Thesis (Ph.D.)--McMaster University, 2004. / Supervisor: David W. Andrews. Includes bibliographical references (leaves 134-148).

Thesis (M.S. )--University of Tennessee Health Science Center, 2008. / Title from title page screen (viewed on July 17, 2008). Research advisor: Linda M. Hendershot, Ph.D. Document formatted into pages (x, 57 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 47-57).

Thesis (Ph. D.)--University of Virginia, 2006. / Includes bibliographical references. Also available online through Digital Dissertations.

Thesis (Ph.D.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 139 pages. Includes Vita. Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karol. inst., 2007. / Härtill 3 uppsatser.

Yao, Yao. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 131-151). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts also in Chinese.

Chen, Shuyan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 91-98). / Abstracts in English and Chinese. / ABSTRACT --- p.i / ACKNOWLEGGMENTS --- p.v / LIST OF FIGURES --- p.vi / LIST OF TABLES --- p.vii / ABBREVIATIONS --- p.viii / CONTENTS --- p.ix / Chapter Chapter I --- Introduction / Chapter 1.1 --- Introduction of BRE / Chapter 1.1.1 --- Discovery of BRE --- p.1 / Chapter 1.1.2 --- Isoforms of BRE --- p.2 / Chapter 1.1.3 --- Homology and orthologs of BRE --- p.3 / Chapter 1.1.4 --- Expression studies of BRE mRNA --- p.4 / Chapter 1.1.5 --- Expression and cellular localization of BRE protein --- p.5 / Chapter 1.1.6 --- Interaction between BRE and death receptor --- p.6 / Chapter 1.1.7 --- Anti-apoptotic effect of BRE in cell line studies --- p.9 / Chapter 1.1.8 --- Anti-apoptotic effect of BRE in vivo --- p.11 / Chapter 1.1.9 --- BRE's role in DNA repair and ubiquitination --- p.12 / Chapter 1.1.10 --- BRE's role in regulation of Prohibitin and p53 expression --- p.13 / Chapter 1.2 --- Hepatocellular carcinoma / Chapter 1.2.1 --- Carcinogenesis --- p.15 / Chapter 1.2.2 --- Diethylnitrosamine -induced HCC --- p.15 / Chapter 1.2.3 --- Mouse model for HCC studies --- p.17 / Chapter 1.2.4 --- BRE in human HCC --- p.18 / Chapter 1.3 --- Green Fluorescent Protein / Chapter 1.3.1 --- Application of GFP in biological research --- p.19 / Chapter 1.3.2 --- Advantage of GFP applied in protein localization --- p.19 / Chapter Chapter II --- Materials and Methods / Chapter 2.1 --- Materials / Chapter 2.1.1 --- Primer used for cloning --- p.20 / Chapter 2.1.2 --- DNA clones used in the studies --- p.21 / Chapter 2.1.3 --- Materials for DNA manipulation --- p.24 / Chapter 2.1.4 --- Materials for protein manipulation --- p.24 / Chapter 2.1.5 --- Antibodies --- p.25 / Chapter 2.1.6 --- Chemicals --- p.25 / Chapter 2.1.7 --- Kits --- p.26 / Chapter 2.1.8 --- Culture media and reagents --- p.26 / Chapter 2.1.9 --- Bacterial strain used for transformation and cloning --- p.26 / Chapter 2.1.10 --- Instrumentation --- p.27 / Chapter 2.1.11 --- Animals --- p.27 / Chapter 2.1.12 --- Slides --- p.27 / Chapter 2.2 --- Methods / Chapter 2.2.1 --- Construction of Plasmids / Chapter 2.2.1.1 --- Polymerase chain reaction (PCR) --- p.28 / Chapter 2.2.1.2 --- Enzyme Digestion and Ligation --- p.29 / Chapter 2.2.1.3 --- Transformaion / Chapter 2.2.1.3.1 --- Preparation of competent cells --- p.29 / Chapter 2.2.1.3.2 --- Heat-shock Transformation --- p.29 / Chapter 2.2.1.4 --- Midi Prep of plasmids --- p.30 / Chapter 2.2.2 --- Cell Culture --- p.30 / Chapter 2.2.3 --- Transfection --- p.30 / Chapter 2.2.4 --- MG-132 treatment --- p.31 / Chapter 2.2.5 --- Flow Cytometry --- p.32 / Chapter 2.2.6 --- Western blotting / Chapter 2.2.6.1 --- SDS-PAGE --- p.32 / Chapter 2.2.6.2 --- Immunoblotting --- p.32 / Chapter 2.2.7 --- Production of Monoclonal Antibody --- p.33 / Chapter 2.2.8 --- Mice --- p.34 / Chapter 2.2.9 --- Tissue Processing --- p.35 / Chapter 2.2.10 --- Tissue Section --- p.35 / Chapter 2.2.11 --- Immunostaining --- p.36 / Chapter 2.2.12 --- H&E staining --- p.36 / Chapter 2.2.13 --- Picture Capture --- p.37 / Chapter 2.2.14 --- Confocal imaging --- p.37 / Chapter 2.2.14 --- Statistical Analysis --- p.37 / Chapter Chapter III --- BRE promotes growth of chemically-induced hepatocellular carcinoma / Chapter 3.1 --- DEN induced HCC in male mice --- p.38 / Chapter 3.2 --- BRE facilitates HCC in female mice --- p.44 / Chapter 3.3 --- Over-expression of BRE in tumor portion --- p.45 / Chapter 3.4 --- Direct effect of DEN on BRE expression --- p.47 / Chapter 3.5 --- Contribution of infiltrating cells in up-regulation of BRE --- p.50 / Chapter Chaper IV --- Subcellular localization of BRE / Chapter 4.1 --- GFP-BRE fusion constructs --- p.55 / Chapter 4.1.1 --- Transfection of GFP-BRE fusions --- p.58 / Chapter 4.1.2 --- Flow cytometry analysis of GFP-BRE fusions --- p.59 / Chapter 4.1.3 --- Western blot analysis of GFP-BRE fusions --- p.62 / Chapter 4.1.4 --- Stabilities of GFP-BRE fusions --- p.64 / Chapter 4.2 --- Fusions between GFP and the deletion mutants of BRE --- p.66 / Chapter 4.2.1 --- Transfection of mutants --- p.68 / Chapter 4.2.2 --- Low expression of mutants --- p.69 / Chapter 4.3 --- MG-132 treatments / Chapter 4.3.1 --- Increased expression of fusion proteins --- p.74 / Chapter 4.3.2 --- Subcellular localization of GFP-BRE fusions --- p.77 / Chapter Chapter V --- Discussion / Chapter 5.1 --- Functional role of BRE in HCC / Chapter 5.1.1 --- Stage model of carcinogenesis --- p.81 / Chapter 5.1.2 --- Anti-apoptotic genes in cancer --- p.84 / Chapter 5.1.3 --- Limitation of the study --- p.85 / Chapter 5.1.4 --- Conclusion --- p.85 / Chapter 5.2 --- Subcellular localization of BRE / Chapter 5.2.1 --- Low expression of GFP-BRE fusions --- p.86 / Chapter 5.2.2 --- Additional study --- p.90 / Chapter 5.2.3 --- Conclusion --- p.90 / Reference --- p.91 / Appendix --- p.99

