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You searched for +publisher:"University of Southern California" +contributor:("Kalra, Vijay K."). Showing records 1 – 22 of 22 total matches.

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University of Southern California

1. Yamamoto, Vicky N. The role of Ryk and Smek in neurogenesis; Mechanisms of CBP/β-catenin signaling inhibitor and IL-6 mediators in head and neck cancer.

Degree: PhD, Biochemistry and Molecular Biology, 2015, University of Southern California

 The Role of Ryk and Smek in Neurogenesis: Ryk, a single-pass membrane receptor and a Wnt co-receptor, is expressed in the brain during neurodevelopment and… (more)

Subjects/Keywords: head and neck cancer; squamous cell carcinoma; IL-6; microRNA; small molecule inhibitor; Epithelial-to-Mesenchymal transition (EMT); Wnt signaling; neurogenesis; neurodevelopment; neuronal stem cell; Ryk; Smek

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APA (6th Edition):

Yamamoto, V. N. (2015). The role of Ryk and Smek in neurogenesis; Mechanisms of CBP/β-catenin signaling inhibitor and IL-6 mediators in head and neck cancer. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/130707/rec/7245

Chicago Manual of Style (16th Edition):

Yamamoto, Vicky N. “The role of Ryk and Smek in neurogenesis; Mechanisms of CBP/β-catenin signaling inhibitor and IL-6 mediators in head and neck cancer.” 2015. Doctoral Dissertation, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/130707/rec/7245.

MLA Handbook (7th Edition):

Yamamoto, Vicky N. “The role of Ryk and Smek in neurogenesis; Mechanisms of CBP/β-catenin signaling inhibitor and IL-6 mediators in head and neck cancer.” 2015. Web. 19 Jun 2019.

Vancouver:

Yamamoto VN. The role of Ryk and Smek in neurogenesis; Mechanisms of CBP/β-catenin signaling inhibitor and IL-6 mediators in head and neck cancer. [Internet] [Doctoral dissertation]. University of Southern California; 2015. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/130707/rec/7245.

Council of Science Editors:

Yamamoto VN. The role of Ryk and Smek in neurogenesis; Mechanisms of CBP/β-catenin signaling inhibitor and IL-6 mediators in head and neck cancer. [Doctoral Dissertation]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/130707/rec/7245


University of Southern California

2. Li, Chen. MicroRNAs involved in the regulation of Endothelin-1 gene expression in endothelial cells.

Degree: MS, Biochemistry and Molecular Biology, 2014, University of Southern California

 We showed that in human dermal microvascular endothelial cell line (HMEC-1), the stability of ET-1 mRNA was increased in response to PlGF treatment. We also… (more)

Subjects/Keywords: endothelial cells; Endothelin-1; microRNA

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APA (6th Edition):

Li, C. (2014). MicroRNAs involved in the regulation of Endothelin-1 gene expression in endothelial cells. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/86172/rec/4069

Chicago Manual of Style (16th Edition):

Li, Chen. “MicroRNAs involved in the regulation of Endothelin-1 gene expression in endothelial cells.” 2014. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/86172/rec/4069.

MLA Handbook (7th Edition):

Li, Chen. “MicroRNAs involved in the regulation of Endothelin-1 gene expression in endothelial cells.” 2014. Web. 19 Jun 2019.

Vancouver:

Li C. MicroRNAs involved in the regulation of Endothelin-1 gene expression in endothelial cells. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/86172/rec/4069.

Council of Science Editors:

Li C. MicroRNAs involved in the regulation of Endothelin-1 gene expression in endothelial cells. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/86172/rec/4069


University of Southern California

3. Jaisinghani, Ruchika. Transcriptional regulation of IFN-γ and PlGF in response to Epo and VEGF in erythroid cells.

Degree: MS, Molecular Microbiology and Immunology, 2014, University of Southern California

 Sickle cell disease (SCD) is a genetic disorder, characterized by a mutation within the β-globin chain of the hemoglobin molecule. The clinical manifestations of SCD… (more)

Subjects/Keywords: molecular biology; cell biology; microbiology; biochemistry; molecular cloning; cell culture; biology; sickle cell; erythroid cells; IFN gamma; PlGF

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APA (6th Edition):

Jaisinghani, R. (2014). Transcriptional regulation of IFN-γ and PlGF in response to Epo and VEGF in erythroid cells. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/250117/rec/7564

Chicago Manual of Style (16th Edition):

Jaisinghani, Ruchika. “Transcriptional regulation of IFN-γ and PlGF in response to Epo and VEGF in erythroid cells.” 2014. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/250117/rec/7564.

