subject:(Nuclear factor erythroid 2 like 2 Nrf 2 )

NSYSU

1. Yang, Shih-Ming. Oxidative Stress and Rejection: Molecular Mechanisms and Diagnostic Potential in Liver Transplantation.

Degree: Master, Biological Sciences, 2015, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0508115-130153

► Liver biopsy is currently the only means of definite diagnosis of acute rejection (AR), while it is invasive and painful, resulting in several complications such… (more)

▼ Liver biopsy is currently the only means of definite diagnosis of acute rejection (AR), while it is invasive and painful, resulting in several complications such as bleeding, infection, and rarely, graft loss. Therefore, the development of noninvasive and feasible diagnosis tool is important for early prediction and diagnosis of AR. AR leads to imbalance of reactive oxygen species (ROS) generation and natural antioxidant defense, and excessive ROS formation induces oxidative stress, which triggers free radical nitric oxide (NO) synthesis. This study aimed to explore molecular mechanisms of AR and diagnostic potential of NO and its oxidation products in liver transplantation. Using a rat orthotopic liver transplantation (OLT) model, we explored mitogen-activated protein kinase (MAPK) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-mediated molecular mechanisms of AR. LEW rats with AR (DA-LEW OLT at day 7) showed significantly higher levels of aspartate transaminase (AST), alanine transaminase (ALT) and lipid peroxidation product (malondialdehyde: MDA) as compared with naive LEW and syngeneic LEW-LEW OLT rats. Proinflammatory cytokines, induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were significantly elevated in DA-LEW OLT livers. Levels of phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphorylated p38 MAPK (p-38 MAPK) were significantly downregulated in DA-LEW OLT livers, resulting in the inactivation of Nrf2-mediated antioxidant defense. Induction of Bax and cleaved caspase-3 suggested ROS-mediated apoptosis in DA-LEW OLT livers. Exhaled breath NO as well as serum nitrite and nitrate (NO2- and NO3-; NOx) were significantly increased in DA-LEW, but not in LEW-LEW OLT rats. Cyclosporine A clearly suppressed the induction of NOx, suggesting the diagnostic potential of NO and its oxidation products in AR. In summary, we present MAPK and Nrf2-mediated molecular mechanisms of AR and a potential of serum NOx and exhaled breath NO for prediction and diagnosis of AR. Advisors/Committee Members: Ming-Hong Tai (committee member), Shigeru Goto (chair), Ching-Mei Hsu (chair), Toshiaki Nakano (committee member).

Subjects/Keywords: nuclear factor (erythroid-derived 2)-like; rejection; liver transplantation; nitric oxide; oxidative stress; noninvasive diagnosis

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APA (6^th Edition):

Yang, S. (2015). Oxidative Stress and Rejection: Molecular Mechanisms and Diagnostic Potential in Liver Transplantation. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0508115-130153

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

Chicago Manual of Style (16^th Edition):

Yang, Shih-Ming. “Oxidative Stress and Rejection: Molecular Mechanisms and Diagnostic Potential in Liver Transplantation.” 2015. Thesis, NSYSU. Accessed February 25, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0508115-130153.

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

MLA Handbook (7^th Edition):

Yang, Shih-Ming. “Oxidative Stress and Rejection: Molecular Mechanisms and Diagnostic Potential in Liver Transplantation.” 2015. Web. 25 Feb 2021.

Vancouver:

Yang S. Oxidative Stress and Rejection: Molecular Mechanisms and Diagnostic Potential in Liver Transplantation. [Internet] [Thesis]. NSYSU; 2015. [cited 2021 Feb 25]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0508115-130153.

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

Council of Science Editors:

Yang S. Oxidative Stress and Rejection: Molecular Mechanisms and Diagnostic Potential in Liver Transplantation. [Thesis]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0508115-130153

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

University of South Carolina

2. Clinton, Sarah Ashley. The Role Of Nuclear Factor-Erythroid-2-Related Factor 2 In Sensitivity To Thymidylate Synthase Inhibitors In Colon Cancer Cells.

Degree: PhD, Biological Sciences, 2016, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/3969

► Nuclear factor-erythroid-2-related factor 2 (NRF2), a member of the cap ‘n’ collar family of bZIP transcription factors, confers protection against oxidative and electrophilic stress.… (more)

▼ Nuclear factor-erythroid-2-related factor 2 (NRF2), a member of the cap ‘n’ collar family of bZIP transcription factors, confers protection against oxidative and electrophilic stress. NRF2 is of great interest in cancer research, due to its role in response to chemotherapy. The class of drugs targeting thymidylate synthase (TYMS) has been useful in the treatment of colorectal cancer, among other cancers. It has long been known that inhibition of TYMS leads to depletion of thymidine levels and the onset of programmed cell death, deriving from the enzyme’s function as the sole de novo source of thymidine for DNA replication and repair. Exposing cells to TYMS inhibitors such as fluoropyrimidine antimetabolites (5-fluorouracil, or FUra; 5’-fluoro-2’-deoxyuridine, or FdUrd), as well as anti-folate analogs (raltitrexed, or RTX), induce intracellular concentrations of reactive oxygen species, which are a primary cause of drug-mediated toxicity. This prompted our focus on assessing the impact of NRF2 on cellular response to TYMS inhibitors. Using human colon tumor-derived cell line HCT116, we have shown by gene expression profiling that drug exposure induces expression of a number of genes that are regulated by NRF2. Quantitative PCR assays of several colon tumor cell lines verified that FUra, FdUrd, and RTX induce transcription of several genes known to be NRF2-targets, including AKR1B10, ALDH3A1, HSPB8, HMOX1, and SERPINE1, among others. Such induction mirrors that in response to the classical NRF2 activator tert-butylhydroquinone (tBHQ). NRF2 protein concentrations in the nucleus are increased by FdUrd treatment, though not to the same extent as with tBHQ. Reporter gene constructs were used to show that both FdUrd and tBHQ induce transcription mediated by the NRF2-binding antioxidant response element (ARE). Furthermore, chromatin-immunoprecipitation experiments revealed that TYMS inhibitors promote occupancy by NRF2 of the ARE regions of several genes; again, tBHQ had a much greater effect. Additionally, chromatin-immunoprecipitation experiments indicated that TYMS inhibitors do not alter the acetylation of histones near the promoter regions. We observed no correlation between the activity of the target gene, and the acetylation of histones. We also showed that the PI3K/AKT pathway does not affect the stability of NRF2 in HCT116 cells. Finally, we observed that increases in the apoptotic index following exposure to TYMS inhibitors were greater in cells in which the transcription factor was subjected to siRNA-mediated “knockdown” or CRISPR/Cas9-mediated “knockout”, indicating that reduced NRF2 expression sensitizes cells to TYMS inhibitors. Overall, we conclude that TYMS inhibitors activate NRF2 and its downstream target genes, thereby constraining drug response. Reducing such activation of NRF2 or its consequences may be an effective strategy to sensitizing tumor cells to chemotherapy. Advisors/Committee Members: Franklin G. Berger, Maria Marjorette O. Peña.

Subjects/Keywords: Biology; Life Sciences; Role Of Nuclear Factor-Erythroid-2-Related; Factor 2 In Sensitivity; Thymidylate Synthase Inhibitors; Colon Cancer Cells

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APA (6^th Edition):

Clinton, S. A. (2016). The Role Of Nuclear Factor-Erythroid-2-Related Factor 2 In Sensitivity To Thymidylate Synthase Inhibitors In Colon Cancer Cells. (Doctoral Dissertation). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/3969

Chicago Manual of Style (16^th Edition):

Clinton, Sarah Ashley. “The Role Of Nuclear Factor-Erythroid-2-Related Factor 2 In Sensitivity To Thymidylate Synthase Inhibitors In Colon Cancer Cells.” 2016. Doctoral Dissertation, University of South Carolina. Accessed February 25, 2021. https://scholarcommons.sc.edu/etd/3969.

MLA Handbook (7^th Edition):

Clinton, Sarah Ashley. “The Role Of Nuclear Factor-Erythroid-2-Related Factor 2 In Sensitivity To Thymidylate Synthase Inhibitors In Colon Cancer Cells.” 2016. Web. 25 Feb 2021.

Vancouver:

Clinton SA. The Role Of Nuclear Factor-Erythroid-2-Related Factor 2 In Sensitivity To Thymidylate Synthase Inhibitors In Colon Cancer Cells. [Internet] [Doctoral dissertation]. University of South Carolina; 2016. [cited 2021 Feb 25]. Available from: https://scholarcommons.sc.edu/etd/3969.

Council of Science Editors:

Clinton SA. The Role Of Nuclear Factor-Erythroid-2-Related Factor 2 In Sensitivity To Thymidylate Synthase Inhibitors In Colon Cancer Cells. [Doctoral Dissertation]. University of South Carolina; 2016. Available from: https://scholarcommons.sc.edu/etd/3969

University of Queensland

3. Hu, Hao. Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53.

Degree: School of Medicine, 2016, University of Queensland

URL: http://espace.library.uq.edu.au/view/UQ:405743

Subjects/Keywords: Cytochrome P450 2A6 (CYP2A6); Bilirubin (BR); Haem oxygenase1 (HMOX1); Benzo[α]pyrene (BaP); Nuclear factor erythroid 2-like 2 (Nrf-2); Tumour suppressor p53; Constitutive androstane receptor (CAR); CEBP α; Octamer-1 (Oct-1); Hepatocyte nuclear factor-4α (HNF-4α); 060107 Enzymes; 060111 Signal Transduction; 060199 Biochemistry and Cell Biology not elsewhere classified

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

APA (6^th Edition):

Hu, H. (2016). Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53. (Thesis). University of Queensland. Retrieved from http://espace.library.uq.edu.au/view/UQ:405743

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

Chicago Manual of Style (16^th Edition):

Hu, Hao. “Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53.” 2016. Thesis, University of Queensland. Accessed February 25, 2021. http://espace.library.uq.edu.au/view/UQ:405743.

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

MLA Handbook (7^th Edition):

Hu, Hao. “Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53.” 2016. Web. 25 Feb 2021.

Vancouver:

Hu H. Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53. [Internet] [Thesis]. University of Queensland; 2016. [cited 2021 Feb 25]. Available from: http://espace.library.uq.edu.au/view/UQ:405743.

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

Council of Science Editors:

Hu H. Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53. [Thesis]. University of Queensland; 2016. Available from: http://espace.library.uq.edu.au/view/UQ:405743

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

University of Louisville

4. Lin, Qian. A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes.

Degree: PhD, 2018, University of Louisville

URL: 10.18297/etd/3016 ; https://ir.library.louisville.edu/etd/3016

► Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder and is strongly associated with type 2 diabetes (T2D). Our recently engineered… (more)

Subjects/Keywords: fibroblast growth factor 1; nonalcoholic fatty liver disease; oxidative stress; AMP-activated protein kinase; nuclear factor erythroid 2-related factor 2; Endocrine System Diseases; Pharmacology

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APA (6^th Edition):

Lin, Q. (2018). A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/3016 ; https://ir.library.louisville.edu/etd/3016

Chicago Manual of Style (16^th Edition):

Lin, Qian. “A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes.” 2018. Doctoral Dissertation, University of Louisville. Accessed February 25, 2021. 10.18297/etd/3016 ; https://ir.library.louisville.edu/etd/3016.

MLA Handbook (7^th Edition):

Lin, Qian. “A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes.” 2018. Web. 25 Feb 2021.

Vancouver:

Lin Q. A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes. [Internet] [Doctoral dissertation]. University of Louisville; 2018. [cited 2021 Feb 25]. Available from: 10.18297/etd/3016 ; https://ir.library.louisville.edu/etd/3016.

Council of Science Editors:

Lin Q. A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes. [Doctoral Dissertation]. University of Louisville; 2018. Available from: 10.18297/etd/3016 ; https://ir.library.louisville.edu/etd/3016

5. HO WANXING EUGENE. INVESTIGATIONS OF ANTI-INFLAMMATORY MECHANISMS OF ANTI-MALARIAL DRUG ARTESUNATE IN ALLERGIC ASTHMA.

Degree: 2014, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/51992

Subjects/Keywords: Artemisinin; Oxidative Stress; Mass Spectrometry; Metabolomics; Bronchoalveolar lavage fluid; Nuclear factor (erythroid-derived 2)-like 2

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

APA (6^th Edition):

EUGENE, H. W. (2014). INVESTIGATIONS OF ANTI-INFLAMMATORY MECHANISMS OF ANTI-MALARIAL DRUG ARTESUNATE IN ALLERGIC ASTHMA. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/51992

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

Chicago Manual of Style (16^th Edition):

EUGENE, HO WANXING. “INVESTIGATIONS OF ANTI-INFLAMMATORY MECHANISMS OF ANTI-MALARIAL DRUG ARTESUNATE IN ALLERGIC ASTHMA.” 2014. Thesis, National University of Singapore. Accessed February 25, 2021. http://scholarbank.nus.edu.sg/handle/10635/51992.

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

MLA Handbook (7^th Edition):

EUGENE, HO WANXING. “INVESTIGATIONS OF ANTI-INFLAMMATORY MECHANISMS OF ANTI-MALARIAL DRUG ARTESUNATE IN ALLERGIC ASTHMA.” 2014. Web. 25 Feb 2021.