Indiana University-Purdue University Indianapolis (IUPUI) / Enhancing osteoblast proliferation, survival, and extracellular matrix protein secretion are potential therapeutic approaches to treat bone fractures and diseases such as osteoporosis. BENS is a traditional medicine used in many countries such as India for thousands of years to treat many diseases including bone diseases. In this study, molecular, cell-based and in vivo approaches were utilized to investigate the effects of BENS on bone and cartilage regeneration. An osteosarcoma cell line (MG63) was incubated in serum free media with and without 0.8 mg/ml of BENS. BENS significantly increased cell survival up to 30 days and these cells retained their ability to proliferate in fresh media with serum. After adding BENS, there were statistically significant decreases in the expression of both anti-apoptotic and pro-apoptotic proteins. An in vivo non-critical size segmental bone defect Xenopus system was used to evaluate the ability of BENS to enhance cartilage formation. After a small segment of the anterior hemisection of the tarsus bone was excised, the frogs were divided into three groups and given subcutaneous injections of either phosphate-buffered saline or BENS once daily for 30 days and then bone/cartilage formation evaluated. The total cartilage area/total section area was significantly increased (2.6 fold) in the BENS treated samples. In an osteoporotic rat model, the anabolic properties of BENS on bone mass were assessed by histomorphometric analyses. Ovariectomized (OVX) rats received daily intraperitoneal injections for 4 weeks. Bone formation rates (BFRs) for the cortical periosteal bone surface of the midshaft tibia were 383.2, 223.9, 308.8, 304.9, and 370.9 µm3/µm2/year, and for the trabecular surface were 82.2, 113, 212.1, 157, and 165 µm3/µm2/year for the sham, OVX, PTH, 3 mg/kg BENS, and 30 mg/kg BENS groups, respectively. BENS increased both trabecular and cortical BFRs. It generated better results on cortical periosteal bone surface than did PTH. Taken together, these findings suggest that BENS promotes osteoblast survival due to its effects on altering the balance between pro-apoptotic and anti-apoptotic proteins. In addition, in vivo studies revealed that BENS enhanced cartilage formation in Xenopus and BFRs in rats. Therefore, BENS may possess anabolic bone/cartilage properties.