MLA Handbook (7th Edition):

Jaisinghani, Ruchika. “Transcriptional regulation of IFN-γ and PlGF in response to Epo and VEGF in erythroid cells.” 2014. Web. 19 Jun 2019.

Vancouver:

Jaisinghani R. Transcriptional regulation of IFN-γ and PlGF in response to Epo and VEGF in erythroid cells. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/250117/rec/7564.

Council of Science Editors:

Jaisinghani R. Transcriptional regulation of IFN-γ and PlGF in response to Epo and VEGF in erythroid cells. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/250117/rec/7564


University of Southern California

4. Gururaj, Sushmitha. Ethanol induced modulation of microglial P2X7 receptor expression and its role in neuroinflammation.

Degree: MS, Biochemistry and Molecular Biology, 2012, University of Southern California

 The present work builds upon a central hypothesis that ATP-gated purinergic P2X7 receptors (P2X7Rs) play an important role in causing ethanol-induced neuroinflammation and neurodegeneration. A… (more)

Subjects/Keywords: ethanol; purinergic; P2X7 receptor; neuroinflammation; neurodenegeration

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APA (6th Edition):

Gururaj, S. (2012). Ethanol induced modulation of microglial P2X7 receptor expression and its role in neuroinflammation. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43372/rec/2511

Chicago Manual of Style (16th Edition):

Gururaj, Sushmitha. “Ethanol induced modulation of microglial P2X7 receptor expression and its role in neuroinflammation.” 2012. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43372/rec/2511.

MLA Handbook (7th Edition):

Gururaj, Sushmitha. “Ethanol induced modulation of microglial P2X7 receptor expression and its role in neuroinflammation.” 2012. Web. 19 Jun 2019.

Vancouver:

Gururaj S. Ethanol induced modulation of microglial P2X7 receptor expression and its role in neuroinflammation. [Internet] [Masters thesis]. University of Southern California; 2012. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43372/rec/2511.

Council of Science Editors:

Gururaj S. Ethanol induced modulation of microglial P2X7 receptor expression and its role in neuroinflammation. [Masters Thesis]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/43372/rec/2511


University of Southern California

5. Hu, Jay. Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes.

Degree: MS, Biochemistry and Molecular Biology, 2015, University of Southern California

 Highly Active Anti Retroviral Therapy (HAART) has become an integral part of modern Human Immunodeficiency Virus (HIV) and Acquired Immunodeficiency Syndrome (AIDS) treatment. Liver damage… (more)

Subjects/Keywords: hepatocytes; ER stress; oxidative stress; Nrf2; HIV protease inhibitor

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APA (6th Edition):

Hu, J. (2015). Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950

Chicago Manual of Style (16th Edition):

Hu, Jay. “Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes.” 2015. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950.

MLA Handbook (7th Edition):

Hu, Jay. “Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes.” 2015. Web. 19 Jun 2019.

Vancouver:

Hu J. Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes. [Internet] [Masters thesis]. University of Southern California; 2015. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950.

Council of Science Editors:

Hu J. Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes. [Masters Thesis]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950


University of Southern California

6. Ravichandran, Monisha. Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation.

Degree: MS, Biochemistry and Molecular Biology, 2012, University of Southern California

 Chronic alcohol consumption leads to liver injury and death. Studies have shown ethanol causes increased inflammation, which leads to liver damage and cirrhosis. To counteract… (more)

Subjects/Keywords: NQO-1; ethanol; miR-566; miR-518; miR-642; Nrf-2; Bach-1; Keap-1

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APA (6th Edition):

Ravichandran, M. (2012). Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/84016/rec/598

Chicago Manual of Style (16th Edition):

Ravichandran, Monisha. “Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation.” 2012. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/84016/rec/598.

MLA Handbook (7th Edition):

Ravichandran, Monisha. “Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation.” 2012. Web. 19 Jun 2019.

Vancouver:

Ravichandran M. Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation. [Internet] [Masters thesis]. University of Southern California; 2012. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/84016/rec/598.

Council of Science Editors:

Ravichandran M. Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation. [Masters Thesis]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/84016/rec/598


University of Southern California

7. Guyon, Timothy A. Evaluation of the role of the basic Helix-Loop-Helix transcription factor Twist-2 in lymphocyte development and activation.

