br>; Gene Expression Regulation, Neoplastic<; br>; MicroRNAs – genetics.<; br>; Neoplasm Metastasis – prevention & control<; br>; Neoplasm Proteins – physiology.<; br>; RNA, Neoplasm – genetics.

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APA (6th Edition):

Spratling, P. M. (2012). Cardiovascular Disease Knowledge And Risk Perception Among Women With Recent Preeclampsia: Interventional Education In Disease Management And Prevention. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1405

Chicago Manual of Style (16th Edition):

Spratling, Patsy M. “Cardiovascular Disease Knowledge And Risk Perception Among Women With Recent Preeclampsia: Interventional Education In Disease Management And Prevention.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1405.

MLA Handbook (7th Edition):

Spratling, Patsy M. “Cardiovascular Disease Knowledge And Risk Perception Among Women With Recent Preeclampsia: Interventional Education In Disease Management And Prevention.” 2012. Web. 22 Feb 2020.

Vancouver:

Spratling PM. Cardiovascular Disease Knowledge And Risk Perception Among Women With Recent Preeclampsia: Interventional Education In Disease Management And Prevention. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1405.

Council of Science Editors:

Spratling PM. Cardiovascular Disease Knowledge And Risk Perception Among Women With Recent Preeclampsia: Interventional Education In Disease Management And Prevention. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1405

3. 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

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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 February 22, 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. 22 Feb 2020.

Vancouver:

Harms PW. Modulation of cell signaling by Tomoregulins in embryogenesis and cancer. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2006. [cited 2020 Feb 22]. 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

4. Grunda, Jessica M. Identification of new strategies for the treatment of glioblastoma multiforme utilizing a pharmacogenomic approach: genetic profiles associated with patient prognosis and outcome to capecitabine treatment.

Degree: PhD, 2009, University of Alabama – Birmingham

Glioblastoma multiforme (GBM) is the most lethal form of primary brain neoplasm with average patient survival between 9 and 15 months even with the most… (more)

Subjects/Keywords: Brain Neoplasms<; br>; Drug Resistance, Neoplasm  – genetics<; br>; Endopeptidases  – metabolism<; br>; Gene Expression Profiling<; br>; Glioblastoma<; br>; Microtubule-Associated Proteins  – metabolism<; br>; Neoplasm Proteins  – metabolism<; br>; Thymidylate Synthase  – metabolism<; br>; Tumor Markers, Biological  – metabolism

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APA (6th Edition):

Grunda, J. M. (2009). Identification of new strategies for the treatment of glioblastoma multiforme utilizing a pharmacogenomic approach: genetic profiles associated with patient prognosis and outcome to capecitabine treatment. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1085

Chicago Manual of Style (16th Edition):

Grunda, Jessica M. “Identification of new strategies for the treatment of glioblastoma multiforme utilizing a pharmacogenomic approach: genetic profiles associated with patient prognosis and outcome to capecitabine treatment.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1085.

MLA Handbook (7th Edition):

Grunda, Jessica M. “Identification of new strategies for the treatment of glioblastoma multiforme utilizing a pharmacogenomic approach: genetic profiles associated with patient prognosis and outcome to capecitabine treatment.” 2009. Web. 22 Feb 2020.

Vancouver:

Grunda JM. Identification of new strategies for the treatment of glioblastoma multiforme utilizing a pharmacogenomic approach: genetic profiles associated with patient prognosis and outcome to capecitabine treatment. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1085.

Council of Science Editors:

Grunda JM. Identification of new strategies for the treatment of glioblastoma multiforme utilizing a pharmacogenomic approach: genetic profiles associated with patient prognosis and outcome to capecitabine treatment. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1085

5. Silveira, Alexandra C. Characterization of SUDS3 as a BRMS1 family member in breast cancer.

Degree: PhD, 2008, University of Alabama – Birmingham

BRMS1 and SUDS3 belong to a protein family characterized by the Sds3-like domain. These proteins are core members of SIN3-HDAC chromatin remodeling complexes and thus,… (more)

Subjects/Keywords: Breast Neoplasms  – metabolism <; br>; Carrier Proteins  – metabolism <; br>; Chromatin Assembly and Disassembly <; br>; Histone Deacetylases  – metabolism <; br>; Neoplasm Proteins  – metabolism <; br>; Repressor Proteins/metabolism

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APA (6th Edition):

Silveira, A. C. (2008). Characterization of SUDS3 as a BRMS1 family member in breast cancer. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,339

Chicago Manual of Style (16th Edition):

Silveira, Alexandra C. “Characterization of SUDS3 as a BRMS1 family member in breast cancer.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,339.

MLA Handbook (7th Edition):

Silveira, Alexandra C. “Characterization of SUDS3 as a BRMS1 family member in breast cancer.” 2008. Web. 22 Feb 2020.

Vancouver:

Silveira AC. Characterization of SUDS3 as a BRMS1 family member in breast cancer. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,339.