Vancouver:

EUGENE HW. INVESTIGATIONS OF ANTI-INFLAMMATORY MECHANISMS OF ANTI-MALARIAL DRUG ARTESUNATE IN ALLERGIC ASTHMA. [Internet] [Thesis]. National University of Singapore; 2014. [cited 2021 Feb 25]. Available from: http://scholarbank.nus.edu.sg/handle/10635/51992.

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

Council of Science Editors:

EUGENE HW. INVESTIGATIONS OF ANTI-INFLAMMATORY MECHANISMS OF ANTI-MALARIAL DRUG ARTESUNATE IN ALLERGIC ASTHMA. [Thesis]. National University of Singapore; 2014. Available from: http://scholarbank.nus.edu.sg/handle/10635/51992

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

6. Lo, Raymond Ho Fai. Activation of Estrogen Receptor Alpha, Aryl Hydrocarbon Receptor, and Nuclear Factor Erythroid-2 Like 2 in Human Breast Cancer Cells.

Degree: 2013, University of Toronto

URL: http://hdl.handle.net/1807/43650

►

There is a strong association between estrogen exposure and breast cancer risk. Estrogen can activate estrogen receptor alpha (ERalpha) to increase cell proliferation. Estrogen can… (more)

▼

There is a strong association between estrogen exposure and breast cancer risk. Estrogen can activate estrogen receptor alpha (ERalpha) to increase cell proliferation. Estrogen can also be metabolized into genotoxic compounds to induce DNA damage and mutations. Activation of the aryl hydrocarbon receptor (AHR) and nuclear factor erythroid-2 like 2 (NFE2L2; NRF2) can alter the production of genotoxic estrogen. The present thesis investigated the signalling mechanisms of ERalpha, AHR, and NRF2 and how their interaction might modulate breast cancer risk. In Chapter 2, genome-wide, but promoter-focused analysis of ERalpha binding sites in T-47D breast cancer cells identified potential cell line specific differences in estrogen signalling between T-47D and the commonly used MCF-7 breast cancer cells. CYP2B6 was identified to be an ERalpha target gene in T-47D cells but not MCF-7 cells, supporting cell line dependent effect in estrogen signalling. In Chapter 3 and 4, genome-wide analyses of AHR binding sites were performed to investigate the molecular criteria governing genomic AHR transactivation in vivo in mouse and in vitro in MCF-7 breast cancer cells. Our analysis identified 1) the previously established aryl hydrocarbon response element to be an important, but not an absolute requirement in AHR transactivation and 2) key epigenetic modifications that modulate AHR-dependent gene regulation. Lastly, in Chapter 5, interaction among ERalpha, AHR, and NRF2 was presented at the regulatory region of two NRF2 target genes, NADPH Quinone Oxidoreductase 1 (NQO1) and Heme Oxygenase 1 (HMOX1). ERalpha repressed, whereas AHR enhanced NRF2-dependent NQO1 and HMOX1 mRNA expression through altered p300 recruitment and Histone H3 Lysine 9 acetylation. Collectively, this thesis examined novel molecular mechanisms that might alter breast cancer development/progression by modulating ER, AHR, and NRF2 activity.

PhD

Advisors/Committee Members: Matthews, Jason, Wells, Peter G., Pharmacology.

Subjects/Keywords: Estrogen Receptor; Aryl Hydrocarbon Receptor; Nuclear Factor Erythroid-2 Like 2; 0383

…factor NRF2; NFE2L2 Nuclear factor erythroid-2 like 2 NURD Nucleosome remodeling Oatp… …x29;, and the nuclear factor erythroid-2 like factor 2 (NRF2) all play important… …factor erythroid-2-related factor 2 (NFE2L2) in MCF-7 breast cancer cells. Accepted… …localization sequence NQO1 NADPH quinone oxidoreductase 1 xiii NR2F Nuclear receptor subfamily 2… …glucuronosyltransferase XAP2 X-associated protein 2 xv List of Tables Table 1 Transcription factor motifs…

11 more images…

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

APA (6^th Edition):

Lo, R. H. F. (2013). Activation of Estrogen Receptor Alpha, Aryl Hydrocarbon Receptor, and Nuclear Factor Erythroid-2 Like 2 in Human Breast Cancer Cells. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/43650

Chicago Manual of Style (16^th Edition):

Lo, Raymond Ho Fai. “Activation of Estrogen Receptor Alpha, Aryl Hydrocarbon Receptor, and Nuclear Factor Erythroid-2 Like 2 in Human Breast Cancer Cells.” 2013. Doctoral Dissertation, University of Toronto. Accessed February 25, 2021. http://hdl.handle.net/1807/43650.

MLA Handbook (7^th Edition):

Lo, Raymond Ho Fai. “Activation of Estrogen Receptor Alpha, Aryl Hydrocarbon Receptor, and Nuclear Factor Erythroid-2 Like 2 in Human Breast Cancer Cells.” 2013. Web. 25 Feb 2021.

Vancouver:

Lo RHF. Activation of Estrogen Receptor Alpha, Aryl Hydrocarbon Receptor, and Nuclear Factor Erythroid-2 Like 2 in Human Breast Cancer Cells. [Internet] [Doctoral dissertation]. University of Toronto; 2013. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/1807/43650.

Council of Science Editors:

Lo RHF. Activation of Estrogen Receptor Alpha, Aryl Hydrocarbon Receptor, and Nuclear Factor Erythroid-2 Like 2 in Human Breast Cancer Cells. [Doctoral Dissertation]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/43650

Universidade do Rio Grande do Sul

7. Moreira, Andréa Cristiane Janz. A melatonina atenua o estresse oxidativo, ativa o estresse de retículo endoplasmático e a apoptose na hepatocarcinogênese experimental.

Degree: 2015, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/157476

►

O carcinoma hepatocelular (CHC) é a quarta causa mais frequente de morte por câncer em todo o mundo. Este estudo teve dois grandes objetivos, o… (more)

▼

O carcinoma hepatocelular (CHC) é a quarta causa mais frequente de morte por câncer em todo o mundo. Este estudo teve dois grandes objetivos, o primeiro foi estabelecer o carcinoma hpatocelular experimental por indução química e o segundo estudar os efeitos da melatonina sobre o estresse oxidativo, estresse de retículo endoplasmático e apoptose durante a hepatocarcinogênese. Foram realizados dois experimentos, ambos utilizaram dietilnitrosamina (DEN) mais acetilaminofluoreno (2-AAF) em ratos Wistar machos pesando 145-150 g. O primeiro estudo testou 3 protocolos de indução do câncer hepático. Os animais foram divididos em três grupos testes: DEN50: que recebeu DEN 50 mg duas vezes por semana até a 6ª semana e uma vez por semana nas semanas 11 a 13. DEN75: recebeu DEN 75mg uma vez por semana nas semanas até a 6ª semana e um reforço nas semanas de 11 a 13. DEN100: recebeu 5 doses de DEN 100mg uma a cada seis semanas por 28 semanas. Todos receberam 2- AAF dose única de 100 mg na 4ª semana. Após a indução foi comprovado por testes bioquímicos, macroscópico e histológico que o protocolo DEN50 desenvolve CHC avançado em 19 semanas, apresentou a fase inflamatória na 5ª semana e cirrose na 12ª semana. O protocolo DEN100 exibe padrão de lesões pré-cancerosas com cirrose em 28 semanas. O protocolo DEN75 foi o mais heterogêneo dos três, pois desenvolveu lesões pré-cancerosas, cancer inicial e CHC avançado. O segundo estudo, repetiu o protocolo DEN50 e administrou melatonina 20mg/L. Os tratamentos começaram nas semanas 5 e 12. Ao final de 19 semanas foi observado que animais do grupo que só recebeu DEN+2-AAF (DEN-CHC) desenvolveram carcinoma avançado, exibiram mais expressão de proteinas pró-inflamatórias (iNOS, COX-2 e NFkB). E animais tratados com Melatonina (DEN+MEL5 e DEN+MEL 12) apresentaram padrão histológico de cirrose e reduzida expressão destas proteinas. Quanto ao comportamento oxidativo foi observado que grupo DEN-CHC apresentou menor lipoperoxidação (LPO) por redução de ácidos graxos poliinsaturados, maior oxidação proteica, menor atividade da SOD e maior índice de danos ao DNA. O tratamento com melatonina ao longo da hepatocarcinogênese se mostrou efetivo para proteger a membrana lipidica, reduziu a oxidação proteica, aumentou a atividade da SOD e atenuou o dano ao DNA. Por fim, referente ao estresse de retículo endoplasmático e apoptose, animais com DEN-CHC não apresentaram ativação das proteinas de estresse de retículo (BiP, ATF6 e CHOP) nem acionaram as rotas apoptóticas. Entretanto, animais tratados com Melatonina tiveram aumento significativo na expressão de proteinas como BiP, ATF6 e CHOP, assim como proteinas pró-apoptóticas. Nossos resultados apontam que a melatonin, durante o processo de hepatocarcinogênese experimental, atuou como anti-inflamatório, antioxidante e pró-apoptótico. E estas ações contribuiram para evitar a progressão do carcinoma hepatocelular.

Hepatocellular carcinoma (HCC) is the fourth most frequent cause of cancer death worldwide. This study had two main objectives, the first was to…

Advisors/Committee Members: Marroni, Norma Anair Possa.

Subjects/Keywords: Melatonina; Hepatocarcinoma; Diethylnitrosamine; Estresse oxidativo; Carcinoma hepatocelular : Induzido quimicamente; Oxidative stress; Nuclear factor erythroid 2-related factor 2; Estresse do retículo endoplasmático; Nitric oxide synthase;

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

APA (6^th Edition):

Moreira, A. C. J. (2015). A melatonina atenua o estresse oxidativo, ativa o estresse de retículo endoplasmático e a apoptose na hepatocarcinogênese experimental. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/157476

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

Chicago Manual of Style (16^th Edition):

Moreira, Andréa Cristiane Janz. “A melatonina atenua o estresse oxidativo, ativa o estresse de retículo endoplasmático e a apoptose na hepatocarcinogênese experimental.” 2015. Thesis, Universidade do Rio Grande do Sul. Accessed February 25, 2021. http://hdl.handle.net/10183/157476.

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

MLA Handbook (7^th Edition):

Moreira, Andréa Cristiane Janz. “A melatonina atenua o estresse oxidativo, ativa o estresse de retículo endoplasmático e a apoptose na hepatocarcinogênese experimental.” 2015. Web. 25 Feb 2021.

Vancouver:

Moreira ACJ. A melatonina atenua o estresse oxidativo, ativa o estresse de retículo endoplasmático e a apoptose na hepatocarcinogênese experimental. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2015. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10183/157476.

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

Council of Science Editors:

Moreira ACJ. A melatonina atenua o estresse oxidativo, ativa o estresse de retículo endoplasmático e a apoptose na hepatocarcinogênese experimental. [Thesis]. Universidade do Rio Grande do Sul; 2015. Available from: http://hdl.handle.net/10183/157476

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

8. CHUA SHU XIAN SERENE. INVESTIGATING THE ROLE OF NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR 2 (NRF2) IN BREAST CANCER CELL-STATE DYNAMICS.

Degree: 2018, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/143082

Subjects/Keywords: Nuclear Factor Erythroid 2-Related Factor 2; Nrf2; Breast Cancer; MCF10CA1h; Cell-State Dynamics; Tumour Cell Plasticity

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

APA (6^th Edition):

SERENE, C. S. X. (2018). INVESTIGATING THE ROLE OF NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR 2 (NRF2) IN BREAST CANCER CELL-STATE DYNAMICS. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/143082

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

Chicago Manual of Style (16^th Edition):

SERENE, CHUA SHU XIAN. “INVESTIGATING THE ROLE OF NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR 2 (NRF2) IN BREAST CANCER CELL-STATE DYNAMICS.” 2018. Thesis, National University of Singapore. Accessed February 25, 2021. http://scholarbank.nus.edu.sg/handle/10635/143082.

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

MLA Handbook (7^th Edition):

SERENE, CHUA SHU XIAN. “INVESTIGATING THE ROLE OF NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR 2 (NRF2) IN BREAST CANCER CELL-STATE DYNAMICS.” 2018. Web. 25 Feb 2021.

Vancouver:

SERENE CSX. INVESTIGATING THE ROLE OF NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR 2 (NRF2) IN BREAST CANCER CELL-STATE DYNAMICS. [Internet] [Thesis]. National University of Singapore; 2018. [cited 2021 Feb 25]. Available from: http://scholarbank.nus.edu.sg/handle/10635/143082.

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

Council of Science Editors:

SERENE CSX. INVESTIGATING THE ROLE OF NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR 2 (NRF2) IN BREAST CANCER CELL-STATE DYNAMICS. [Thesis]. National University of Singapore; 2018. Available from: http://scholarbank.nus.edu.sg/handle/10635/143082

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

University of Illinois – Urbana-Champaign

9. Keever, Marissa R. Comparison of the molecular phenotypes of pigs carrying different IGF2 alleles at four developmental time points.