Degree: MS, Molecular Microbiology and Immunology, 2011, University of Southern California

 Transcription factors belonging to the basic helix-loop-helix (bHLH) family have been shown to regulate a variety of signaling pathway and the development and activity of… (more)

Subjects/Keywords: Immunology; lymphocytes; T cells; Twist-2; TWIST 2

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APA (6th Edition):

Guyon, T. A. (2011). Evaluation of the role of the basic Helix-Loop-Helix transcription factor Twist-2 in lymphocyte development and activation. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/613295/rec/2543

Chicago Manual of Style (16th Edition):

Guyon, Timothy A. “Evaluation of the role of the basic Helix-Loop-Helix transcription factor Twist-2 in lymphocyte development and activation.” 2011. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/613295/rec/2543.

MLA Handbook (7th Edition):

Guyon, Timothy A. “Evaluation of the role of the basic Helix-Loop-Helix transcription factor Twist-2 in lymphocyte development and activation.” 2011. Web. 19 Jun 2019.

Vancouver:

Guyon TA. Evaluation of the role of the basic Helix-Loop-Helix transcription factor Twist-2 in lymphocyte development and activation. [Internet] [Masters thesis]. University of Southern California; 2011. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/613295/rec/2543.

Council of Science Editors:

Guyon TA. Evaluation of the role of the basic Helix-Loop-Helix transcription factor Twist-2 in lymphocyte development and activation. [Masters Thesis]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/613295/rec/2543


University of Southern California

8. Lee, Jo. Differential effect of ethanol and r-sulforaphane on regulation of heme oxygenase-1 in endothelial cells.

Degree: MS, Biochemistry and Molecular Biology, 2014, University of Southern California

 Alcoholism is one of the leading causes of liver disease in the United States. The liver metabolizes 80% of ethanol consumed. Ethanol and its metabolite,… (more)

Subjects/Keywords: r-sulforaphane; heme oxygenase-1

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APA (6th Edition):

Lee, J. (2014). Differential effect of ethanol and r-sulforaphane on regulation of heme oxygenase-1 in endothelial cells. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/121882/rec/1983

Chicago Manual of Style (16th Edition):

Lee, Jo. “Differential effect of ethanol and r-sulforaphane on regulation of heme oxygenase-1 in endothelial cells.” 2014. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/121882/rec/1983.

MLA Handbook (7th Edition):

Lee, Jo. “Differential effect of ethanol and r-sulforaphane on regulation of heme oxygenase-1 in endothelial cells.” 2014. Web. 19 Jun 2019.

Vancouver:

Lee J. Differential effect of ethanol and r-sulforaphane on regulation of heme oxygenase-1 in endothelial cells. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/121882/rec/1983.

Council of Science Editors:

Lee J. Differential effect of ethanol and r-sulforaphane on regulation of heme oxygenase-1 in endothelial cells. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/121882/rec/1983


University of Southern California

9. Gonsalves, Caryn Suzanne. A novel role for hypoxia-inducible factor-1alpha (HIF-1alpha) in the regulation of inflammatory chemokines and leukotriene expression in sickle cell disease.

Degree: PhD, Biochemistry & Molecular Biology, 2009, University of Southern California

 In sickle cell disease (SCD), low oxygen tension results in sickle cell hemoglobin polymerization, causing the sickling of red blood cells, with subsequent vaso-occlusions (137).… (more)

Subjects/Keywords: leukotrienes; sickle cell disease

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APA (6th Edition):

Gonsalves, C. S. (2009). A novel role for hypoxia-inducible factor-1alpha (HIF-1alpha) in the regulation of inflammatory chemokines and leukotriene expression in sickle cell disease. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/252837/rec/288

Chicago Manual of Style (16th Edition):

Gonsalves, Caryn Suzanne. “A novel role for hypoxia-inducible factor-1alpha (HIF-1alpha) in the regulation of inflammatory chemokines and leukotriene expression in sickle cell disease.” 2009. Doctoral Dissertation, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/252837/rec/288.

MLA Handbook (7th Edition):

Gonsalves, Caryn Suzanne. “A novel role for hypoxia-inducible factor-1alpha (HIF-1alpha) in the regulation of inflammatory chemokines and leukotriene expression in sickle cell disease.” 2009. Web. 19 Jun 2019.