Council of Science Editors:

Silveira AC. Characterization of SUDS3 as a BRMS1 family member in breast cancer. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,339

6. 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

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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 February 22, 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. 22 Feb 2020.

Vancouver:

Nash KT(T. KISS1 metastasis suppressor secretion is required for metastasis suppression. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2006. [cited 2020 Feb 22]. 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

7. Cook, Leah M. (Leah Marie). Understanding molecular mechanisms of breast cancer metastasis using genetically-engineered mice.

Degree: PhD, 2011, University of Alabama – Birmingham

Morbidity and mortality of breast cancer patients are drastically increased when primary tumor cells metastasize to distant organ sites. Effective treatment of metastatic disease has… (more)

Subjects/Keywords: Breast Neoplasms  – pathology<; br>; Mammary Neoplasms, Animal<; br>; Mice, Transgenic<; br>; Neoplasm Metastasis  – pathology<; br>; Tumor Microenvironment<; br>; Tumor Suppressor Proteins  – genetics<; br>; Tumor Suppressor Proteins  – metabolism

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APA (6th Edition):

Cook, L. M. (. M. (2011). Understanding molecular mechanisms of breast cancer metastasis using genetically-engineered mice. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1045

Chicago Manual of Style (16th Edition):

Cook, Leah M (Leah Marie). “Understanding molecular mechanisms of breast cancer metastasis using genetically-engineered mice.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1045.

MLA Handbook (7th Edition):

Cook, Leah M (Leah Marie). “Understanding molecular mechanisms of breast cancer metastasis using genetically-engineered mice.” 2011. Web. 22 Feb 2020.

Vancouver:

Cook LM(M. Understanding molecular mechanisms of breast cancer metastasis using genetically-engineered mice. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1045.

Council of Science Editors:

Cook LM(M. Understanding molecular mechanisms of breast cancer metastasis using genetically-engineered mice. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1045

8. Swindall, Amanda F. The Role Of St6gal-I Sialylation In Fas (cd95) Death Receptor Function And Tumorigenesis.

Degree: PhD, 2012, University of Alabama – Birmingham

The golgi glycosyltransferase, ST6Gal-I, adds a negatively-charged sialic acid in an alpha-2-6 linkage to N-linked glycans. ST6Gal-I is upregulated in many cancers, and is associated… (more)

Subjects/Keywords: Antigens, CD – metabolism.<; br>; Antigens, CD95 – metabolism.<; br>; Apoptosis<; br>; Tumor Cells, Cultured<; br>; Colonic Neoplasms<; br>; Neoplasm Proteins – metabolism.<; br>; Sialyltransferases – metabolism.

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APA (6th Edition):

Swindall, A. F. (2012). The Role Of St6gal-I Sialylation In Fas (cd95) Death Receptor Function And Tumorigenesis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1392

Chicago Manual of Style (16th Edition):

Swindall, Amanda F. “The Role Of St6gal-I Sialylation In Fas (cd95) Death Receptor Function And Tumorigenesis.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1392.

MLA Handbook (7th Edition):

Swindall, Amanda F. “The Role Of St6gal-I Sialylation In Fas (cd95) Death Receptor Function And Tumorigenesis.” 2012. Web. 22 Feb 2020.

Vancouver:

Swindall AF. The Role Of St6gal-I Sialylation In Fas (cd95) Death Receptor Function And Tumorigenesis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1392.

Council of Science Editors:

Swindall AF. The Role Of St6gal-I Sialylation In Fas (cd95) Death Receptor Function And Tumorigenesis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1392

9. Dong, Shengli. Characterization of the oligosaccharides of B. anthracis exosporium.

Degree: PhD, 2010, University of Alabama – Birmingham

Fatal systemic anthrax is caused by exposure to spores of Bacillus anthracis. The outermost layer of the B. anthracis spore is called the exosporium. It… (more)

Subjects/Keywords: Amino Sugars  – biosynthesis<; br>; Bacillus anthracis  – genetics<; br>; Bacillus anthracis  – metabolism<; br>; Bacterial Proteins  – metabolism<; br>; Carbohydrate Epimerases  – metabolism<; br>; Deoxyglucose  – analogs & derivatives<; br>; Glycoproteins<; br>; Oligosaccharides<; br>; Operon

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APA (6th Edition):

Dong, S. (2010). Characterization of the oligosaccharides of B. anthracis exosporium. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1237

Chicago Manual of Style (16th Edition):

Dong, Shengli. “Characterization of the oligosaccharides of B. anthracis exosporium.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1237.

MLA Handbook (7th Edition):

Dong, Shengli. “Characterization of the oligosaccharides of B. anthracis exosporium.” 2010. Web. 22 Feb 2020.

Vancouver:

Dong S. Characterization of the oligosaccharides of B. anthracis exosporium. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1237.

Council of Science Editors:

Dong S. Characterization of the oligosaccharides of B. anthracis exosporium. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1237

10. Hertz, Marla (Marla Ilene). In vivo analysis of the natural diversity of the IGR IRES family and characterizaton of the role of ribosomal protein S25 in IRES-mediated translation.