Degree: MS, Animal Sciences, 2017, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/97301

► A single nucleotide polymorphism in insulin-like growth factor 2 (IGF2 intron3-G3072A) is associated with greater muscle mass and decreased subcutaneous fat deposition in pigs carrying… (more)

▼ A single nucleotide polymorphism in insulin-like growth factor 2 (IGF2 intron3-G3072A) is associated with greater muscle mass and decreased subcutaneous fat deposition in pigs carrying a paternal copy of the A allele (Apat). While many studies have focused on the differences in between the gross phenotypes of these animals, relatively little has been done to understand how these animals differ at the molecular level. It was the objective of this study to compare the molecular phenotypes of animals carrying the Apat allele and those carrying the Gpat allele in order to gain insight into how those differences may result in the differences seen at the whole-animal level. RNA was extracted from longissimus (LM) samples taken from six animals of each genotype (Apat and Gpat) at four different time points, fetal day 90 (d90), birth (0d), weaning (21d), and market weight (176d). In total 46 samples were sequenced on the Illumina HiSeq 2000 with a target depth of 20 million reads per sample. Analysis of the RNA-seq data using tweeDEseq determined differentially expressed genes between Apat and Gpat pigs at each time point. Additionally, IPA analysis was used to determine if there were any differentially activated pathways between the two phenotypes. IGF2 was not found to be upregulated in Apat pigs compared to Gpat at d90 or 0d; however, IGF2 expression was found to be increased in Apat pigs compared to Gpat pigs at 21d and 176d. Though there was not differential expression of IGF2 at d90 and 0d, there was still differential expression of several other genes at these time points. At d90, Apat pigs tended to have an increase in the expression anti-apoptotic genes and a decrease in pro-apoptotic genes, possibly indicating enhanced myoblast survival, while Gpat pigs had greater expression of genes associated with protein synthesis. At 0d, there was an increased expression of genes associated with proliferation and protein synthesis in Apat pigs, and Gpat pigs appeared to have upregulation of genes involved in inflammation. At both 0d and 21d Apat and Gpat pigs had displayed upregulation of markers of myogenesis, suggesting different stages of muscle development. At 176d, Apat animals had decreased expression of genes involved in adipose signaling, including inflammation, stress, and autophagy and greater expression of genes associated with tissue development and the cell cycle. Thus, throughout the developmental timepoints, there appear to be markedly different processes taking place in the muscle tissue of Apat pigs and Gpat pigs. Advisors/Committee Members: Beever, Jonathan E (advisor), Dilger, Anna C (committee member), Kukekova, Anna V (committee member).

Subjects/Keywords: Insulin-like growth factor 2 (IGF2); Pig; RNA-seq; Muscle

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

APA (6^th Edition):

Keever, M. R. (2017). Comparison of the molecular phenotypes of pigs carrying different IGF2 alleles at four developmental time points. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/97301

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

Chicago Manual of Style (16^th Edition):

Keever, Marissa R. “Comparison of the molecular phenotypes of pigs carrying different IGF2 alleles at four developmental time points.” 2017. Thesis, University of Illinois – Urbana-Champaign. Accessed February 25, 2021. http://hdl.handle.net/2142/97301.

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

MLA Handbook (7^th Edition):

Keever, Marissa R. “Comparison of the molecular phenotypes of pigs carrying different IGF2 alleles at four developmental time points.” 2017. Web. 25 Feb 2021.

Vancouver:

Keever MR. Comparison of the molecular phenotypes of pigs carrying different IGF2 alleles at four developmental time points. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2017. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/2142/97301.

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

Council of Science Editors:

Keever MR. Comparison of the molecular phenotypes of pigs carrying different IGF2 alleles at four developmental time points. [Thesis]. University of Illinois – Urbana-Champaign; 2017. Available from: http://hdl.handle.net/2142/97301

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

McMaster University

10. Habib, Eric. Regulation of xCT by NRF-2 in Breast Cancer Cells.

Degree: MSc, 2014, McMaster University

URL: http://hdl.handle.net/11375/16535

►

Cancer cells adapt to high levels of oxidative stress in order to survive and proliferate, making the transcription factors involved in antioxidant defence regulation targets… (more)

▼

Cancer cells adapt to high levels of oxidative stress in order to survive and proliferate, making the transcription factors involved in antioxidant defence regulation targets of interest. The transcription factor NF E2 Related Factor 2 (NRF-2) regulates cellular defence genes including those encoding intracellular redox-balancing proteins such as enzymes involved in glutathione metabolism. Glutathione in particular is an important intracellular antioxidant molecule. NRF-2 binds to the Antioxidant Response Element (ARE) in the promoter of its target genes. Under basal conditions, Kelch-like ECH-associated protein 1 (KEAP1) acts as an inhibitor that targets NRF-2 for ubiquitination. During oxidative stress, NRF-2 dissociates from KEAP1 and enters the nucleus to bind to the ARE sequence. It is hypothesized that the elevated Reactive Oxygen Species may be depleting the glutathione levels within the cancer cell. System xc- is a cystine/glutamate antiporter that exports glutamate while importing cystine to synthesize glutathione. In response to oxidative stress, the cells increase system xc- activity in order to provide cystine for glutathione synthesis. There is evidence that expression of xCT, the specific subunit of system xc-,is regulated by NRF-2. However this has not yet been demonstrated in human breast cancer cells, which is the focus of this project. Basal expression of NRF-2, KEAP1 and xCT was characterized in three breast cancer cell lines (MDA-MB-231, MCF-7 and T47D) and compared to two non-cancer cell lines (184B5 and MCF10A). Basal protein levels of NRF-2 and KEAP1 showed no differences between cell lines. Basal protein levels of xCT were increased in MCF10A cells than T47D cells. MCF-7 cells were treated with hydrogen peroxide (H2O2) resulting in NRF-2 protein accumulation in the nucleus. With H2O2 treatment, xCT mRNA levels increased in MCF-7 cells. Additionally, transient overexpression of NRF-2 increased extracellular glutamate levels in MCF-7 cells. These data support a model that under oxidative stress, NRF-2 is localized to the nucleus and transcriptionally upregulates xCT. This is the first study in which the regulation of xCT has been linked to oxidative stress via NRF-2 in human breast cancer cells.

Thesis

Master of Science (MSc)

Advisors/Committee Members: Singh, Gurmit, Medical Sciences (Division of Physiology/Pharmacology).

Subjects/Keywords: Breast Cancer; Reactive Oxygen Species; System X; xCT; NRF-2; Glutamate

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

APA (6^th Edition):

Habib, E. (2014). Regulation of xCT by NRF-2 in Breast Cancer Cells. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/16535

Chicago Manual of Style (16^th Edition):

Habib, Eric. “Regulation of xCT by NRF-2 in Breast Cancer Cells.” 2014. Masters Thesis, McMaster University. Accessed February 25, 2021. http://hdl.handle.net/11375/16535.

MLA Handbook (7^th Edition):

Habib, Eric. “Regulation of xCT by NRF-2 in Breast Cancer Cells.” 2014. Web. 25 Feb 2021.

Vancouver:

Habib E. Regulation of xCT by NRF-2 in Breast Cancer Cells. [Internet] [Masters thesis]. McMaster University; 2014. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/11375/16535.

Council of Science Editors:

Habib E. Regulation of xCT by NRF-2 in Breast Cancer Cells. [Masters Thesis]. McMaster University; 2014. Available from: http://hdl.handle.net/11375/16535

University of Oulu

11. Kari, E. (Esa). Clinical impact of antioxidant enzymes Prx6 and Trx and their regulators Nrf1 and Nrf2 in diffuse Large B-cell lymphoma.

Degree: 2020, University of Oulu

URL: http://urn.fi/urn:isbn:9789526225289

►

Abstract Diffuse large B-cell lymphoma (DLBCL) is the single most common lymphoid malignancy in Western world. Excess oxidative stress and antioxidative enzyme expression have previously… (more)

▼

Abstract Diffuse large B-cell lymphoma (DLBCL) is the single most common lymphoid malignancy in Western world. Excess oxidative stress and antioxidative enzyme expression have previously been associated with adverse disease presentation and poor prognosis in DLBCL. The present study evaluated the clinical relevance of two antioxidant enzymes—peroxiredoxin 6 (Prx6) and thioredoxin-1 (Trx)—, one oxidative stress marker—8-hydroxydeoxyguanosine (8-OHdG)—, and four antioxidative, response-related transcription factors nuclear factor erythroid 2-related factor 1 (Nrf1) and factor 2 (Nrf2), Kelch ECH associating protein 1 (Keap1) and BTB (broad complex (BR-C), tramtrack (ttk), bric-a-brac/poxvirus (bab)) domain and Cap’n’collar (CNC) homolog 1 (Bach1) in DLBCL patients and cell culture (Trx). The pre-treatment blood serum levels of Prx6 were found to be significantly lower among DLBCL patients compared to healthy controls, and these levels were observed to rise to the controls’ levels after treatments. Low Prx6 levels were associated with neutropenic infections; thus, Prx6 might be a potential marker for selecting patients to receive white blood cell growth factors. All tissue assessed transcription factors, excluding Bach1, had prognostic implications among high-risk DLBCL patients. Low nuclear expression of Nrf1, high cytoplasmic expression of Nrf1, high nuclear expression of Nrf2 and low cytoplasmic expression of Keap1 were related to poor overall survival. Nuclear Nrf2 and Bach1 expressions were associated with adverse clinical features in DLBCL. Lymphoma cell’s cytoplasmic Trx expression was associated with superior survival with DLBCL patients who received etoposide-containing, high-dose chemotherapy or R-CHOEP. In the cell culture model, knockdown of Trx resulted in sensitization of lymphoma cells to doxorubicin and decreased the response to etoposide. Trx appears to be predict the response to etoposide (R-CHOEP).

Tiivistelmä Diffuusi suurten B-solujen lymfooma (DLBCL) on yleisin yksittäinen imusolmukesyöpä länsimaissa. Runsas oksidatiivinen stressi ja antioksidatiivisten entsyymien ilmentyminen on aiemmin yhdistetty huonoon taudinkuvaan ja ennusteeseen DLBCL:ssä. Tässä tutkimuksessa arvioitiin kahden antioksidatiivisen entsyymin peroksiredoksiini 6 (Prx6) ja tioredoksiini-1 (Trx), yhden oksidatiivisen stressin markkerin 8-hydroksideoksyguanosiinin (8-OHdG) sekä neljän antioksidatiivivasteeseen liittyvän transkriptiotekijän tumafaktori erytoidi 2-liittyvä faktori 1 (Nrf1) ja faktori 2 (Nrf2), Kelch ECH assosioituva proteiini 1 (Keap1) ja BTB (broad complex (BR-C), tramtrack (ttk), bric-a-brac/poxvirus (bab)) domeeni ja Cap’n’collar (CNC) homologi 1 (Bach1) kliinistä merkitystä DLBCL-potilailla sekä soluviljelyssä (Trx). Hoitoja edeltävien Prx6-seerumipitoisuuksien havaittiin olevan huomattavasti pienempiä verrattuna terveisiin kontrolleihin. Nämä pitoisuudet nousivat hoitojen jälkeen kontrollien tasolle. Matala seerumin Prx6 assosioitui neutropeenisiin infektioihin, minkä vuoksi Prx6 voisi olla potentiaalinen…

Advisors/Committee Members: Kuittinen, O. (Outi), Turpeenniemi-Hujanen, T. (Taina).

Subjects/Keywords: 8-hydroxydeoxyguanosine (8-OHdG); BTB domain and CNC homolog 1 (Bach1); Kelch ECH associating protein 1; diffuse large b-cell lymphoma; nuclear factor erythroid 2-related factor 1 &2; peroxiredoxin 6; thioredoxin-1; 8-hydroksideoksyguanosiini (8-OHdG); BTB (BR-C; Kelch ECH assosioituva proteiini 1 (Keap1); diffuusi suurten B-solujen lymfooma; peroksiredoksiini 6; tioredoksiini-1; ttk ja bab) domeeni ja CNC homologi 1 (Bach1); tumafaktori erytoidi 2-liittyvä faktori 1 (Nrf1) ja faktori 2 (Nrf2)

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

APA (6^th Edition):

Kari, E. (. (2020). Clinical impact of antioxidant enzymes Prx6 and Trx and their regulators Nrf1 and Nrf2 in diffuse Large B-cell lymphoma. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789526225289

Chicago Manual of Style (16^th Edition):

Kari, E (Esa). “Clinical impact of antioxidant enzymes Prx6 and Trx and their regulators Nrf1 and Nrf2 in diffuse Large B-cell lymphoma.” 2020. Doctoral Dissertation, University of Oulu. Accessed February 25, 2021. http://urn.fi/urn:isbn:9789526225289.

MLA Handbook (7^th Edition):

Kari, E (Esa). “Clinical impact of antioxidant enzymes Prx6 and Trx and their regulators Nrf1 and Nrf2 in diffuse Large B-cell lymphoma.” 2020. Web. 25 Feb 2021.