Tam Ka-ying. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 164-179). / Abstracts in English and Chinese. / Chapter Chapter one: --- Introduction --- p.4 / Chapter 1.1 --- Introduction of BRE --- p.4 / Chapter 1.1.1 --- Discovery of BRE --- p.4 / Chapter 1.1.2 --- cDNA sequence and amino acids sequence of BRE --- p.4 / Chapter 1.1.3 --- BRE expression level in Human and rat organs --- p.5 / Chapter 1.1.4 --- Expression of Human and mouse BRE in multiple isoforms --- p.6 / Chapter 1.1.4.1 --- BRE isoforms in Human --- p.6 / Chapter 1.1.4.2 --- BRE isoforms in mouse --- p.6 / Chapter 1.1.5 --- mRNA level of BRE upon stress --- p.7 / Chapter 1.1.6 --- BRE and steroidogenesis --- p.8 / Chapter 1.1.7 --- BRE and p55 tumor necrosis factor α (TNF) receptor --- p.9 / Chapter 1.1.8 --- BRE and NFkB activity --- p.9 / Chapter 1.1.9 --- Anti-apoptotic effect of BRE --- p.10 / Chapter 1.1.10 --- BRE enhances the growth of tumor cells --- p.12 / Chapter 1.1.11 --- BRE and its ubiquitination activity --- p.12 / Chapter 1.1.12 --- Regulation of Prohibitin and p53 expression and proliferation by BRE --- p.13 / Chapter 1.2 --- Regulation of transcription --- p.15 / Chapter 1.2.1 --- Cis-acting elements --- p.17 / Chapter 1.2.1.1 --- The TATA box --- p.18 / Chapter 1.2.1.2 --- The GC box and CAAT box --- p.18 / Chapter 1.2.1.3 --- The initiator (Inr) --- p.19 / Chapter 1.2.1.4 --- CpG islands --- p.20 / Chapter 1.2.2 --- Trans- acting protein factors --- p.21 / Chapter 1.2.2.1 --- Zinc finger domain --- p.21 / Chapter 1.2.2.2 --- Basic helix-turn-helix domain (bHLH) --- p.22 / Chapter 1.3 --- Hypothesis and Objectives --- p.23 / Chapter Chapter two: --- Materials and Methods --- p.25 / Chapter 2.1 --- Materials --- p.25 / Chapter 2.1.1 --- Primers used in polymerase chain reaction (PCR) and sequencing --- p.25 / Chapter 2.1.2 --- DNA clones used in the studies --- p.26 / Chapter 2.1.3 --- Materials for DNA manipulation --- p.27 / Chapter 2.1.4 --- Materials for protein manipulation --- p.28 / Chapter 2.1.5 --- Antibodies --- p.28 / Chapter 2.1.6 --- Chemical used in treatments --- p.29 / Chapter 2.1.7 --- Kits --- p.29 / Chapter 2.1.8 --- Culture media and reagents --- p.30 / Chapter 2.1.9 --- Instrumentation --- p.30 / Chapter 2.1.10 --- Bacterial strain used for transfection and cloning --- p.31 / Chapter 2.2 --- Methodologies --- p.36 / Chapter 2.2.1 --- Cell culture --- p.36 / Chapter 2.2.1.1 --- Monolayer cells --- p.36 / Chapter 2.2.1.2 --- Suspension cell --- p.36 / Chapter 2.2.2 --- Identification of the transcriptional start site (TSS) of BRE by RNA ligase- mediated rapid amplification of 5，and 3，cDNA ends (RLM-RACE) --- p.37 / Chapter 2.2.3 --- Preparation of the 5' untranslated region (UTR) fragments of BRE --- p.39 / Chapter 2.2.3.1 --- Polymerase chain reaction (PCR) with Taq polymerase --- p.39 / Chapter 2.2.3.2 --- Polymerase chain reaction (PCR) with PhusiońёØ high-fidelity DNA.