Degree: PhD, 2011, University of Alabama – Birmingham

Translation of the majority of eukaryotic mRNAs is initiated upon recognition of its 5′ cap structure by translation initiation factors in so-called cap-dependent translation. Capdependent… (more)

Subjects/Keywords: Dicistroviridae  – metabolism<; br>; Gene Expression Regulation<; br>; Hepacivirus  – metabolism<; br>; Prostatic Neoplasms<; br>; Protein Biosynthesis<; br>; Ribosomal Proteins  – metabolism<; br>; Saccharomyces cerevisiae Proteins  – metabolism

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APA (6th Edition):

Hertz, M. (. I. (2011). In vivo analysis of the natural diversity of the IGR IRES family and characterizaton of the role of ribosomal protein S25 in IRES-mediated translation. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,953

Chicago Manual of Style (16th Edition):

Hertz, Marla (Marla Ilene). “In vivo analysis of the natural diversity of the IGR IRES family and characterizaton of the role of ribosomal protein S25 in IRES-mediated translation.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,953.

MLA Handbook (7th Edition):

Hertz, Marla (Marla Ilene). “In vivo analysis of the natural diversity of the IGR IRES family and characterizaton of the role of ribosomal protein S25 in IRES-mediated translation.” 2011. Web. 22 Feb 2020.

Vancouver:

Hertz M(I. In vivo analysis of the natural diversity of the IGR IRES family and characterizaton of the role of ribosomal protein S25 in IRES-mediated translation. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,953.

Council of Science Editors:

Hertz M(I. In vivo analysis of the natural diversity of the IGR IRES family and characterizaton of the role of ribosomal protein S25 in IRES-mediated translation. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,953

11. Pandya, Ashka Y. Structural and functional analysis of KLF4.

Degree: PhD, 2007, University of Alabama – Birmingham

KLF4, a C2H2 type zinc finger transcription factor, plays an essential role in maturation of normal stratified squamous epithelium. In normal squamous epithelium its expression… (more)

Subjects/Keywords: Breast Neoplasms  – metabolism<; br>; Breast Neoplasms  – pathology<; br>; Cell Nucleus  – metabolism<; br>; DNA-Binding Proteins  – biosynthesis<; br>; Kruppel-Like Transcription Factors<; br>; Prognosis Transcription Factors  – biosynthesis

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APA (6th Edition):

Pandya, A. Y. (2007). Structural and functional analysis of KLF4. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,531

Chicago Manual of Style (16th Edition):

Pandya, Ashka Y. “Structural and functional analysis of KLF4.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,531.

MLA Handbook (7th Edition):

Pandya, Ashka Y. “Structural and functional analysis of KLF4.” 2007. Web. 22 Feb 2020.

Vancouver:

Pandya AY. Structural and functional analysis of KLF4. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,531.

Council of Science Editors:

Pandya AY. Structural and functional analysis of KLF4. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,531

12. Mayhew, David Lawrence. Translation Initiation Signaling Components Altered By Mechanical Load Dictate Skeletal Muscle Hypertrophy.

Degree: PhD, 2010, University of Alabama – Birmingham

The regulation of protein synthesis (i.e., mRNA translation) is an energetically costly and extensively regulated process, which is primarily regulated at the initiation step. Mechanical… (more)

Subjects/Keywords: Eukaryotic Initiation Factor-2B – metabolism.<; br>; Muscle Proteins – metabolism.<; br>; Muscle, Skeletal<; br>; Physical Exertion<; br>; Physical Stimulation<; br>; Protein Biosynthesis<; br>; Resistance Training – adverse effects.<; br>; Signal Transduction

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APA (6th Edition):

Mayhew, D. L. (2010). Translation Initiation Signaling Components Altered By Mechanical Load Dictate Skeletal Muscle Hypertrophy. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1427

Chicago Manual of Style (16th Edition):

Mayhew, David Lawrence. “Translation Initiation Signaling Components Altered By Mechanical Load Dictate Skeletal Muscle Hypertrophy.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1427.

MLA Handbook (7th Edition):

Mayhew, David Lawrence. “Translation Initiation Signaling Components Altered By Mechanical Load Dictate Skeletal Muscle Hypertrophy.” 2010. Web. 22 Feb 2020.

Vancouver:

Mayhew DL. Translation Initiation Signaling Components Altered By Mechanical Load Dictate Skeletal Muscle Hypertrophy. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1427.

Council of Science Editors:

Mayhew DL. Translation Initiation Signaling Components Altered By Mechanical Load Dictate Skeletal Muscle Hypertrophy. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1427

13. 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

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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 February 22, 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. 22 Feb 2020.

Vancouver:

Kallmeyer AK(K. Regulatory mechanisms of eukaryotic translation termination. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Feb 22]. 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

14. 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.

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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 February 22, 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. 22 Feb 2020.