Vancouver:

Kari E(. Clinical impact of antioxidant enzymes Prx6 and Trx and their regulators Nrf1 and Nrf2 in diffuse Large B-cell lymphoma. [Internet] [Doctoral dissertation]. University of Oulu; 2020. [cited 2021 Feb 25]. Available from: http://urn.fi/urn:isbn:9789526225289.

Council of Science Editors:

Kari E(. Clinical impact of antioxidant enzymes Prx6 and Trx and their regulators Nrf1 and Nrf2 in diffuse Large B-cell lymphoma. [Doctoral Dissertation]. University of Oulu; 2020. Available from: http://urn.fi/urn:isbn:9789526225289

University of Alberta

12. Lim, David W. Trophic peptide therapies for neonatal short bowel syndrome: actions and mechanisms studied in a preclinical model.

Degree: PhD, Department of Surgery, 2016, University of Alberta

URL: https://era.library.ualberta.ca/files/c4x51hj32q

► Short bowel syndrome (SBS) occurs when a significant length of intestine is surgically resected for both congenital and acquired intestinal abnormalities and remains a significant… (more)

▼ Short bowel syndrome (SBS) occurs when a significant length of intestine is surgically resected for both congenital and acquired intestinal abnormalities and remains a significant cause of morbidity and mortality in neonates. With an insufficient amount of intestine available for nutrient absorption, neonates with SBS are dependent on parenteral nutrition (PN) for survival but many continue to develop and succumb to PN-associated complications such liver disease and sepsis. In order for these children to survive, the remnant intestine must adapt and improve nutrient absorption over time. Glucagon-like peptide-2 (GLP-2) is a distal intestinal-derived peptide that is trophic to the intestine and stimulates intestinal adaptation after major resection. Diseases that lead to SBS in neonates, such as necrotizing enterocolitis, most commonly affect and require removal of the distal intestine, including ileum. Thus, GLP-2 may be the limiting factor for adaptation in human neonates with SBS. Furthermore, the intestinotrophic effects of GLP-2 may be augmented by the simultaneous delivery of either enteral nutrition (EN) or epidermal growth factor (EGF). We thus hypothesized that GLP-2 therapy stimulates intestinal growth and function in neonatal SBS, and that the intestinotrophic effects of GLP-2 are augmented when given in combination with either EN or EGF therapy. For these studies, neonatal piglets were block-randomized to either a 75% mid-intestinal resection (JI model) with jejunoileal anastomosis (leaving equal lengths of jejunum and ileum) or 75% distal-intestinal resection (JC model) (removing all ileum) with jejunocolic anastomosis or sham (no resection) control. Piglets also received a jugular venous catheter and a gastrostomy tube for the provision of PN and EN, respectively. Piglets were subsequently maintained for 7 days. In the first study, piglets received either intravenous GLP-2 (42 μg/kg/day) or saline control and either remained on total PN (0% EN) or received EN at 40% of nutritional requirement. In the second study, piglets received saline control, intravenous GLP-2 (42 μg /kg/day), enteral EGF (80 µg/kg/day), or combined GLP-2 and EGF and all piglets received EN at 20% of nutritional requirement. Structural adaptation was assessed by the change in intestinal length, mucosal and intestinal weight, and histopathology. Functional adaptation was assessed by measuring several parameters: the relative gene expression of nutrient transporters, digestive enzymes and tight junction proteins, measurement of intestinal permeability using the Üssing chamber apparatus, fat absorption and weight gain. In the first study, we observed that in piglets maintained on total PN in the absence of treatment, the JI model demonstrated intrinsic structural adaptation, including increased intestinal weight and villus height, while the JC model did not. In this group that was not enterally fed, GLP-2 treatment induced histological adaptation in the JC model. In contrast, enteral feeding at 40% of nutritional requirement resulted in…

Subjects/Keywords: short bowel syndrome; intestinal failure; neonatal; glucagon-like peptide-2; epidermal growth factor; intestinal adaptation

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

APA (6^th Edition):

Lim, D. W. (2016). Trophic peptide therapies for neonatal short bowel syndrome: actions and mechanisms studied in a preclinical model. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/c4x51hj32q

Chicago Manual of Style (16^th Edition):

Lim, David W. “Trophic peptide therapies for neonatal short bowel syndrome: actions and mechanisms studied in a preclinical model.” 2016. Doctoral Dissertation, University of Alberta. Accessed February 25, 2021. https://era.library.ualberta.ca/files/c4x51hj32q.

MLA Handbook (7^th Edition):

Lim, David W. “Trophic peptide therapies for neonatal short bowel syndrome: actions and mechanisms studied in a preclinical model.” 2016. Web. 25 Feb 2021.

Vancouver:

Lim DW. Trophic peptide therapies for neonatal short bowel syndrome: actions and mechanisms studied in a preclinical model. [Internet] [Doctoral dissertation]. University of Alberta; 2016. [cited 2021 Feb 25]. Available from: https://era.library.ualberta.ca/files/c4x51hj32q.

Council of Science Editors:

Lim DW. Trophic peptide therapies for neonatal short bowel syndrome: actions and mechanisms studied in a preclinical model. [Doctoral Dissertation]. University of Alberta; 2016. Available from: https://era.library.ualberta.ca/files/c4x51hj32q

University of Texas Southwestern Medical Center

13. Huynh, Hoang Dinh. Insulin-Like Growth Factor-Binding Protein 2 Supports Hematopoietic Stem Cell Expansion: From In Vitro to In Vivo.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/882

► Successful hematopoietic stem cell (HSC) transplantation is often limited by the numbers of HSCs, and robust methods to expand HSCs ex vivo are needed. We… (more)

▼ Successful hematopoietic stem cell (HSC) transplantation is often limited by the numbers of HSCs, and robust methods to expand HSCs ex vivo are needed. We previously showed that angiopoietin-like proteins (Angptls), a group of growth factors isolated from a fetal liver HSC supportive cell population, improved ex vivo expansion of HSCs. Here we demonstrate that insulin-like growth factor binding protein 2 (IGFBP2), secreted by a tumorigenic cell line, also enhanced ex vivo expansion of mouse HSCs. As measured by competitive repopulation analyses, there was a 48-fold increase in numbers of long-term repopulating mouse HSCs after 21 days of culture. This is the first demonstration that IGFBP2 stimulates expansion or proliferation of murine stem cells. Our finding also suggests that certain cancer cells synthesize proteins that can stimulate HSC expansion. To further study the function of IGFBP2 in vivo, we showed that IGFBP2-null mice have fewer HSCs than wild-type mice. While IGFBP2 has little cell-autonomous effect on HSC function, we found decreased in vivo repopulation of HSCs in primary and secondary transplanted IGFBP2-null recipients. Importantly, bone marrow stromal cells that are deficient for IGFBP2 have significantly decreased ability to support the expansion of repopulating HSCs. To investigate the mechanism by which IGFBP2 supports HSC activity, we demonstrated that HSCs in IGFBP2-null mice had decreased survival and cycling, downregulated expression of anti-apoptotic factor Bcl-2, and upregulated expression of cell cycle inhibitors p21, p16, p19, p57, and PTEN. Moreover, we found that the C-terminus, but not the RGD domain, of extrinsic IGFBP2 was essential for support of HSC activity. Defective signaling of the IGF type I receptor did not rescue the decreased repopulation of HSCs in IGFBP2-null recipients, suggesting that the environmental effect of IGFBP2 on HSCs is independent of IGF-IR mediated signaling. Therefore, as an environmental factor, IGFBP2 supports the survival and cycling of HSCs. Advisors/Committee Members: Zhang, Chengcheng "Alec".

Subjects/Keywords: Hematopoietic Stem Cell Transplantation; Insulin-Like Growth Factor Binding Protein 2; Cell Division

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

APA (6^th Edition):

Huynh, H. D. (2011). Insulin-Like Growth Factor-Binding Protein 2 Supports Hematopoietic Stem Cell Expansion: From In Vitro to In Vivo. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/882

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

Chicago Manual of Style (16^th Edition):

Huynh, Hoang Dinh. “Insulin-Like Growth Factor-Binding Protein 2 Supports Hematopoietic Stem Cell Expansion: From In Vitro to In Vivo.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed February 25, 2021. http://hdl.handle.net/2152.5/882.

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

MLA Handbook (7^th Edition):

Huynh, Hoang Dinh. “Insulin-Like Growth Factor-Binding Protein 2 Supports Hematopoietic Stem Cell Expansion: From In Vitro to In Vivo.” 2011. Web. 25 Feb 2021.

Vancouver:

Huynh HD. Insulin-Like Growth Factor-Binding Protein 2 Supports Hematopoietic Stem Cell Expansion: From In Vitro to In Vivo. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/2152.5/882.

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

Council of Science Editors:

Huynh HD. Insulin-Like Growth Factor-Binding Protein 2 Supports Hematopoietic Stem Cell Expansion: From In Vitro to In Vivo. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/882

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

University of Miami

14. Grieco, Steven F. Antidepressant and Molecular Responses to Ketamine Linked to its Inhibition of Glycogen Synthase Kinase-3 (GSK3).

Degree: PhD, Biochemistry and Molecular Biology (Medicine), 2016, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/1737

► Herein are described two novel outcomes, the up-regulation of 5HTR2C cluster miRNAs and IGF2, as a result of GSK3 inhibition by an antidepressant dose… (more)

Subjects/Keywords: Depression; Glycogen Synthase Kinase-3; Ketamine; Hippocampus, microRNA; Insulin-Like Growth Factor 2

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

APA (6^th Edition):

Grieco, S. F. (2016). Antidepressant and Molecular Responses to Ketamine Linked to its Inhibition of Glycogen Synthase Kinase-3 (GSK3). (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1737

Chicago Manual of Style (16^th Edition):

Grieco, Steven F. “Antidepressant and Molecular Responses to Ketamine Linked to its Inhibition of Glycogen Synthase Kinase-3 (GSK3).” 2016. Doctoral Dissertation, University of Miami. Accessed February 25, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/1737.

MLA Handbook (7^th Edition):

Grieco, Steven F. “Antidepressant and Molecular Responses to Ketamine Linked to its Inhibition of Glycogen Synthase Kinase-3 (GSK3).” 2016. Web. 25 Feb 2021.

Vancouver:

Grieco SF. Antidepressant and Molecular Responses to Ketamine Linked to its Inhibition of Glycogen Synthase Kinase-3 (GSK3). [Internet] [Doctoral dissertation]. University of Miami; 2016. [cited 2021 Feb 25]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1737.

Council of Science Editors:

Grieco SF. Antidepressant and Molecular Responses to Ketamine Linked to its Inhibition of Glycogen Synthase Kinase-3 (GSK3). [Doctoral Dissertation]. University of Miami; 2016. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1737

Boston University

15. Thomas, Dolly. The role of IGF2 in the regulation of hematopoietic stem cell function.

Degree: PhD, Cell & Molecular Biology, 2014, Boston University

URL: http://hdl.handle.net/2144/15084

► Maintenance of the hematopoietic system is dependent upon the proper regulation and orchestrated functions of the hematopoietic stem cell (HSC) pool. A number of extrinsic… (more)

▼ Maintenance of the hematopoietic system is dependent upon the proper regulation and orchestrated functions of the hematopoietic stem cell (HSC) pool. A number of extrinsic signaling pathways and intrinsic regulators have been found to regulate HSC processes. However a full understanding of the ability of HSC to balance the processes of self-renewal, quiescence, and lineage specification is not yet clear. We therefore set out to identify novel HSC regulators by comparative gene expression analysis of whole genome transcriptomes generated for long-term (LT)-HSC (Hoechst low/- Lin- Sca1+ cKit+ CD34-), short-term (ST)-HSC (Hoechst low/- Lin- Sca1+ cKit+ CD34+), and non-HSC (Hoechst+) of the bone marrow. These studies identified IGF2 as one of the most differentially expressed genes within LT-HSC, suggesting a potential role for IGF2 in the regulation of HSC. Using a combination of lentiviral-mediated overexpression and knockdown experiments, we found IGF2 to confer enhanced self-renewal in vitro and in vivo. Overexpression of IGF2 resulted in an increased percentage of multi-lineage colonies within colony-forming unit (CFU) assays without affecting lineage specification. In vivo, serial bone marrow transplantation revealed that IGF2 within HSC enhances short-term and long-term donor contribution. Analysis of the expression of key cell cycle regulators revealed that IGF2 induced upregulation of p57 expression specifically within HSC. This upregulation could be attributed to differences in the methylation status of the p57 promoter in HSC compared to other progenitor and mature blood cell populations. p57, a member of the Cip/Kip family of cyclin dependent kinase inhibitors, has recently been shown to be required for the regulation of HSC quiescence and long-term self-renewal. Analysis of bone marrow obtained from primary and secondary transplant recipients showed that overexpression of IGF2 resulted in an increased percentage of quiescent HSC. Treatment of HSC overexpressing IGF2 with LY294002, a PI3K-Akt inhibitor, prevented IGF2-mediated upregulation of p57 expression. These findings demonstrate that within HSC, IGF2 induces p57 expression through activation of the PI3K-Akt pathway to regulate HSC quiescence. We have identified a novel role for IGF2 in HSC function, providing new insights into the biology of HSC and opening potential platforms for the development of better therapies involving HSC-mediated hematopoietic reconstitution.