… --- p.40 / Chapter 2.2.4 --- Construction of the reporter constructs --- p.42 / Chapter 2.2.5 --- Cell transfection --- p.42 / Chapter 2.2.6 --- Dual-luciferase reporter assay --- p.43 / Chapter 2.2.7 --- Western blotting --- p.44 / Chapter 2.2.8 --- Cell cycle analysis by flow cytometry --- p.45 / Chapter 2.2.9 --- BRE antibody production --- p.43 / Chapter Chapter Three: --- Identification of transcriptional start sites and promoter region for BRE --- p.52 / Chapter 3.1 --- Identification of the transcriptional start sites for BRE --- p.52 / Chapter 3.2 --- Computational analysis of the 5' region of BRE --- p.57 / Chapter 3.2.1 --- Putative transcriptional factor binding sites --- p.57 / Chapter 3.2.2 --- CpG island --- p.58 / Chapter 3.3 --- Identification of BRE promoter --- p.64 / Chapter Chapter Four: --- Characterization of transcriptional regulation of BRE --- p.70 / Chapter 4.1 --- Regulation of BRE promoter by genotoxic stimuli and retinoic acid --- p.71 / Chapter 4.1.1 --- Etoposide --- p.71 / Chapter 4.1.2 --- 4-nitroquinoline-l -oxide (4NQO) --- p.79 / Chapter 4.1.3 --- Retinoic acid (RA) --- p.87 / Chapter 4.2 --- Regulation of BRE promoter by p53 protein and gamma irradiation --- p.90 / Chapter 4.2.1 --- Co-transfection with p53 plasmid --- p.90 / Chapter 4.2.2 --- Gamma irradiation (y irradiation) --- p.96 / Chapter 4.2.2.1 --- γ irradiation treatment of HeLa cells --- p.96 / Chapter 4.2.2.2 --- γ irradiation treatment of Balb/c 3T3 cells --- p.99 / Chapter 4.3 --- Regulation of BRE promoter by BRE --- p.103 / Chapter 4.3.1 --- Co-transfection with V5-tagged BRE (GS-BRE) --- p.103 / Chapter 4.3 2 --- Co-transfection with untagged BRE (pcDNA3-BRE) --- p.107 / Chapter 4.4 --- Regulation of BRE promoter by culture condition --- p.110 / Chapter 4.4.1 --- Cell density --- p.110 / Chapter 4.4.2 --- Serum deprivation --- p.114 / Chapter 4.5 --- Regulation of BRE promoter by kinase inhibitors --- p.120 / Chapter Chapter Five: --- BRE and cell cycle analysis --- p.127 / Chapter 5.1 --- Cell synchronization in G1 phase by aphidicolin (APC) --- p.127 / Chapter 5.1.1 --- Flow analysis --- p.128 / Chapter 5.1.2 --- Luciferase reporter assay --- p.128 / Chapter 5.1.3 --- Western blot analysis --- p.129 / Chapter 5.2 --- Cell synchronization in G2/M phase by colchicine (COL) --- p.137 / Chapter 5.2.1 --- Flow analysis --- p.137 / Chapter 5.2.2 --- Luciferase reporter assay --- p.137 / Chapter 5.2.3 --- Western blot analysis --- p.138 / Chapter 5.3 --- Cell cycle analysis of the treatments investigated by luciferase assays --- p.144 / Chapter Chapter Six: --- Discussion --- p.149 / Chapter 6.1 --- Study of BRE expression --- p.149 / Chapter 6.2 --- Study of BRE regulation --- p.154 / Chapter 6.3 --- Conclusion --- p.163 / Reference --- p.164 / Appendix (Raw data and statistical information of luciferase assays)

Thesis--University of Oklahoma. / Bibliography: leaves 71-78.