Vancouver:

Cheetham CC. Pathophysiology Of Dyt1 Dystonia: Targeted Mouse Models. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Feb 22]. 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


University of Texas Southwestern Medical Center

15. Kocabas, Fatih. MEIS1: At the Crossroads Between Metabolic and Cell Cycle Regulation.

Degree: 2013, University of Texas Southwestern Medical Center

 Stem cells undergo self-renewal, maintaining themselves in an undifferentiated state while generating differentiated cells that are required for the tissue homeostasis or repair. One intriguing… (more)

Subjects/Keywords: Neoplasm Proteins; Hematopoietic Stem Cells; Homeodomain Proteins

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APA (6th Edition):

Kocabas, F. (2013). MEIS1: At the Crossroads Between Metabolic and Cell Cycle Regulation. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1251

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Kocabas, Fatih. “MEIS1: At the Crossroads Between Metabolic and Cell Cycle Regulation.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed February 22, 2020. http://hdl.handle.net/2152.5/1251.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Kocabas, Fatih. “MEIS1: At the Crossroads Between Metabolic and Cell Cycle Regulation.” 2013. Web. 22 Feb 2020.

Vancouver:

Kocabas F. MEIS1: At the Crossroads Between Metabolic and Cell Cycle Regulation. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2020 Feb 22]. Available from: http://hdl.handle.net/2152.5/1251.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kocabas F. MEIS1: At the Crossroads Between Metabolic and Cell Cycle Regulation. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/1251

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

16. Harms, Kelly Lynn. Mechanisms of P53-mediated apoptosis.

Degree: PhD, 2007, University of Alabama – Birmingham

The p53 tumor suppressor is the most commonly inactivated gene in human cancers. The ability of p53, a transcription factor, to regulate genes that mediate… (more)

Subjects/Keywords: Apoptosis  – genetics<; br>; DNA, Neoplasm  – metabolism<; br>; Gene Expression Regulation  – physiology<; br>; Histone Deacetylases  – metabolism<; br>; Insulin-Like Growth Factor Binding Protein 3  – genetics<; br>; Repressor Proteins  – metabolism<; br>; Transcriptional Activation  – physiology<; br>; Tumor Suppressor Protein p53

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

APA (6th Edition):

Harms, K. L. (2007). Mechanisms of P53-mediated apoptosis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,446

Chicago Manual of Style (16th Edition):

Harms, Kelly Lynn. “Mechanisms of P53-mediated apoptosis.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,446.

MLA Handbook (7th Edition):

Harms, Kelly Lynn. “Mechanisms of P53-mediated apoptosis.” 2007. Web. 22 Feb 2020.

Vancouver:

Harms KL. Mechanisms of P53-mediated apoptosis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,446.

Council of Science Editors:

Harms KL. Mechanisms of P53-mediated apoptosis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,446

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

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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 February 22, 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. 22 Feb 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 Feb 22]. 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


Hong Kong University of Science and Technology

18. Feng, Yitao. Macromolecular crowding effect on function, stability and dynamics of selected protein systems.

Degree: 2012, Hong Kong University of Science and Technology

 In the cellular environment, biomacromolecules together occupy about 20-30% of the total volume and sometimes up to 40% by estimation. The occupied volume is not… (more)

Subjects/Keywords: Macromolecules ; Synthesis ; Polyketides ; Proteins ; Biosynthesis

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APA (6th Edition):

Feng, Y. (2012). Macromolecular crowding effect on function, stability and dynamics of selected protein systems. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-91980 ; https://doi.org/10.14711/thesis-b1207874 ; http://repository.ust.hk/ir/bitstream/1783.1-91980/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Feng, Yitao. “Macromolecular crowding effect on function, stability and dynamics of selected protein systems.” 2012. Thesis, Hong Kong University of Science and Technology. Accessed February 22, 2020. http://repository.ust.hk/ir/Record/1783.1-91980 ; https://doi.org/10.14711/thesis-b1207874 ; http://repository.ust.hk/ir/bitstream/1783.1-91980/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Feng, Yitao. “Macromolecular crowding effect on function, stability and dynamics of selected protein systems.” 2012. Web. 22 Feb 2020.

Vancouver:

Feng Y. Macromolecular crowding effect on function, stability and dynamics of selected protein systems. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2012. [cited 2020 Feb 22]. Available from: http://repository.ust.hk/ir/Record/1783.1-91980 ; https://doi.org/10.14711/thesis-b1207874 ; http://repository.ust.hk/ir/bitstream/1783.1-91980/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Feng Y. Macromolecular crowding effect on function, stability and dynamics of selected protein systems. [Thesis]. Hong Kong University of Science and Technology; 2012. Available from: http://repository.ust.hk/ir/Record/1783.1-91980 ; https://doi.org/10.14711/thesis-b1207874 ; http://repository.ust.hk/ir/bitstream/1783.1-91980/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Texas Southwestern Medical Center

19. Pineda, Carlos Tyler. The Cancer Specific Ubiquitin Ligase MAGE-A3/6-TRIM28 Drives Tumorigenesis by Ubiquitination and Proteasomal Degradation of AMPK.