Subjects/Keywords: Medicine; Hematopoiesis; Hematopoietic stem cells; Insulin-like growth factor 2; p57; Self-renewal; Stem cells

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

APA (6^th Edition):

Thomas, D. (2014). The role of IGF2 in the regulation of hematopoietic stem cell function. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/15084

Chicago Manual of Style (16^th Edition):

Thomas, Dolly. “The role of IGF2 in the regulation of hematopoietic stem cell function.” 2014. Doctoral Dissertation, Boston University. Accessed February 25, 2021. http://hdl.handle.net/2144/15084.

MLA Handbook (7^th Edition):

Thomas, Dolly. “The role of IGF2 in the regulation of hematopoietic stem cell function.” 2014. Web. 25 Feb 2021.

Vancouver:

Thomas D. The role of IGF2 in the regulation of hematopoietic stem cell function. [Internet] [Doctoral dissertation]. Boston University; 2014. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/2144/15084.

Council of Science Editors:

Thomas D. The role of IGF2 in the regulation of hematopoietic stem cell function. [Doctoral Dissertation]. Boston University; 2014. Available from: http://hdl.handle.net/2144/15084

16. Abdalrahman, Akrm. Isolation of Natural Nrf2 Activators from American Ginseng.

Degree: MS, Biomedical Engineering, 2014, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/2662

► Nuclear factor erythroid-2 related factor 2 (Nrf2), a major transcription factor of the endogenous antioxidant defense system, has been proposed as a potential therapeutic… (more)

▼ Nuclear factor erythroid-2 related factor 2 (Nrf2), a major transcription factor of the endogenous antioxidant defense system, has been proposed as a potential therapeutic target for the treatment of various diseases. However, a small molecule-driven Nrf2 signaling therapeutic approach remains to be established. Herein, we report one such possibility discovered by the bioassay-based fractionation of American ginseng. Since crude extract of American ginseng was found to suppress the expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-inflamed macrophages via activating Nrf2, we further fractioned the crude extract using solvents including hexane, dichloromethane, ethyl acetate, butanol, and water, and found that the hexane fraction was the most effective fraction in activating Nrf2-mediated suppression of iNOS expression in macrophages. By utilizing preparative, reverse-phase HPLC and a comparative analysis by analytical scale LC-UV, we found that hexane fraction contains predominantly polyacetylenes and linolenic acid, and we identified panaxynol as the major compound in polyacetylenes. We report a unique and Nrf2-dependent anti-inflammatory profile of panaxynol in inflamed macrophages. In lipopolysaccharide (LPS)-inflamed RAW264.7 macrophages, panaxynol dramatically suppressed the expression of pro-inflammatory cytokines including inducible nitric oxide synthase (iNOS) and monocyte chemotactic protein-1 (MCP-1), but it has no effects on regulate expression of interleulin-6 (IL-6), interleulin-1B (IL-1B), and tumor necrosis factor alpha (TNF-a), this results suggested activation of specific pathway; that is Panaxynol potently activated Nrf2 signaling; but, it did not affect NF-kB activity in LPS inflamed macrophages. Moreover, knockout of Nrf2 blocked the panaxynol induced anti-inflammatory responses in LPS-inflamed macrophages. These results demonstrated that panaxynol suppresses pro-inflammatory responses in macrophages via an activation of Nrf2 independently of NF-kB, suggesting a potential mechanism responsible for the American ginseng-mediated health benefits and a unique therapeutic potential of panaxynol for specific targeting Nrf2-mediated resolution of inflammation. Advisors/Committee Members: Taixing Cui.

Subjects/Keywords: Biomedical Engineering and Bioengineering; Engineering; Natural; Nrf2 Activators; American Ginseng; Nuclear factor erythroid-2

…6 1.4 Nuclear factor erythroid-2 related factors pathway… …not fully understood. Nuclear factor erythroid-2 related factors (NF-E2-related factors… …Osthoff et al., 1997). 1.4. Nuclear factor erythroid-2 related factors (NF-E2-related… …7 1.5. Nuclear factor kappa B (NF-κB) pathway… …released from Keap1 or just partially dissociated (Zhang, 2006). 1.5. Nuclear factor…

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APA (6^th Edition):

Abdalrahman, A. (2014). Isolation of Natural Nrf2 Activators from American Ginseng. (Masters Thesis). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/2662

Chicago Manual of Style (16^th Edition):

Abdalrahman, Akrm. “Isolation of Natural Nrf2 Activators from American Ginseng.” 2014. Masters Thesis, University of South Carolina. Accessed February 25, 2021. https://scholarcommons.sc.edu/etd/2662.

MLA Handbook (7^th Edition):

Abdalrahman, Akrm. “Isolation of Natural Nrf2 Activators from American Ginseng.” 2014. Web. 25 Feb 2021.

Vancouver:

Abdalrahman A. Isolation of Natural Nrf2 Activators from American Ginseng. [Internet] [Masters thesis]. University of South Carolina; 2014. [cited 2021 Feb 25]. Available from: https://scholarcommons.sc.edu/etd/2662.

Council of Science Editors:

Abdalrahman A. Isolation of Natural Nrf2 Activators from American Ginseng. [Masters Thesis]. University of South Carolina; 2014. Available from: https://scholarcommons.sc.edu/etd/2662

University of Southern California

17. 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

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/84016/rec/598

► 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 (6^th 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 (16^th 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 February 25, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/84016/rec/598.

MLA Handbook (7^th Edition):

Ravichandran, Monisha. “Alcohol mediated expression of cyto-protective enzyme - NQO-1 and its post translational regulation.” 2012. Web. 25 Feb 2021.

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 2021 Feb 25]. 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

18. Kroscher, Kellie Ann. Creation and characterization of mice with a mutation disrupting binding of a transcriptional repressor of insulin-like growth factor 2.

Degree: MS, Animal Sciences, 2017, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/98425

► Insulin-like growth factor-2 (IGF2) is a key regulator of myogenesis as it promotes differentiation of myoblasts during embryonic and fetal development. A single nucleotide polymorphism… (more)

▼ Insulin-like growth factor-2 (IGF2) is a key regulator of myogenesis as it promotes differentiation of myoblasts during embryonic and fetal development. A single nucleotide polymorphism (SNP) identified in pigs in intron 3 of IGF2 disrupts a binding site for the transcriptional repressor ZBED6 leading to increased expression of IGF2. The SNP prevents binding of ZBED6 increasing IGF2 expression prenatally as well as postnatally compared with their wild type counterparts. Pigs with this mutation have a 10 % increase in muscle mass and a 15% decrease in subcutaneous fat deposition despite similar body weights. Though IGF2 is a highly conserved gene across species, similar mutations in IGF2 have not been detected. Therefore, the effect of mutations preventing the binding of ZBED6 to IGF2 in species other than pigs remains unknown. In order to characterize how a mutation in the ZBED6 binding site of IGF2 impacts growth, a mouse model was created using transcription activator-like effector nucleases (TALEN) with co-injection of oligo donors. Two founders were generated containing mutations that disrupted the ZBED6 binding site. One founder mouse contained the targeted G>A point mutation that mimicked the mutation in pigs, and the other founder had an A>G point mutation from the designed oligo donor on one allele and a G>A point mutation at the target site (A>G/G>A), with the other allele containing a C insertion in the target site (C+). All of these mutations inhibited the binding of ZBED6. Founders were bred to wild type (WT) females. The offspring produced contained either the C-insertion or A>G/G>A mutations and were bred to WT females to create two different mutant lines. Offspring lean and fat mass were evaluated through ECHO MRI at 21, 35, 49, 63, and 77 days of age. Offspring were euthanized at 21, 49, or 77 days of age and muscle, organ, and fat depot weights were collected. As expected, body weight, fat, and lean mass increased with increasing age (P<0.01). Mice with a mutation disrupting ZBED6 binding sites were 10.09-12.73 % heavier than their WT counterparts at 49d, 63d and 77d. Additionally, lean mass at 77d of age and fat mass at 45d and after were increased (P≤0.05) in mutated mice compared with WT mice as determined by ECHO MRI. However, as a percentage of body weight, lean and fat mass did not differ between genotypes (P≥0.12). The tibialis anterior was increased (P=0.03) by 20% in mutated mice compared with WT mice at 77d, but there were no differences in muscle fiber size and fiber cross sectional area (P≥0.64). Liver expression of IGF2 decreased with increasing age in all genotypes (P=0.02), and IGF2 expression was increased by 12-32 fold in mutated mice compared with their WT counterparts (P≤0.01). In contrast, protein quantification of IGF2 in serum of 77d mice did not differ between genotypes (P=0.16). We had hypothesized that mice with mutations disrupting the ZBED6 binding site in IGF2 would have increased muscle mass and reduced fat deposition at the same body weight, similar to the phenotype of… Advisors/Committee Members: Dilger, Anna C (advisor).

Subjects/Keywords: Insulin-like growth factor-2 (IGF2); Mice; Transcription activator-like effector nucleases (TALEN); Single nucleotide polymorphism (SNP)

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APA (6^th Edition):

Kroscher, K. A. (2017). Creation and characterization of mice with a mutation disrupting binding of a transcriptional repressor of insulin-like growth factor 2. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/98425

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

Chicago Manual of Style (16^th Edition):

Kroscher, Kellie Ann. “Creation and characterization of mice with a mutation disrupting binding of a transcriptional repressor of insulin-like growth factor 2.” 2017. Thesis, University of Illinois – Urbana-Champaign. Accessed February 25, 2021. http://hdl.handle.net/2142/98425.

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

MLA Handbook (7^th Edition):

Kroscher, Kellie Ann. “Creation and characterization of mice with a mutation disrupting binding of a transcriptional repressor of insulin-like growth factor 2.” 2017. Web. 25 Feb 2021.

Vancouver:

Kroscher KA. Creation and characterization of mice with a mutation disrupting binding of a transcriptional repressor of insulin-like growth factor 2. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2017. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/2142/98425.

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

Council of Science Editors:

Kroscher KA. Creation and characterization of mice with a mutation disrupting binding of a transcriptional repressor of insulin-like growth factor 2. [Thesis]. University of Illinois – Urbana-Champaign; 2017. Available from: http://hdl.handle.net/2142/98425

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

Duke University

19. Gilroy, Caslin Anne. Controlled Release Systems for Treating Type 2 Diabetes and Their Application Toward Multi-Agonist Combination Therapies .

Degree: 2019, Duke University

URL: http://hdl.handle.net/10161/19873

► Over 30 million people in the United States suffer from type 2 diabetes (T2D), and this figure is rapidly increasing. Currently available glucose-lowering drugs… (more)

▼ Over 30 million people in the United States suffer from type 2 diabetes (T2D), and this figure is rapidly increasing. Currently available glucose-lowering drugs largely treat the symptoms of diabetes and not the underlying pathology, leaving one third of diabetes patients with improperly managed disease. Thus, there exists an urgent need for novel drugs that slow T2D progression while posing a minimal burden on the patient. The metabolic regulatory factor fibroblast growth factor 21 (FGF21) is under investigation as a T2D therapeutic due to its favorable effects on glycemic control and body weight. However, the feasibility of native FGF21 as a drug candidate is impeded by its rapid in vivo clearance and by costly production methods associated with poor protein solubility. To address these issues, FGF21 was recombinantly expressed in E. coli as a fusion with an elastin-like polypeptide (ELP), a repetitive peptide polymer with reversible thermal phase behavior. Below their transition temperature (Tt), ELPs exist as soluble unimers, while above their Tt, they aggregate into an insoluble coacervate. The thermal responsiveness of the ELP was retained when genetically fused to FGF21, with several notably positive impacts for the synthesis and efficacy of this protein drug. First, the ELP fusion partner acted as a solubility enhancer, yielding 50 mg/L of active FGF21 protein from the soluble cell lysate fraction in shaker flask culture, and eliminating the need for protein refolding. Second, the phase transition behavior of the ELP was exploited for chromatography-free FGF21 purification. Third, the Tt of the ELP was tuned to below body temperature, such that the phase transition was initiated solely by body heat. Indeed, in vivo injection of the fusion resulted in an immiscible viscous phase in the subcutaneous (s.c.) space that dissolved at a steady rate, temporally releasing fusion unimers into circulation. The injectable FGF21 drug depot was tested in diabetic ob/ob mice, and conferred dose-dependent glucose-and weight-lowering effects that were sustained out to 5 days following a single s.c. injection. Once an optimized ELP-based FGF21 delivery strategy was established, the fusion concept was applied to a combination therapy to afford even greater metabolic benefits, while providing controlled release properties exclusive to the ELP platform. Recent evidence supports the development of combination drug treatments that incorporate complementary mechanisms of action to more effectively treat T2D. Thus, we developed a unimolecular dual agonist by combining the incretin glucagon-like peptide-1 (GLP1) with FGF21, hypothesizing that this agent would merge the insulinotropic and anorectic effects of GLP1 with the enhanced insulin sensitivity and energy expenditure associated with FGF21 signaling. The dual agonist was designed as a single polypeptide fusion, with GLP1 located at the N terminus and FGF21 at the C terminus. This orientation allowed each peptide to activate its endogenous receptor, while the… Advisors/Committee Members: Chilkoti, Ashutosh (advisor).