Vancouver:

Gonsalves CS. A novel role for hypoxia-inducible factor-1alpha (HIF-1alpha) in the regulation of inflammatory chemokines and leukotriene expression in sickle cell disease. [Internet] [Doctoral dissertation]. University of Southern California; 2009. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/252837/rec/288.

Council of Science Editors:

Gonsalves CS. A novel role for hypoxia-inducible factor-1alpha (HIF-1alpha) in the regulation of inflammatory chemokines and leukotriene expression in sickle cell disease. [Doctoral Dissertation]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/252837/rec/288


University of Southern California

10. Ramrakhiani, Ambika. Hepatic c-Jun overexpression metabolically reprograms cancer cells through mTORC2/AKT pathway.

Degree: MS, Molecular Microbiology and Immunology, 2014, University of Southern California

 The term metabolic syndrome describes the association between obesity, insulin resistance, and the risk of several prominent chronic diseases, including cancer. The link between many… (more)

Subjects/Keywords: c-Jun; diabetes; insulin pathway

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APA (6th Edition):

Ramrakhiani, A. (2014). Hepatic c-Jun overexpression metabolically reprograms cancer cells through mTORC2/AKT pathway. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/445587/rec/3147

Chicago Manual of Style (16th Edition):

Ramrakhiani, Ambika. “Hepatic c-Jun overexpression metabolically reprograms cancer cells through mTORC2/AKT pathway.” 2014. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/445587/rec/3147.

MLA Handbook (7th Edition):

Ramrakhiani, Ambika. “Hepatic c-Jun overexpression metabolically reprograms cancer cells through mTORC2/AKT pathway.” 2014. Web. 19 Jun 2019.

Vancouver:

Ramrakhiani A. Hepatic c-Jun overexpression metabolically reprograms cancer cells through mTORC2/AKT pathway. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/445587/rec/3147.

Council of Science Editors:

Ramrakhiani A. Hepatic c-Jun overexpression metabolically reprograms cancer cells through mTORC2/AKT pathway. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/445587/rec/3147


University of Southern California

11. Wei, Hsiao-Fan. Studies on the expression and function of the human TMEM56 protein.

Degree: MS, Biochemistry and Molecular Biology, 2011, University of Southern California

 Transmembrane 56 (TMEM56) is a 30 KDa protein and it is highly conserved in most species. The protein was identified as an IKKβ-interacting protein by… (more)

Subjects/Keywords: ATP synthease enzyme activity assay; LTQ-ETD; mitochondria; TMEM56; transmembrane protein; western blotting

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APA (6th Edition):

Wei, H. (2011). Studies on the expression and function of the human TMEM56 protein. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/615287/rec/6171

Chicago Manual of Style (16th Edition):

Wei, Hsiao-Fan. “Studies on the expression and function of the human TMEM56 protein.” 2011. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/615287/rec/6171.

MLA Handbook (7th Edition):

Wei, Hsiao-Fan. “Studies on the expression and function of the human TMEM56 protein.” 2011. Web. 19 Jun 2019.

Vancouver:

Wei H. Studies on the expression and function of the human TMEM56 protein. [Internet] [Masters thesis]. University of Southern California; 2011. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/615287/rec/6171.

Council of Science Editors:

Wei H. Studies on the expression and function of the human TMEM56 protein. [Masters Thesis]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/615287/rec/6171


University of Southern California

12. Yeligar, Samantha Mahadevappa. Ethanol-HIF-1 alpha axis in inflammatory gene expression in liver cells.

Degree: PhD, Biochemistry & Molecular Biology, 2009, University of Southern California

 Chronic alcohol consumption leads to liver inflammation and cirrhosis. Portal hypertension and its complications contribute to mortality in patients with cirrhosis. Concomitant to inflammation and… (more)

Subjects/Keywords: ethanol; HIF-1α

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APA (6th Edition):

Yeligar, S. M. (2009). Ethanol-HIF-1 alpha axis in inflammatory gene expression in liver cells. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/572744/rec/2512

Chicago Manual of Style (16th Edition):

Yeligar, Samantha Mahadevappa. “Ethanol-HIF-1 alpha axis in inflammatory gene expression in liver cells.” 2009. Doctoral Dissertation, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/572744/rec/2512.

MLA Handbook (7th Edition):

Yeligar, Samantha Mahadevappa. “Ethanol-HIF-1 alpha axis in inflammatory gene expression in liver cells.” 2009. Web. 19 Jun 2019.