Degree: 2015, University of Texas Southwestern Medical Center

 The genes MAGE-A3 and MAGE-A6 (MAGE-A3/6) have a unique expression pattern in which they are normally expressed in the adult testis but are aberrantly expressed… (more)

Subjects/Keywords: AMP-Activated Protein Kinases; Antigens, Neoplasm; Neoplasm Proteins; Neoplasms; Ubiquitination; Ubiquitin-Protein Ligases

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APA (6th Edition):

Pineda, C. T. (2015). The Cancer Specific Ubiquitin Ligase MAGE-A3/6-TRIM28 Drives Tumorigenesis by Ubiquitination and Proteasomal Degradation of AMPK. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/4447

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Pineda, Carlos Tyler. “The Cancer Specific Ubiquitin Ligase MAGE-A3/6-TRIM28 Drives Tumorigenesis by Ubiquitination and Proteasomal Degradation of AMPK.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed February 22, 2020. http://hdl.handle.net/2152.5/4447.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Pineda, Carlos Tyler. “The Cancer Specific Ubiquitin Ligase MAGE-A3/6-TRIM28 Drives Tumorigenesis by Ubiquitination and Proteasomal Degradation of AMPK.” 2015. Web. 22 Feb 2020.

Vancouver:

Pineda CT. The Cancer Specific Ubiquitin Ligase MAGE-A3/6-TRIM28 Drives Tumorigenesis by Ubiquitination and Proteasomal Degradation of AMPK. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2020 Feb 22]. Available from: http://hdl.handle.net/2152.5/4447.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pineda CT. The Cancer Specific Ubiquitin Ligase MAGE-A3/6-TRIM28 Drives Tumorigenesis by Ubiquitination and Proteasomal Degradation of AMPK. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/4447

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Prakash, Anand, M.S. Characterization of synergistic effect of iododeoxyuridine and clofarabine in cisplatin-resistant ovarian cancer cells .

Degree: MS, 2009, University of Alabama – Birmingham

Epithelial ovarian cancer (EOC) is the most common gynecological cancer and the fifth most frequent cause of cancer deaths in women. Cytoreductive surgery (CRS) followed… (more)

Subjects/Keywords: Cisplatin  – pharmacology<; br>; Drug Resistance, Neoplasm<; br>; Drug Synergism<; br>; Ovarian Neoplasms  – drug therapy

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APA (6th Edition):

Prakash, Anand, M. S. (2009). Characterization of synergistic effect of iododeoxyuridine and clofarabine in cisplatin-resistant ovarian cancer cells . (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,421

Chicago Manual of Style (16th Edition):

Prakash, Anand, M S. “Characterization of synergistic effect of iododeoxyuridine and clofarabine in cisplatin-resistant ovarian cancer cells .” 2009. Masters Thesis, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,421.

MLA Handbook (7th Edition):

Prakash, Anand, M S. “Characterization of synergistic effect of iododeoxyuridine and clofarabine in cisplatin-resistant ovarian cancer cells .” 2009. Web. 22 Feb 2020.

Vancouver:

Prakash, Anand MS. Characterization of synergistic effect of iododeoxyuridine and clofarabine in cisplatin-resistant ovarian cancer cells . [Internet] [Masters thesis]. University of Alabama – Birmingham; 2009. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,421.

Council of Science Editors:

Prakash, Anand MS. Characterization of synergistic effect of iododeoxyuridine and clofarabine in cisplatin-resistant ovarian cancer cells . [Masters Thesis]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,421

21. Shaikh, Faheem M. Role of variant sialylation in regulating tumor cell behavior.

Degree: PhD, 2008, University of Alabama – Birmingham

Many different tumors have been documented to have elevated levels of the enzyme ST6Gal I, a Golgi glycosyltransferase that adds [alpha]2-6 sialic acids to glycoproteins.… (more)

Subjects/Keywords: Cell Movement  – physiology <; br>; Colonic Neoplasms <; br>; Integrins  – chemistry <; br>; Integrins  – metabolism <; br>; Neoplasm Invasiveness <; br>; Sialic Acids  – metabolism

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APA (6th Edition):

Shaikh, F. M. (2008). Role of variant sialylation in regulating tumor cell behavior. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,266

Chicago Manual of Style (16th Edition):

Shaikh, Faheem M. “Role of variant sialylation in regulating tumor cell behavior.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,266.

MLA Handbook (7th Edition):

Shaikh, Faheem M. “Role of variant sialylation in regulating tumor cell behavior.” 2008. Web. 22 Feb 2020.

Vancouver:

Shaikh FM. Role of variant sialylation in regulating tumor cell behavior. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,266.

Council of Science Editors:

Shaikh FM. Role of variant sialylation in regulating tumor cell behavior. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,266

22. Cody, James Joseph. A dual-action, armed replicating adenovirus for the treatment of bone metastases of breast cancer.