Subjects/Keywords: Biomedical engineering; Endocrinology; Controlled release; Drug delivery; Elastin-like polypeptides; Fibroblast growth factor 21; Glucagon-like peptide-1; Type 2 diabetes

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APA (6^th Edition):

Gilroy, C. A. (2019). Controlled Release Systems for Treating Type 2 Diabetes and Their Application Toward Multi-Agonist Combination Therapies . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/19873

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

Chicago Manual of Style (16^th Edition):

Gilroy, Caslin Anne. “Controlled Release Systems for Treating Type 2 Diabetes and Their Application Toward Multi-Agonist Combination Therapies .” 2019. Thesis, Duke University. Accessed February 25, 2021. http://hdl.handle.net/10161/19873.

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

MLA Handbook (7^th Edition):

Gilroy, Caslin Anne. “Controlled Release Systems for Treating Type 2 Diabetes and Their Application Toward Multi-Agonist Combination Therapies .” 2019. Web. 25 Feb 2021.

Vancouver:

Gilroy CA. Controlled Release Systems for Treating Type 2 Diabetes and Their Application Toward Multi-Agonist Combination Therapies . [Internet] [Thesis]. Duke University; 2019. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10161/19873.

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

Council of Science Editors:

Gilroy CA. Controlled Release Systems for Treating Type 2 Diabetes and Their Application Toward Multi-Agonist Combination Therapies . [Thesis]. Duke University; 2019. Available from: http://hdl.handle.net/10161/19873

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

University of Melbourne

20. Chao, Mindy Hsiang-Ning. Dissecting the FGF-2 and IGF-I crosstalk in neuronal differentiation of Ewing Sarcoma Family of Tumours (ESFT).

Degree: 2016, University of Melbourne

URL: http://hdl.handle.net/11343/191280

► Ewing sarcoma family of tumours (ESFTs) are poorly differentiated tumours which exhibit evidence of limited neuronal differentiation. Although the cell-of-origin of ESFT remains unclear, prevailing… (more)

Subjects/Keywords: fibroblast growth factor 2; insulin-like growth factor I; Ewing Sarcoma Family of Tumours; p21WAF1/Cip1, EWS/FLI-1, neuronal differentiation

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APA (6^th Edition):

Chao, M. H. (2016). Dissecting the FGF-2 and IGF-I crosstalk in neuronal differentiation of Ewing Sarcoma Family of Tumours (ESFT). (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/191280

Chicago Manual of Style (16^th Edition):

Chao, Mindy Hsiang-Ning. “Dissecting the FGF-2 and IGF-I crosstalk in neuronal differentiation of Ewing Sarcoma Family of Tumours (ESFT).” 2016. Doctoral Dissertation, University of Melbourne. Accessed February 25, 2021. http://hdl.handle.net/11343/191280.

MLA Handbook (7^th Edition):

Chao, Mindy Hsiang-Ning. “Dissecting the FGF-2 and IGF-I crosstalk in neuronal differentiation of Ewing Sarcoma Family of Tumours (ESFT).” 2016. Web. 25 Feb 2021.

Vancouver:

Chao MH. Dissecting the FGF-2 and IGF-I crosstalk in neuronal differentiation of Ewing Sarcoma Family of Tumours (ESFT). [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/11343/191280.

Council of Science Editors:

Chao MH. Dissecting the FGF-2 and IGF-I crosstalk in neuronal differentiation of Ewing Sarcoma Family of Tumours (ESFT). [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/191280

University of Alberta

21. Baghirova, Sabina. Nuclear matrix metalloproteinase-2 and investigation of its potential targets in myocardial ischemia-reperfusion injury.

Degree: MS, Department of Pharmacology, 2016, University of Alberta

URL: https://era.library.ualberta.ca/files/c7s75dc42x

► Matrix metalloproteinases (MMPs) are zinc-dependent proteases involved in intra- and extra-cellular matrix remodeling. MMP-2 was the first to be localized to the nucleus; however the… (more)

▼ Matrix metalloproteinases (MMPs) are zinc-dependent proteases involved in intra- and extra-cellular matrix remodeling. MMP-2 was the first to be localized to the nucleus; however the biological functions and substrates of nuclear MMP-2 are mostly unknown. We hypothesized that MMP‐2 is present in the nucleus under normal physiological conditions but increases during myocardial ischemia‐reperfusion (I/R) injury induced oxidative stress, proteolyzing nuclear structural proteins (lamins). Lamin A/C, a putative nuclear MMP‐2 target, is an intermediate filament protein that provides structural support to the nucleus. Immunofluorescent confocal microscopy and subcellular fractionation showed the presence of MMP-2 in cytoplasm and nuclei of neonatal rat ventricular myocytes. The distribution of MMP-2 in cytoplasm and nuclei was verified by immunofluorescent confocal microscopy in the human fibrosarcoma HT 1080 cells. Further analysis by flow cytometry determined that 88.6% of a sample of ~10,000 HT 1080 cells had MMP-2 concentrated to the nucleus. Rat hearts were isolated and perfused by the Langendorff method aerobically, or subjected to global, no-flow ischemia followed by aerobic reperfusion in the presence or absence of an MMP inhibitor (100 µM o-phenanthroline). Nuclear fractions extracted from the rat hearts showed increased MMP-2 activity, but not protein level in hearts subjected to I/R injury. To identify possible targets, an in vitro proteolysis assay was performed with lamin A or B incubated with MMP-2. Lamin A, but not lamin B, was proteolysed by MMP-2 in to a putative 50 kDa fragment, which was also predicted by in silico cleavage site analysis. Protein levels of troponin I, a known sarcomeric target of MMP-2 showed a trend for decrease in I/R hearts and was normalized by o-phenanthroline, demonstrating efficacy of the MMP inhibitor. However, lamin A and lamin C protein levels remained unchanged in I/R hearts. PARP-1, a nuclear DNA repair protein, previously shown to be proteolysed by MMP-2 in vitro was measured in I/R hearts. It was observed that PARP-1 protein levels were decreased in I/R hearts treated with o-phenanthroline compared to I/R hearts without o-phenanthroline. Nuclear MMP-2 is present in cardiomyocytes under normal physiological conditions, and is increased as a result of I/R injury. This increase of MMP-2 activity in extracts from I/R hearts leads to proteolysis of troponin I, but not, PARP-1, lamin A or C. The activation of genes in myocardial I/R injury suggests that other nuclear functions of MMP-2 are likely.

Subjects/Keywords: Nuclear MMP-2; Nuclear matrix metalloproteinase-2; myocardial ischemia-reperfusion injury

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

APA (6^th Edition):

Baghirova, S. (2016). Nuclear matrix metalloproteinase-2 and investigation of its potential targets in myocardial ischemia-reperfusion injury. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/c7s75dc42x

Chicago Manual of Style (16^th Edition):

Baghirova, Sabina. “Nuclear matrix metalloproteinase-2 and investigation of its potential targets in myocardial ischemia-reperfusion injury.” 2016. Masters Thesis, University of Alberta. Accessed February 25, 2021. https://era.library.ualberta.ca/files/c7s75dc42x.

MLA Handbook (7^th Edition):

Baghirova, Sabina. “Nuclear matrix metalloproteinase-2 and investigation of its potential targets in myocardial ischemia-reperfusion injury.” 2016. Web. 25 Feb 2021.

Vancouver:

Baghirova S. Nuclear matrix metalloproteinase-2 and investigation of its potential targets in myocardial ischemia-reperfusion injury. [Internet] [Masters thesis]. University of Alberta; 2016. [cited 2021 Feb 25]. Available from: https://era.library.ualberta.ca/files/c7s75dc42x.

Council of Science Editors:

Baghirova S. Nuclear matrix metalloproteinase-2 and investigation of its potential targets in myocardial ischemia-reperfusion injury. [Masters Thesis]. University of Alberta; 2016. Available from: https://era.library.ualberta.ca/files/c7s75dc42x

University of Toronto

22. Trivedi, Shivangi. Role of Glucagon-like Peptide-2 in Rodent Models of Colon Cancer.

Degree: 2011, University of Toronto

URL: http://hdl.handle.net/1807/31613

►

Glucagon-like peptide-2 (GLP-2) is an intestinotrophic and intestinal anti-inflammatory hormone. Hence, I hypothesized that treatment with degradation-resistant hGly2GLP-2 increases, while blocking endogenous GLP-2 decreases colorectal… (more)

Subjects/Keywords: Glucagon-like peptide-2; Colon cancer; 0719

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

APA (6^th Edition):

Trivedi, S. (2011). Role of Glucagon-like Peptide-2 in Rodent Models of Colon Cancer. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/31613

Chicago Manual of Style (16^th Edition):

Trivedi, Shivangi. “Role of Glucagon-like Peptide-2 in Rodent Models of Colon Cancer.” 2011. Masters Thesis, University of Toronto. Accessed February 25, 2021. http://hdl.handle.net/1807/31613.

MLA Handbook (7^th Edition):

Trivedi, Shivangi. “Role of Glucagon-like Peptide-2 in Rodent Models of Colon Cancer.” 2011. Web. 25 Feb 2021.

Vancouver:

Trivedi S. Role of Glucagon-like Peptide-2 in Rodent Models of Colon Cancer. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/1807/31613.

Council of Science Editors:

Trivedi S. Role of Glucagon-like Peptide-2 in Rodent Models of Colon Cancer. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/31613

23. Kotsantis, Ioannis. Διερεύνηση του μοριακού μονοπατιού και της κλινικής συσχέτισης του αυξητικού παράγοντα της ινσουλίνης τύπου Ι σε ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα.

Degree: 2019, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/46637

►

Insulin-like growth factor 1(IGF-1) signaling pathway has been suggested as an important oncogenic mediator in various malignancies, including lung cancer. In this study, we aimed… (more)

▼

Insulin-like growth factor 1(IGF-1) signaling pathway has been suggested as an important oncogenic mediator in various malignancies, including lung cancer. In this study, we aimed to evaluate serum levels of IGF-1, IGF-2 and IGF Binding Protein 3 (IGF-BP3) before and after chemotherapy or chemoradiotherapy treatment in patients with locally advanced/metastatic non-small cell lung cancer (NSCLC) and their potential correlation with response to therapy and patient survival. Methods: Seventy-three patients with stage III/IV NSCLC were included in the study. Expression of IGF1, IGF2, and IGFBP3 was evaluated in peripheral blood samples in two separate time points, at baseline and 3 months post treatment. Analysis and quantification of circulating levels of IGF-1, IGF-2, IGF-BP3 were performed by total ELISA technique. IGF-1/IGF-BP3 ratio is considered an indicator of IGF-1bioavailability. Results: In univariate analysis, the median value of IGF-1 after treatment (130.80 vs 98.00 ng/ml, p=0.087), and the median ratio of IGF-1/IGF-BP3 (0.01044 vs 0.00678,p=0.056) were higher in responders. Further analysis of the variation of each biomarker before and after treatment showed that the median value of IGF-1 was decreased after treatment in the total population (125.82 from 133.4 ng/ml, p=0.087), albeit no difference was found between subgroups. In addition, the median value of IGF-1/IGF-BP3 ratio was found to be lower after treatment in the total population (0.01006 from 0.01252, p=0.011). Importantly, the post-treatment value of the ratio was significantly reduced in responders (0.01044 from 0.01255, p=0.02). No correlation was found between variation in biomarker values, patient OS and PFS. Conclusions: In a cohort of patients with stage III/IV NSCLC treated with chemotherapy or chemoradiotherapy, reduction of IGF-1/IGF-BP3 ratio, which is anindicator of IGF-1 bioavailability, was statistically significant in patients that responded to treatment. If validated in larger cohorts, our results support the use ofIGF-1/IGFBP3 as a predictive tool for response to chemotherapy in NSCLC.