Vancouver:

Yeligar SM. Ethanol-HIF-1 alpha axis in inflammatory gene expression in liver cells. [Internet] [Doctoral dissertation]. University of Southern California; 2009. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/572744/rec/2512.

Council of Science Editors:

Yeligar SM. Ethanol-HIF-1 alpha axis in inflammatory gene expression in liver cells. [Doctoral Dissertation]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/572744/rec/2512


University of Southern California

13. Wang, Min-chuan. RNA polymerase III-dependent transcription is repressed under prolonged hypoxic conditions.

Degree: MS, Biochemistry & Molecular Biology, 2010, University of Southern California

 RNA polymerase III is important for the transcription of non-protein coding RNAs which are important for protein synthesis, RNA processing and protein trafficking. In recent… (more)

Subjects/Keywords: hypoxia; RNA pol III; HIF-1

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APA (6th Edition):

Wang, M. (2010). RNA polymerase III-dependent transcription is repressed under prolonged hypoxic conditions. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/397293/rec/5602

Chicago Manual of Style (16th Edition):

Wang, Min-chuan. “RNA polymerase III-dependent transcription is repressed under prolonged hypoxic conditions.” 2010. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/397293/rec/5602.

MLA Handbook (7th Edition):

Wang, Min-chuan. “RNA polymerase III-dependent transcription is repressed under prolonged hypoxic conditions.” 2010. Web. 19 Jun 2019.

Vancouver:

Wang M. RNA polymerase III-dependent transcription is repressed under prolonged hypoxic conditions. [Internet] [Masters thesis]. University of Southern California; 2010. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/397293/rec/5602.

Council of Science Editors:

Wang M. RNA polymerase III-dependent transcription is repressed under prolonged hypoxic conditions. [Masters Thesis]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/397293/rec/5602


University of Southern California

14. Ybanez, Maria Cecilia D. Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways.

Degree: MS, Biochemistry and Molecular Biology, 2013, University of Southern California

 Our previous studies have shown that acetaminophen (APAP)-induced hepatocyte necrosis is mediated by JNK. In the present study we show that protein kinase C (PKC)… (more)

Subjects/Keywords: acetaminophen (APAP); AMPK; p70S6K; necrosis

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APA (6th Edition):

Ybanez, M. C. D. (2013). Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5294

Chicago Manual of Style (16th Edition):

Ybanez, Maria Cecilia D. “Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways.” 2013. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5294.

MLA Handbook (7th Edition):

Ybanez, Maria Cecilia D. “Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways.” 2013. Web. 19 Jun 2019.

Vancouver:

Ybanez MCD. Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5294.

Council of Science Editors:

Ybanez MCD. Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5294


University of Southern California

15. Vendryes, Christopher Lee. Fibroblast growth factors and notch signaling in a diethoxycarbonyl dihydrocollidine-induced hepatic progenitor cell liver injury model.

Degree: MS, Biochemistry & Molecular Biology, 2010, University of Southern California

 INTRODUCTION: The liver is a multi-purposeful organ, susceptible to injury. Following acute injury, cells such as hepatocytes, regenerate, while latent hepatic progenitor cell (HPC) become… (more)

Subjects/Keywords: fibroblast growth factors; cirrhosis; notch; liver

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APA (6th Edition):

Vendryes, C. L. (2010). Fibroblast growth factors and notch signaling in a diethoxycarbonyl dihydrocollidine-induced hepatic progenitor cell liver injury model. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/427535/rec/2799

Chicago Manual of Style (16th Edition):

Vendryes, Christopher Lee. “Fibroblast growth factors and notch signaling in a diethoxycarbonyl dihydrocollidine-induced hepatic progenitor cell liver injury model.” 2010. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/427535/rec/2799.

MLA Handbook (7th Edition):

Vendryes, Christopher Lee. “Fibroblast growth factors and notch signaling in a diethoxycarbonyl dihydrocollidine-induced hepatic progenitor cell liver injury model.” 2010. Web. 19 Jun 2019.

Vancouver:

Vendryes CL. Fibroblast growth factors and notch signaling in a diethoxycarbonyl dihydrocollidine-induced hepatic progenitor cell liver injury model. [Internet] [Masters thesis]. University of Southern California; 2010. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/427535/rec/2799.