Degree: PhD, 2008, University of Alabama – Birmingham

Most patients with advanced breast cancer develop osteolytic bone metastases, which have numerous complications. Because current therapies are not curative, new treatments are needed. Conditionally… (more)

Subjects/Keywords: Adenoviridae  – genetics <; br>; Bone Neoplasms  – secondary <; br>; Breast Neoplasms <; br>; Gene Expression Regulation, Neoplastic <; br>; Neoplasm Metastasis  – genetics <; br>; Neoplasm Metastasis  – therapy <; br>; Virus Replication  – genetics

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APA (6th Edition):

Cody, J. J. (2008). A dual-action, armed replicating adenovirus for the treatment of bone metastases of breast cancer. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,320

Chicago Manual of Style (16th Edition):

Cody, James Joseph. “A dual-action, armed replicating adenovirus for the treatment of bone metastases of breast cancer.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,320.

MLA Handbook (7th Edition):

Cody, James Joseph. “A dual-action, armed replicating adenovirus for the treatment of bone metastases of breast cancer.” 2008. Web. 22 Feb 2020.

Vancouver:

Cody JJ. A dual-action, armed replicating adenovirus for the treatment of bone metastases of breast cancer. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,320.

Council of Science Editors:

Cody JJ. A dual-action, armed replicating adenovirus for the treatment of bone metastases of breast cancer. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,320


University of Texas Southwestern Medical Center

23. Gao, Wenhua. Characterizaton of Mcl-1 in Regulating Different Forms of Cell Death.

Degree: 2007, University of Texas Southwestern Medical Center

 Programmed Cell Deaths (apoptosis, autophagic cell death and necrosis) play essential roles in animal development and certain diseases. Autophagy is a cellular process that provides… (more)

Subjects/Keywords: Apoptosis; Neoplasm Proteins; Ubiquitin

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APA (6th Edition):

Gao, W. (2007). Characterizaton of Mcl-1 in Regulating Different Forms of Cell Death. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/426

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Gao, Wenhua. “Characterizaton of Mcl-1 in Regulating Different Forms of Cell Death.” 2007. Thesis, University of Texas Southwestern Medical Center. Accessed February 22, 2020. http://hdl.handle.net/2152.5/426.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Gao, Wenhua. “Characterizaton of Mcl-1 in Regulating Different Forms of Cell Death.” 2007. Web. 22 Feb 2020.

Vancouver:

Gao W. Characterizaton of Mcl-1 in Regulating Different Forms of Cell Death. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2007. [cited 2020 Feb 22]. Available from: http://hdl.handle.net/2152.5/426.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gao W. Characterizaton of Mcl-1 in Regulating Different Forms of Cell Death. [Thesis]. University of Texas Southwestern Medical Center; 2007. Available from: http://hdl.handle.net/2152.5/426

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Texas Southwestern Medical Center

24. Reynoso, Eduardo. Thioredoxin-1 Inhibition Promotes MLKL Activation: Biochemical Insights Into a Suppressor of the Necroptotic Pathway.

Degree: 2017, University of Texas Southwestern Medical Center

 Necroptosis is an immunogenic caspase-independent cell death program. While mainly serving to defend against viral infection, dysregulated necroptotic signaling contributes to the pathology of a… (more)

Subjects/Keywords: Neoplasm Proteins; Neoplasms; Protein Kinases; Protein Multimerization; Thioredoxins

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APA (6th Edition):

Reynoso, E. (2017). Thioredoxin-1 Inhibition Promotes MLKL Activation: Biochemical Insights Into a Suppressor of the Necroptotic Pathway. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7729

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Reynoso, Eduardo. “Thioredoxin-1 Inhibition Promotes MLKL Activation: Biochemical Insights Into a Suppressor of the Necroptotic Pathway.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed February 22, 2020. http://hdl.handle.net/2152.5/7729.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Reynoso, Eduardo. “Thioredoxin-1 Inhibition Promotes MLKL Activation: Biochemical Insights Into a Suppressor of the Necroptotic Pathway.” 2017. Web. 22 Feb 2020.

Vancouver:

Reynoso E. Thioredoxin-1 Inhibition Promotes MLKL Activation: Biochemical Insights Into a Suppressor of the Necroptotic Pathway. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2020 Feb 22]. Available from: http://hdl.handle.net/2152.5/7729.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Reynoso E. Thioredoxin-1 Inhibition Promotes MLKL Activation: Biochemical Insights Into a Suppressor of the Necroptotic Pathway. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/7729

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


McGill University

25. Goh, Siew-Lee. Functional studies of MEIS1, a HOX co-factor.

Degree: PhD, Division of Experimental Medicine., 2007, McGill University

 HOX proteins are evolutionarily conserved homeodomain-containing transcription factors involved in hematopoiesis and patterning during embryogenesis. Their tasks as master regulators of embryonic development are achieved… (more)

Subjects/Keywords: Homeodomain Proteins  – genetics.; Neoplasm Proteins  – genetics.