Ο Insulin-like growth factor–1 (IGF-1) έχει προταθεί ως σημαντικό σηματοδοτικό μονοπάτι παθογένεσης διαφόρων κακοηθειών, συμπεριλαμβανομένου του καρκίνου του πνεύμονα. Μέθοδοι: Εβδομήντα τρεις ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα (ΜΜΚΠ) συμπεριλήφθηκαν στη μελέτη. Η έκφραση των IGF1, IGF2, και IGFBP3 αξιολογήθηκε σε δείγματα περιφερικού αίματος, πριν την έναρξη οποιασδήποτε θεραπείας και 3 μήνες μετά. Η ανάλυση και η ποσοτικοποίηση των κυκλοφορούντων επιπέδων των IGF-1,IGF-2,και IGF-BP3 έγιναν με τεχνική ELISA. Σκοπός: Σκοπός της παρούσας μελέτης ήταν η αξιολόγηση των επιπέδων των παραγόντων IGF-1, IGF-2 και IGF-BP3 στον ορό πριν και μετά τη χορήγηση θεραπείας ασθενών με τοπικά προχωρημένο/μεταστατικό ΜΜΚΠ και η συσχέτισή τους με την ανταπόκριση στη θεραπεία και την επιβίωση. Αποτελέσματα: Στη μονοπαραγοντική ανάλυση, η διάμεση τιμή του IGF-1 μετά τη θεραπεία (130.80 έναντι 98.00 ng/ml, p=0.087) και ο διάμεσος λόγος…

Subjects/Keywords: Αυξητικός παράγοντας ινσουλίνης τύπου ένα (1); Αυξητικός παράγοντας ινσουλίνης τύπου δύο (2); Μη μικροκυτταρικός καρκίνος πνεύμονα; Χημειοθεραπεία; Insulin-like growth factor 1(IGF-1); Insulin-like growth factor 2 (IGF-2); NSCLC; Chemotherapy

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APA (6^th Edition):

Kotsantis, I. (2019). Διερεύνηση του μοριακού μονοπατιού και της κλινικής συσχέτισης του αυξητικού παράγοντα της ινσουλίνης τύπου Ι σε ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/46637

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

Chicago Manual of Style (16^th Edition):

Kotsantis, Ioannis. “Διερεύνηση του μοριακού μονοπατιού και της κλινικής συσχέτισης του αυξητικού παράγοντα της ινσουλίνης τύπου Ι σε ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα.” 2019. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed February 25, 2021. http://hdl.handle.net/10442/hedi/46637.

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

MLA Handbook (7^th Edition):

Kotsantis, Ioannis. “Διερεύνηση του μοριακού μονοπατιού και της κλινικής συσχέτισης του αυξητικού παράγοντα της ινσουλίνης τύπου Ι σε ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα.” 2019. Web. 25 Feb 2021.

Vancouver:

Kotsantis I. Διερεύνηση του μοριακού μονοπατιού και της κλινικής συσχέτισης του αυξητικού παράγοντα της ινσουλίνης τύπου Ι σε ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10442/hedi/46637.

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

Council of Science Editors:

Kotsantis I. Διερεύνηση του μοριακού μονοπατιού και της κλινικής συσχέτισης του αυξητικού παράγοντα της ινσουλίνης τύπου Ι σε ασθενείς με προχωρημένο μη μικροκυτταρικό καρκίνο πνεύμονα. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. Available from: http://hdl.handle.net/10442/hedi/46637

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

University of Melbourne

24. Rodda, Felicity Ann. Investigation of the genetic mechanisms regulating embryonic skeletal development.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/38277

► Endochondral ossification is the process by which the majority of the bones of the body are formed. It occurs via the differentiation of mesenchymal cells… (more)

▼ Endochondral ossification is the process by which the majority of the bones of the body are formed. It occurs via the differentiation of mesenchymal cells into chondrocytes to produce a cartilage template of the skeleton (chondrogenesis), followed by replacement of cartilage with bone (osteogenesis). This complex process is not completely understood, particularly given the large number of genes of unknown function differentially regulated during chondrogenesis (Cameron, Belluoccio et al. 2009). This project investigated several of these genes, demonstrating the utility of the avian retroviral system for testing the function of candidate skeletal regulator genes in vivo. Kruppel-like factor 2 (Klf2) is a zinc finger transcription factor upregulated 30-fold during chondrogenesis. With known roles in regulating development of the lungs, blood vessels, T-cells and adipocytes, it had not previously been linked to skeletal development. Presented here is the first demonstration of a skeletal regulatory activity for Klf2. Ubiquitous overexpression of Klf2 in chick embryos was able to transform digit identity, alter pelvic girdle morphology, and reduce the length of skeletal elements in the chick limb. Conversely, cartilage-specific Klf2 overexpression elongated skeletal elements, suggesting differential regulation of development by Klf2 when expressed in different tissues. Constitutive activation and repression variants of the gene were also used to explore Klf2 activity in vivo, and indicated that Klf2 functions as a repressor in skeletal development. None of the known patterning and skeletal regulator genes investigated were shown to be altered by Klf2 overexpression. Finally, the expression of two other Kruppel-like family members dynamically expressed during chondrogenesis were examined. Of particular interest, a complementary expression pattern was demonstrated for Klf2 and Klf7 in skeletal tissues, suggesting an importance for Klf7 in regulating skeletal development. A comprehensive understanding of individual gene function in skeletal development is important for understanding normal development, provides possible links to genetic diseases of bone development, and enhances our ability to treat skeletal disease and injury.

Subjects/Keywords: developmental biology; skeletal; endochondral ossification; patterning; chondrogenesis; osteogenesis; RCAS; avian; chick; retrovirus; transcription factor; Klf2; Kruppel-like factor 2; Kruppel-like factor two

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

APA (6^th Edition):

Rodda, F. A. (2012). Investigation of the genetic mechanisms regulating embryonic skeletal development. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38277

Chicago Manual of Style (16^th Edition):

Rodda, Felicity Ann. “Investigation of the genetic mechanisms regulating embryonic skeletal development.” 2012. Doctoral Dissertation, University of Melbourne. Accessed February 25, 2021. http://hdl.handle.net/11343/38277.

MLA Handbook (7^th Edition):

Rodda, Felicity Ann. “Investigation of the genetic mechanisms regulating embryonic skeletal development.” 2012. Web. 25 Feb 2021.

Vancouver:

Rodda FA. Investigation of the genetic mechanisms regulating embryonic skeletal development. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/11343/38277.

Council of Science Editors:

Rodda FA. Investigation of the genetic mechanisms regulating embryonic skeletal development. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/38277

25. Estil·les Altimiras, Elisabet. Efectes de la sobreexpressió d’IGF2 en la protecció i la regeneració de les cèl·lules beta pancreàtiques.

Degree: Departament de Ciències Clíniques, 2014, Universitat de Barcelona

URL: http://hdl.handle.net/10803/285812

► β-Cell mass reduction has a central role in the development of type 1 and type 2 diabetes, and in both conditions the loss of β-cells… (more)

▼ β-Cell mass reduction has a central role in the development of type 1 and type 2 diabetes, and in both conditions the loss of β-cells has been largely attributed to increased β-cell death. Furthermore several reports have highlighted the fundamental contribution of β-cell replication to the physiological maintenance of β-cell mass, and to β-cell mass regeneration in models with reduced β-cell mass. This may suggest that impaired β-cell replication could contribute to the reduction of β-cell mass in diabetes. Islet transplantation restores normoglycemia in type 1 diabetic patients. However, islet transplantation presents some important limitations. A basic restriction is the low organ availability and high requirement, which is exacerbated by the high islet mass that must be transplanted to achieve normoglycemia, probably due to the massive destruction of islets taking place in the initial days after transplantation due to increased beta-cell apoptosis, necrosi and impaired beta-cell replication. IL-1β is an important contributor to β-cell damage in type 1 diabetes, and recently it has also been related to the development of type 2 diabetes. IL-1beta also could contribute to the dramatic beta cell loss that takes place after islet transplantation IGF2 is a growth promoting peptide which is able to stimulate cell differentiation, proliferation and survival. Thus, IGF2 may play a dual beneficial role on β-cell mass, acting both as a mitogenic and as a survival factor for β-cells. We investigated in vitro and in vivo effects of the IGF2 overexpression on β-cell survival and regeneration. The aim of the in vitro study was to characterise the effect of IL-1β on β-cell replication, and the potential modulation by IGF2. Since the induction of β-cell proliferation by IGFs is dependent on ambient glucose concentration, low and high glucose concentrations were used to better define the effects of IL-1β and IGF2 on β-cell replication. The aim of the in vivo study was to determine the effect of IGF2 overexpression on β-cell mass in transplanted islets. In the in vitro study, control-uninfected and adenovirus encoding for IGF2 (Ad-IGF2)-infected rat islets were cultured at 5.5 or 22.2 mmol/l glucose with or without 1, 10, 30, and 50 U/ml of IL-1β. β-Cell replication was markedly reduced by 10 U/ml of IL-1β and was almost nullified with 30 or 50 U/ml of IL-1β. Higher concentrations of IL-1β were required to increase β-cell apoptosis. Although IGF2 overexpression had a strong mitogenic effect on β-cells, IGF2 could preserve β-cell proliferation only in islets cultured with 10 U/ml IL-1β, and had no effect with 30 and 50 U/ml of IL-1β. In contrast, IGF2 overexpression induced a clear protection against IL-1β-induced apoptosis, and higher concentrations of the cytokine were needed to increase β-cell apoptosis in Ad-IGF2-infected islets. These results indicate that β-cell replication is highly sensitive to the deleterious effects of the IL-1β as shown by the inhibition of replication by relatively low IL-1β concentrations, and… Advisors/Committee Members: [email protected] (authoremail), false (authoremailshow), Montanya Mias, Eduard (director), true (authorsendemail).

Subjects/Keywords: Malalties del pàncrees; Enfermedades del páncreas; Pancréas diseases; Diabetis; Diabetes; Illots de Langerhans; Islotes de Langerhans; Islands of Langerhans; Insulin-like growth factor 2 (IGF2); Factor de crecimiento insulínico tipo 2; Factor de creixement insulínic tipus 2; Ciències de la Salut; 616.4

10 more images…

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APA (6^th Edition):

Estil·les Altimiras, E. (2014). Efectes de la sobreexpressió d’IGF2 en la protecció i la regeneració de les cèl·lules beta pancreàtiques. (Thesis). Universitat de Barcelona. Retrieved from http://hdl.handle.net/10803/285812

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

Chicago Manual of Style (16^th Edition):

Estil·les Altimiras, Elisabet. “Efectes de la sobreexpressió d’IGF2 en la protecció i la regeneració de les cèl·lules beta pancreàtiques.” 2014. Thesis, Universitat de Barcelona. Accessed February 25, 2021. http://hdl.handle.net/10803/285812.

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

MLA Handbook (7^th Edition):

Estil·les Altimiras, Elisabet. “Efectes de la sobreexpressió d’IGF2 en la protecció i la regeneració de les cèl·lules beta pancreàtiques.” 2014. Web. 25 Feb 2021.

Vancouver:

Estil·les Altimiras E. Efectes de la sobreexpressió d’IGF2 en la protecció i la regeneració de les cèl·lules beta pancreàtiques. [Internet] [Thesis]. Universitat de Barcelona; 2014. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/10803/285812.

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

Council of Science Editors:

Estil·les Altimiras E. Efectes de la sobreexpressió d’IGF2 en la protecció i la regeneració de les cèl·lules beta pancreàtiques. [Thesis]. Universitat de Barcelona; 2014. Available from: http://hdl.handle.net/10803/285812

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

Queensland University of Technology

26. Lubik, Amy Anne. The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression.

Degree: 2011, Queensland University of Technology

URL: https://eprints.qut.edu.au/49029/

► Prostate cancer (CaP) is the most commonly diagnosed cancer in males in Australia, North America, and Europe. If found early and locally confined, CaP can… (more)

▼ Prostate cancer (CaP) is the most commonly diagnosed cancer in males in Australia, North America, and Europe. If found early and locally confined, CaP can be treated with radical prostatectomy or radiation therapy; however, 25-40% patients will relapse and go on to advanced disease. The most common therapy in these cases is androgen deprivation therapy (ADT), which suppresses androgen production from the testis. Lack of the testicular androgen supply causes cells of the prostate to undergo apoptosis. However, in some cases the regression initially seen with ADT eventually gives way to a growth of a population of cancerous cells that no longer require testicular androgens. This phenotype is essentially fatal and is termed castrate resistant prostate cancer (CRPC). In addition to eventual regression, there are many undesirable side effects which accompany ADT, including development of a metabolic syndrome, which is defined by the U.S. National Library of Medicine as “a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes.” This project will focus on the effect of ADT induced hyperinsulinemia, as mimicked by treating androgen receptor positive CaP cells with insulin in a serum (hormone) deprived environment. While this side effect is not widely explored, in this thesis it is demonstrated for the first time that insulin upregulates pathways important to CaP progression. Our group has previously shown that during CaP progression, the enzymes necessary for de novo steroidogenesis are upregulated in the LNCaP xenograft model, total steroid levels are increased in tumours compared to pre castrate levels, and de novo steroidogenesis from radio-labelled acetate has been demonstrated. Because of the CaP dependence on AR for survival, we and other groups believe that CaP cells carry out de novo steroidogenesis to survive in androgen deprived conditions. Because (a) men on ADT often develop metabolic syndrome, and (b) men with lifestyle-induced obesity and hyperinsulinemia have worse prognosis and faster disease progression, and because (c) insulin causes steroidogenesis in other cell lines, the hypothesis that insulin may contribute to CaP progression through upregulation of steroidogenesis was explored. Insulin upregulates steroidogenesis enzymes at the mRNA level in three AR positive cell lines, as well as upregulating these enzymes at the protein level in two cell lines. It has also been demonstrated that insulin increases mitochondrial (functional) levels of steroid acute regulatory protein (StAR). Furthermore, insulin causes increased levels of total steroids in and induction of de novo steroid synthesis by insulin has been demonstrated at levels induced sufficient to activate AR. The effect of insulin analogs on CaP steroidogenesis in LNCaP and VCaP cells has also been investigated because epidemiological studies suggest that some of the analogs developed may have more cancer stimulatory effects than normal insulin. In this project, despite the signalling differences…

Subjects/Keywords: prostate cancer; metabolic syndrome; insulin; insulin-like growth factor (IGF) 2; steroidogenesis; lipogenesis; sterol response element binding protein (SREBP); metformin; simvastatin

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

APA (6^th Edition):

Lubik, A. A. (2011). The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression. (Thesis). Queensland University of Technology. Retrieved from https://eprints.qut.edu.au/49029/

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

Chicago Manual of Style (16^th Edition):

Lubik, Amy Anne. “The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression.” 2011. Thesis, Queensland University of Technology. Accessed February 25, 2021. https://eprints.qut.edu.au/49029/.