Council of Science Editors:

Vendryes CL. Fibroblast growth factors and notch signaling in a diethoxycarbonyl dihydrocollidine-induced hepatic progenitor cell liver injury model. [Masters Thesis]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/427535/rec/2799


University of Southern California

16. Yang, Kai-Ting. Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression.

Degree: MS, Biochemistry and Molecular Biology, 2013, University of Southern California

 β-cells, which produce and release insulin play a major role in maintaining glucose homeostasis. PTEN is a lipid phosphatase that antagonizes PI3K/AKT signaling pathway and… (more)

Subjects/Keywords: Pten; beta-cell; cell proliferation

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APA (6th Edition):

Yang, K. (2013). Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5314

Chicago Manual of Style (16th Edition):

Yang, Kai-Ting. “Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression.” 2013. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5314.

MLA Handbook (7th Edition):

Yang, Kai-Ting. “Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression.” 2013. Web. 19 Jun 2019.

Vancouver:

Yang K. Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5314.

Council of Science Editors:

Yang K. Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5314


University of Southern California

17. Rengarajan, Srinivas. Regulation of potassium homeostasis during acute potassium loading.

Degree: MS, Biochemistry and Molecular Biology, 2013, University of Southern California

 Potassium is important for the maintenance of acid-base balance, electrolyte homeostasis and optimal cellular excitability. It is vital that the plasma K⁺ level is maintained… (more)

Subjects/Keywords: homeostasis; potassium; ion transport; NCC; SPAK; phosphorylation; metabolic cage; plasma potassium; kidney

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APA (6th Edition):

Rengarajan, S. (2013). Regulation of potassium homeostasis during acute potassium loading. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/318608/rec/5494

Chicago Manual of Style (16th Edition):

Rengarajan, Srinivas. “Regulation of potassium homeostasis during acute potassium loading.” 2013. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/318608/rec/5494.

MLA Handbook (7th Edition):

Rengarajan, Srinivas. “Regulation of potassium homeostasis during acute potassium loading.” 2013. Web. 19 Jun 2019.

Vancouver:

Rengarajan S. Regulation of potassium homeostasis during acute potassium loading. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/318608/rec/5494.

Council of Science Editors:

Rengarajan S. Regulation of potassium homeostasis during acute potassium loading. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/318608/rec/5494


University of Southern California

18. Fata, Azadeh. Study of bone morphogenetic protein-2 and stromal cell derived factor-1 in prostate cancer.

Degree: MS, Pathobiology, 2012, University of Southern California

 The focus of this study is to better understand the role of bone morphogenetic protein-2 (BMP-2), and stromal cell-derived factor-1 (SDF-1) that occur in the… (more)

Subjects/Keywords: androgen-dependent primary tumor (AD cancer); castration resistant prostate cancer (CRPC); bone morphogenetic protein-2; malignant epithelial cells; malignant fibroblastic cells; prostate cancer; tumor microenvironment; stromal cell derived factor-1

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APA (6th Edition):

Fata, A. (2012). Study of bone morphogenetic protein-2 and stromal cell derived factor-1 in prostate cancer. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/34271/rec/6177

Chicago Manual of Style (16th Edition):

Fata, Azadeh. “Study of bone morphogenetic protein-2 and stromal cell derived factor-1 in prostate cancer.” 2012. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/34271/rec/6177.

MLA Handbook (7th Edition):

Fata, Azadeh. “Study of bone morphogenetic protein-2 and stromal cell derived factor-1 in prostate cancer.” 2012. Web. 19 Jun 2019.

Vancouver:

Fata A. Study of bone morphogenetic protein-2 and stromal cell derived factor-1 in prostate cancer. [Internet] [Masters thesis]. University of Southern California; 2012. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/34271/rec/6177.

Council of Science Editors:

Fata A. Study of bone morphogenetic protein-2 and stromal cell derived factor-1 in prostate cancer. [Masters Thesis]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/34271/rec/6177


University of Southern California

19. Tabbakhian, Melia A. KcsA: mutational analysis of ion selectivity with molecular dynamics.

Degree: MS, Physiology and Biophysics, 2013, University of Southern California

 The mechanism of ion selectivity in K⁺-selective ion channels has not yet been determined. In previous studies it was found that K⁺ ions were allowed… (more)

Subjects/Keywords: ion channel; KcsA; ions; potassium; sodium; molecular dynamics; step-wise pulling

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APA (6th Edition):

Tabbakhian, M. A. (2013). KcsA: mutational analysis of ion selectivity with molecular dynamics. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316791/rec/3699

Chicago Manual of Style (16th Edition):

Tabbakhian, Melia A. “KcsA: mutational analysis of ion selectivity with molecular dynamics.” 2013. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316791/rec/3699.