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APA (6th Edition):

Goh, S. (2007). Functional studies of MEIS1, a HOX co-factor. (Doctoral Dissertation). McGill University. Retrieved from http://digitool.library.mcgill.ca/thesisfile103200.pdf

Chicago Manual of Style (16th Edition):

Goh, Siew-Lee. “Functional studies of MEIS1, a HOX co-factor.” 2007. Doctoral Dissertation, McGill University. Accessed February 22, 2020. http://digitool.library.mcgill.ca/thesisfile103200.pdf.

MLA Handbook (7th Edition):

Goh, Siew-Lee. “Functional studies of MEIS1, a HOX co-factor.” 2007. Web. 22 Feb 2020.

Vancouver:

Goh S. Functional studies of MEIS1, a HOX co-factor. [Internet] [Doctoral dissertation]. McGill University; 2007. [cited 2020 Feb 22]. Available from: http://digitool.library.mcgill.ca/thesisfile103200.pdf.

Council of Science Editors:

Goh S. Functional studies of MEIS1, a HOX co-factor. [Doctoral Dissertation]. McGill University; 2007. Available from: http://digitool.library.mcgill.ca/thesisfile103200.pdf


Indian Institute of Science

26. Sapa, Hima Rani. Implications of Soluble Diacylglycerol Acyltransferases in Triacylglycerol Biosynthesis in Yeast and Plants.

Degree: 2013, Indian Institute of Science

 Lipids are stored in a cell for providing energy. The main advantages of storing lipids over carbohydrates like glycogen is that, lipids yield more energy… (more)

Subjects/Keywords: Proteins; Diacylglycerol Acyltransferases; Triacylglycerol Biosynthesis; Storage Lipids; Yeast - Triacylglycerol Biosynthesis; Plants - Triacylglycerol Biosynthesis; Cutin Biosynthesis; Rhodotorula Glutinis - Storage Lipid Formation; Fatty Acids - Biosynthesis; Arabidopsis thaliana - Cutin Biosynthesis; Biochemistry

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APA (6th Edition):

Sapa, H. R. (2013). Implications of Soluble Diacylglycerol Acyltransferases in Triacylglycerol Biosynthesis in Yeast and Plants. (Thesis). Indian Institute of Science. Retrieved from http://etd.iisc.ernet.in/2005/3399 ; http://etd.iisc.ernet.in/abstracts/4265/G25862-Abs.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Sapa, Hima Rani. “Implications of Soluble Diacylglycerol Acyltransferases in Triacylglycerol Biosynthesis in Yeast and Plants.” 2013. Thesis, Indian Institute of Science. Accessed February 22, 2020. http://etd.iisc.ernet.in/2005/3399 ; http://etd.iisc.ernet.in/abstracts/4265/G25862-Abs.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Sapa, Hima Rani. “Implications of Soluble Diacylglycerol Acyltransferases in Triacylglycerol Biosynthesis in Yeast and Plants.” 2013. Web. 22 Feb 2020.

Vancouver:

Sapa HR. Implications of Soluble Diacylglycerol Acyltransferases in Triacylglycerol Biosynthesis in Yeast and Plants. [Internet] [Thesis]. Indian Institute of Science; 2013. [cited 2020 Feb 22]. Available from: http://etd.iisc.ernet.in/2005/3399 ; http://etd.iisc.ernet.in/abstracts/4265/G25862-Abs.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sapa HR. Implications of Soluble Diacylglycerol Acyltransferases in Triacylglycerol Biosynthesis in Yeast and Plants. [Thesis]. Indian Institute of Science; 2013. Available from: http://etd.iisc.ernet.in/2005/3399 ; http://etd.iisc.ernet.in/abstracts/4265/G25862-Abs.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

27. Liu, Jia. Increased hexosamine biosynthesis and protein O-GLCNAC protect isolated rat heart from ischemia/reperfusion injury.

Degree: PhD, 2006, University of Alabama – Birmingham

Increased levels of protein-associated O-linked N-acetylglucosamine (O-GlcNAc) have been correlated with increased tolerance to stress. Therefore the goal of this study was to determine whether… (more)

Subjects/Keywords: Acetylglucosamine  – metabolism <; br>; Hexosamines  – biosynthesis <; br>; Reperfusion Injury  – prevention & control

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APA (6th Edition):

Liu, J. (2006). Increased hexosamine biosynthesis and protein O-GLCNAC protect isolated rat heart from ischemia/reperfusion injury. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,307

Chicago Manual of Style (16th Edition):

Liu, Jia. “Increased hexosamine biosynthesis and protein O-GLCNAC protect isolated rat heart from ischemia/reperfusion injury.” 2006. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,307.

MLA Handbook (7th Edition):

Liu, Jia. “Increased hexosamine biosynthesis and protein O-GLCNAC protect isolated rat heart from ischemia/reperfusion injury.” 2006. Web. 22 Feb 2020.

Vancouver:

Liu J. Increased hexosamine biosynthesis and protein O-GLCNAC protect isolated rat heart from ischemia/reperfusion injury. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2006. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,307.