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

MLA Handbook (7^th Edition):

Lubik, Amy Anne. “The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression.” 2011. Web. 25 Feb 2021.

Vancouver:

Lubik AA. The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression. [Internet] [Thesis]. Queensland University of Technology; 2011. [cited 2021 Feb 25]. Available from: https://eprints.qut.edu.au/49029/.

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

Council of Science Editors:

Lubik AA. The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression. [Thesis]. Queensland University of Technology; 2011. Available from: https://eprints.qut.edu.au/49029/

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

Univerzitet u Beogradu

27. Robajac, Dragana B., 1985-. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.

Degree: Hemijski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

►

Biohemija - Biohemija proteina / Biochemistry - Biochemistry of proteins

Funkcije membranskih proteina su brojne: međućelijska komunikacija, adhezija, signalna transdukcija. Većina membranskih proteina je glikozilovana… (more)

▼

Biohemija - Biohemija proteina / Biochemistry - Biochemistry of proteins

Funkcije membranskih proteina su brojne: međućelijska komunikacija, adhezija, signalna transdukcija. Većina membranskih proteina je glikozilovana i N-glikani imaju važnu ulogu u formiranju trodimenzionalne strukture membranskih proteina, kao i u ispoljavanju njihove funkcije. Receptori za insulin (IR) i faktor rasta sličan insulinu tip 1 (IGF1R) su transmembranske tirozin-kinaze sa visokim stepenom homologije (u nekim domenima čak i 80%). Familija IGF receptora, pored IR i IGF1R, uključuje i receptor za faktore rasta slične insulinu tip 2 (IGF2R). Sva tri receptora (IR, IGF1R i IGF2R) su glikozilovani i obilno prisutni u placenti, gde imaju važne uloge u njenom razvoju i funkcionisanju. Placenta raste i razvija se da bi ispunila različite potrebe fetusa, pa se struktura i funkcija placente menjaju tokom gestacije. Znajući da su proteini odgovorni za biološke funkcije placente pretpostavljeno je da tokom gestacije može doći i do promene u sadržaju različitih tipova N-glikana prisutnih na membranskim proteinima. U ovoj tezi analizirani su tipovi N-glikana koji se mogu naći u sastavu membranskih glikoproteina, odnosno membranski N-glikom proteina humane placente. Ispitana je podložnost membranskog N-glikoma individualnim varijacijama i uticaju starosti majke/trudnice, kao i uticaj gestacije na membranski N-glikom. Znajući da je izmenjena glikozilacija često povezana sa izmenjenom funkcijom, kao i da izmenjena funkcija jednog ili više proteina može biti uzrok bolesti, ispitane su potencijalne promene membranskog N-glikoma u patološkim trudnoćama (kod preeklampsije) i trudnoćama komplikovanim patologijom majki (dijabetes). Uporedo je ispitan i uticaj starosti, gestacije i patologije na tip i zastupljenost različitih N-glikana koji ulaze u sastav receptora IGF sistema. Cilj je bio da se ispita da li promene na ukupnim membranskim proteinima (na N-glikomu) prate promene N-glikana prisutnih na pojedinačnim membranskim glikoproteinima važnim za rast i funkcionisanje placente...

Advisors/Committee Members: Mandić, Ljuba, 1953-.

Subjects/Keywords: membrane proteins; N-glycans; N-glycome; insulin receptor; insulin-like growth factor receptors type 1 and 2; gestational changes; aging; placenta

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

APA (6^th Edition):

Robajac, Dragana B., 1. (2016). N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Robajac, Dragana B., 1985-. “N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.” 2016. Thesis, Univerzitet u Beogradu. Accessed February 25, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Robajac, Dragana B., 1985-. “N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.” 2016. Web. 25 Feb 2021.

Vancouver:

Robajac, Dragana B. 1. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Feb 25]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get.

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

Council of Science Editors:

Robajac, Dragana B. 1. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

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

Universidade Estadual de Campinas

28. Freria, Camila Marques, 1980-. Influência da glia na sobrevivência, capacidade regenerativa axonal e estabilidade sináptica de motoneurônios medulares após lesão central e periférica: Influence of glial cells on survival, axonal regeneration and synaptic plasticity of spinal motoneurons after peripheral and central injury.

Degree: 2013, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313787

► Abstract: Central or peripheral lesions result in local and retrograde inflammation, leading to axonal degeneration, synaptic and/or neuronal loss. Additionally, after injury, reactive glial cells… (more)

Subjects/Keywords: Fator estimulador de colônias de granulócitos; Receptor 4 Toll-like; Receptor 2 Toll-like; CX3CR1; Neurônios motores; Granulocyte colony-stimulating factor; Toll-Like receptor 4; Toll-Like receptor 2; CX3CR1; Motor neurons

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APA (6^th Edition):

Freria, Camila Marques, 1. (2013). Influência da glia na sobrevivência, capacidade regenerativa axonal e estabilidade sináptica de motoneurônios medulares após lesão central e periférica: Influence of glial cells on survival, axonal regeneration and synaptic plasticity of spinal motoneurons after peripheral and central injury. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/313787

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

Chicago Manual of Style (16^th Edition):

Freria, Camila Marques, 1980-. “Influência da glia na sobrevivência, capacidade regenerativa axonal e estabilidade sináptica de motoneurônios medulares após lesão central e periférica: Influence of glial cells on survival, axonal regeneration and synaptic plasticity of spinal motoneurons after peripheral and central injury.” 2013. Thesis, Universidade Estadual de Campinas. Accessed February 25, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313787.

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

MLA Handbook (7^th Edition):

Freria, Camila Marques, 1980-. “Influência da glia na sobrevivência, capacidade regenerativa axonal e estabilidade sináptica de motoneurônios medulares após lesão central e periférica: Influence of glial cells on survival, axonal regeneration and synaptic plasticity of spinal motoneurons after peripheral and central injury.” 2013. Web. 25 Feb 2021.

Vancouver:

Freria, Camila Marques 1. Influência da glia na sobrevivência, capacidade regenerativa axonal e estabilidade sináptica de motoneurônios medulares após lesão central e periférica: Influence of glial cells on survival, axonal regeneration and synaptic plasticity of spinal motoneurons after peripheral and central injury. [Internet] [Thesis]. Universidade Estadual de Campinas; 2013. [cited 2021 Feb 25]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313787.

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

Council of Science Editors:

Freria, Camila Marques 1. Influência da glia na sobrevivência, capacidade regenerativa axonal e estabilidade sináptica de motoneurônios medulares após lesão central e periférica: Influence of glial cells on survival, axonal regeneration and synaptic plasticity of spinal motoneurons after peripheral and central injury. [Thesis]. Universidade Estadual de Campinas; 2013. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313787

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

Universiteit Utrecht

29. Kort, R.A.L. de. The Biological Role of Insulin-Like Growth Factor binding Protein-2 in Tumorigenesis and Metabolic Homeostasis.

Degree: 2010, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/42360

► The Insulin-Like Growth Factor (IGF) system is involved in the regulation of cell growth, differentiation and sustains survival in several tissues. The Insulin-Like Growth Factor… (more)

Subjects/Keywords: Geneeskunde; Insulin-Like Growth Factor system, Insulin-Like Growth Factor Binding Protein-2, Tumorigenesis, Metabolic Homeostasis, IGF-dependent effects, IGF-independent effects

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

APA (6^th Edition):

Kort, R. A. L. d. (2010). The Biological Role of Insulin-Like Growth Factor binding Protein-2 in Tumorigenesis and Metabolic Homeostasis. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/42360

Chicago Manual of Style (16^th Edition):

Kort, R A L de. “The Biological Role of Insulin-Like Growth Factor binding Protein-2 in Tumorigenesis and Metabolic Homeostasis.” 2010. Masters Thesis, Universiteit Utrecht. Accessed February 25, 2021. http://dspace.library.uu.nl:8080/handle/1874/42360.

MLA Handbook (7^th Edition):

Kort, R A L de. “The Biological Role of Insulin-Like Growth Factor binding Protein-2 in Tumorigenesis and Metabolic Homeostasis.” 2010. Web. 25 Feb 2021.

Vancouver:

Kort RALd. The Biological Role of Insulin-Like Growth Factor binding Protein-2 in Tumorigenesis and Metabolic Homeostasis. [Internet] [Masters thesis]. Universiteit Utrecht; 2010. [cited 2021 Feb 25]. Available from: http://dspace.library.uu.nl:8080/handle/1874/42360.

Council of Science Editors:

Kort RALd. The Biological Role of Insulin-Like Growth Factor binding Protein-2 in Tumorigenesis and Metabolic Homeostasis. [Masters Thesis]. Universiteit Utrecht; 2010. Available from: http://dspace.library.uu.nl:8080/handle/1874/42360

Queens University

30. Berridge, Joanne. Elucidating the interaction between the Fragment 2 domain of Prothrombin and Factor Va .

Degree: Biochemistry, 2012, Queens University

URL: http://hdl.handle.net/1974/7344

► The prothrombinase (IIase) complex is an essential component of the coagulation cascade and is composed of a serine protease, Factor Xa (FXa), its non-enzymatic cofactor,… (more)

▼ The prothrombinase (IIase) complex is an essential component of the coagulation cascade and is composed of a serine protease, Factor Xa (FXa), its non-enzymatic cofactor, Factor Va (FVa), calcium and a phospholipid membrane surface. It activates prothrombin (FII) to thrombin, the principal stimulator of clot formation in vivo. FII activation by IIase is mediated by specific interactions between FII and FVa. Preliminary NMR and peptidyl mimicry studies identified six residues within the FII Fragment 2 (F2) domain (S160, Q177, R181, L182, V184 and T185) that likely mediate an interaction between it and the heavy chain of FVa. Therefore, six recombinant FII derivatives were prepared whereby each of the aforementioned residues was mutated to alanine. FII activation kinetics by FXa in the presence or absence of FVa was measured by DAPA-thrombin complex formation. The results show that FII-S160A, -R181A, -L182A, -V184A and -T185A had no significant effect on the catalytic efficiency of the reaction in the presence of FVa. In the absence of FVa, the catalytic efficiency of FII-R181A, -L182A, -V184A, and -T185A derivatives decreased by 17-27% compared with wildtype, while FII-S160A had no effect. FII-Q177A, however, showed a significant increase of 17% in catalytic efficiency in the presence of FVa but no change in its absence. Two double (FII-Q177A/R181A and FII-R181A/T185A) and one triple (FII-Q177A/R181A/T185) mutants were generated to determine if multiple mutations would have an additive effect. These derivatives were indistinguishable from wildtype in the presence of FVa. In the absence of FVa, however, their catalytic efficiency values decreased 12-25% compared with wildtype. Further comparison of these values showed that FII-R181A and -Q177A/R181A both decreased by 25%, while FII-R181A/T185A and -Q177A/R181A/T185A decreased by 12% and 24% with respect to the wildtype, respectively. Both comparisons, where the only difference was an additional mutation at Q177, suggest that Q177 does not affect the activation kinetics of FII in the absence of FVa. Taken together, our data suggest that Q177 in the F2 domain of FII is likely involved in interacting with IIase through a FVa-dependent mechanism while residues R181, L182, V184 and T185 may be involved through a FVa-independent mechanism.

Subjects/Keywords: Fragment 2 domain ; Factor Va ; Prothrombinase ; Prothrombin

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

APA (6^th Edition):

Berridge, J. (2012). Elucidating the interaction between the Fragment 2 domain of Prothrombin and Factor Va . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7344

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

Chicago Manual of Style (16^th Edition):

Berridge, Joanne. “Elucidating the interaction between the Fragment 2 domain of Prothrombin and Factor Va .” 2012. Thesis, Queens University. Accessed February 25, 2021. http://hdl.handle.net/1974/7344.

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

MLA Handbook (7^th Edition):

Berridge, Joanne. “Elucidating the interaction between the Fragment 2 domain of Prothrombin and Factor Va .” 2012. Web. 25 Feb 2021.

Vancouver:

Berridge J. Elucidating the interaction between the Fragment 2 domain of Prothrombin and Factor Va . [Internet] [Thesis]. Queens University; 2012. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/1974/7344.

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

Council of Science Editors:

Berridge J. Elucidating the interaction between the Fragment 2 domain of Prothrombin and Factor Va . [Thesis]. Queens University; 2012. Available from: http://hdl.handle.net/1974/7344

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

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Open Access Theses and Dissertations