MLA Handbook (7th Edition):

Tabbakhian, Melia A. “KcsA: mutational analysis of ion selectivity with molecular dynamics.” 2013. Web. 19 Jun 2019.

Vancouver:

Tabbakhian MA. KcsA: mutational analysis of ion selectivity with molecular dynamics. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316791/rec/3699.

Council of Science Editors:

Tabbakhian MA. KcsA: mutational analysis of ion selectivity with molecular dynamics. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316791/rec/3699


University of Southern California

20. Fang, Hua. Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis.

Degree: Doctor of Medicine, Pathobiology, 2012, University of Southern California

 Resistance to cell death, especially to apoptosis, is an important feature of tumor cells, which is also described as one of the hallmarks in cancer.… (more)

Subjects/Keywords: apoptosis; Bcl-2; ABT-737; plasminogen activator inhibitor-1; cancer

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APA (6th Edition):

Fang, H. (2012). Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6314

Chicago Manual of Style (16th Edition):

Fang, Hua. “Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis.” 2012. Doctoral Dissertation, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6314.

MLA Handbook (7th Edition):

Fang, Hua. “Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis.” 2012. Web. 19 Jun 2019.

Vancouver:

Fang H. Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6314.

Council of Science Editors:

Fang H. Targeting BCL-2 family proteins and plasminogen activator inhibitor-1 in turmor cell apoptosis. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/33557/rec/6314


University of Southern California

21. Amet, Nurmamet. Human growth hormone-transferrin recombinant fusion protein for oral delivery.

Degree: PhD, Pharmaceutical Sciences, 2008, University of Southern California

 Protein drug delivery is limited to needle injection associating with pain, inconvenience, and non- compliance. Therefore, protein drug with oral dosage form is preferred. We… (more)

Subjects/Keywords: fusion protein; oral delivery; helical linker; protein drug; human growth hormone; transferrin

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APA (6th Edition):

Amet, N. (2008). Human growth hormone-transferrin recombinant fusion protein for oral delivery. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/109040/rec/3274

Chicago Manual of Style (16th Edition):

Amet, Nurmamet. “Human growth hormone-transferrin recombinant fusion protein for oral delivery.” 2008. Doctoral Dissertation, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/109040/rec/3274.

MLA Handbook (7th Edition):

Amet, Nurmamet. “Human growth hormone-transferrin recombinant fusion protein for oral delivery.” 2008. Web. 19 Jun 2019.

Vancouver:

Amet N. Human growth hormone-transferrin recombinant fusion protein for oral delivery. [Internet] [Doctoral dissertation]. University of Southern California; 2008. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/109040/rec/3274.

Council of Science Editors:

Amet N. Human growth hormone-transferrin recombinant fusion protein for oral delivery. [Doctoral Dissertation]. University of Southern California; 2008. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/109040/rec/3274


University of Southern California

22. Kuo, Cheng-Fu. Role of hepatitis C virus F protein in viral protein expression and RNA replication.

Degree: MS, 2008, University of Southern California

 Programmed ribosomal frameshift is a novel mechanism used by virus to translate protein from 0 reading frame to -2/+1 reading frame. An A-rich slippery sequence… (more)

Subjects/Keywords: hepatitus C virus; frameshift

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APA (6th Edition):

Kuo, C. (2008). Role of hepatitis C virus F protein in viral protein expression and RNA replication. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/144769/rec/5636

Chicago Manual of Style (16th Edition):

Kuo, Cheng-Fu. “Role of hepatitis C virus F protein in viral protein expression and RNA replication.” 2008. Masters Thesis, University of Southern California. Accessed June 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/144769/rec/5636.

MLA Handbook (7th Edition):

Kuo, Cheng-Fu. “Role of hepatitis C virus F protein in viral protein expression and RNA replication.” 2008. Web. 19 Jun 2019.

Vancouver:

Kuo C. Role of hepatitis C virus F protein in viral protein expression and RNA replication. [Internet] [Masters thesis]. University of Southern California; 2008. [cited 2019 Jun 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/144769/rec/5636.

Council of Science Editors:

Kuo C. Role of hepatitis C virus F protein in viral protein expression and RNA replication. [Masters Thesis]. University of Southern California; 2008. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/144769/rec/5636

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