Council of Science Editors:

Liu J. Increased hexosamine biosynthesis and protein O-GLCNAC protect isolated rat heart from ischemia/reperfusion injury. [Doctoral Dissertation]. University of Alabama – Birmingham; 2006. Available from: http://contentdm.mhsl.uab.edu/u?/etd,307

28. Moore, Lakisha Dionne. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.

Degree: PhD, 2008, University of Alabama – Birmingham

Overexpresssion of transforming growth factor (TGF)-[beta] has been implicated in promoting immune suppression, tumor angiogenesis, tumor cell migration, and invasion in many cancers including carcinoma… (more)

Subjects/Keywords: Breast Neoplasms  – genetics <; br>; Neoplasm Metastasis <; br>; RNA Interference <; br>; Transforming Growth Factor beta1  – genetics <; br>; Transforming Growth Factor beta1  – metabolism

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

APA (6th Edition):

Moore, L. D. (2008). Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,233

Chicago Manual of Style (16th Edition):

Moore, Lakisha Dionne. “Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,233.

MLA Handbook (7th Edition):

Moore, Lakisha Dionne. “Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.” 2008. Web. 22 Feb 2020.

Vancouver:

Moore LD. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,233.

Council of Science Editors:

Moore LD. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,233

29. Ritchie, Joseph P. Heparanase drives the aggressive myeloma phenotype: preclinical development of a heparanase inhibitor for the treatment of multiple myeloma.

Degree: PhD, 2010, University of Alabama – Birmingham

Heparanase, an endoglycosidase which cleaves heparan sulfate chains at specific sites, is rarely expressed in normal tissues but becomes evident in many human cancers. We… (more)

Subjects/Keywords: Heparin  – metabolism<; br>; Heparitin Sulfate  – metabolism<; br>; Multiple Myeloma  – pathology<; br>; Neoplasm Invasiveness<; br>; Syndecan-1  – metabolism

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

APA (6th Edition):

Ritchie, J. P. (2010). Heparanase drives the aggressive myeloma phenotype: preclinical development of a heparanase inhibitor for the treatment of multiple myeloma. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,852

Chicago Manual of Style (16th Edition):

Ritchie, Joseph P. “Heparanase drives the aggressive myeloma phenotype: preclinical development of a heparanase inhibitor for the treatment of multiple myeloma.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,852.

MLA Handbook (7th Edition):

Ritchie, Joseph P. “Heparanase drives the aggressive myeloma phenotype: preclinical development of a heparanase inhibitor for the treatment of multiple myeloma.” 2010. Web. 22 Feb 2020.

Vancouver:

Ritchie JP. Heparanase drives the aggressive myeloma phenotype: preclinical development of a heparanase inhibitor for the treatment of multiple myeloma. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,852.

Council of Science Editors:

Ritchie JP. Heparanase drives the aggressive myeloma phenotype: preclinical development of a heparanase inhibitor for the treatment of multiple myeloma. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,852

30. Calderon, Christopher. O-Linked Beta-N-Acetylglucosamine (o-Glcnac) And The Mitochondrion.

Degree: 2013, University of Alabama – Birmingham

O-linked beta-N-acetylglucosamine (O-GlcNAc) is a dynamic and ubiquitous posttranslational modification of serine and threonine residues on nuclear and cytoplasmic proteins. O-GlcNAc has emerged as an… (more)

Subjects/Keywords: Acetylglucosamine – metabolism<; /br>; Glycosylation<; /br>; Hexosamines – biosynthesis<; /br>; Mitochondrial Membrane Transport Proteins – metabolism.<; /br>; Oxidative Stress.

…52 O-GlcNAcylation of Mitochondrial Proteins ...........................................52… …x29;, onto proteins. The removal of O-GlcNAc is regulated via a unique hexosaminidase, β… …neurodegenerative diseases [9], and many oncogenic proteins and tumor suppressor proteins are… …x28;OGT) catalyzes the addition of UDP‐GlcNAc, onto ser/thr residues of naked proteins… …cytoplasmic proteins in an attempt to characterize potential differentiation and histocompatibility… 

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

APA (6th Edition):

Calderon, C. (2013). O-Linked Beta-N-Acetylglucosamine (o-Glcnac) And The Mitochondrion. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1660

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Calderon, Christopher. “O-Linked Beta-N-Acetylglucosamine (o-Glcnac) And The Mitochondrion.” 2013. Thesis, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1660.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Calderon, Christopher. “O-Linked Beta-N-Acetylglucosamine (o-Glcnac) And The Mitochondrion.” 2013. Web. 22 Feb 2020.

Vancouver:

Calderon C. O-Linked Beta-N-Acetylglucosamine (o-Glcnac) And The Mitochondrion. [Internet] [Thesis]. University of Alabama – Birmingham; 2013. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1660.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Calderon C. O-Linked Beta-N-Acetylglucosamine (o-Glcnac) And The Mitochondrion. [Thesis]. University of Alabama – Birmingham; 2013. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1660

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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