subject:(APOPTOSIS)

University of Rochester

1. McAvoy, Kathleen M. The Role of the Von Hippel-Lindau Protein in Developmental Cell Death in Sympathetic Neurons.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/19818

► While cell death of excess neurons is critical for the development of the nervous system, cell death in adulthood is a primary cause of neurodegenerative… (more)

▼ While cell death of excess neurons is critical for the development of the nervous system, cell death in adulthood is a primary cause of neurodegenerative disease. Thus, understanding the signaling mechanisms that regulate programmed cell death is of primary importance. In development, production of excess neurons and subsequent competition to acquire limited target-derived survival-promoting trophic factors ensures that appropriate numbers of correctly targeted neurons survive. Developing sympathetic neurons are an example of this process, and undergo cell death in the absence of nerve growth factor (NGF). Recent evidence suggests that cell signaling pathways that regulate the hypoxia inducible factor transcription factor (HIF) also regulate neuronal survival. In normoxia, HIFα is hydroxylated on proline residues by the EGLNs, allowing the von Hippel-Lindau protein (VHL) to recognize and ubiquitinate HIFα to target it for degradation. One EGLN, EGLN3, is induced after NGF withdrawal and can promote death when overexpressed. Stabilization of HIF through overexpression or EGLN inhibition reduces cell death after NGF withdrawal. Thus VHL, a pivotal regulator of HIF, may regulate cell death after NGF withdrawal. Additional evidence for a role for VHL in cell death comes from studies of VHL in cancer. Germline mutation of VHL in humans confers increased susceptibility to select cancers. Based on the finding that knockdown of VHL in NGF-differentiated PC12 pheochromocytoma cells reduced cell death caused by NGF withdrawal, it has been proposed that 1) VHL plays a normal role in the regulation of programmed cell death of sympathetic neurons and 2) that lack of VHL may allow NGF-dependent cells to escape development cell death and go on to contribute to pheochromocytoma. Here we directly test the hypothesis that VHL functions to regulate cell death in developing sympathetic neurons after NGF withdrawal. Disruption of Vhl delays cell death after NGF withdrawal by inhibiting cytochrome c release and caspase-3 activation. Although loss of VHL results in increased HIF protein and transcription factor activity, HIF is not required for the increased survival of VHL deficient neurons. Both JUNB and NF-κB can promote survival of NGF-deprived sympathetic neurons and appear to be negatively regulated by VHL in tumor cells. Despite increased JUNB in VHL null sympathetic neurons, reducing JUNB did not reverse the survival advantage of VHL null neurons. However, inhibition of NF-κB reversed the neuroprotection seen in the absence of VHL. Thus, loss of VHL leads to delayed cell death in sympathetic neurons after NGF withdrawal through a mechanism that is largely HIF-independent but requires NF-κB.

Subjects/Keywords: Apoptosis

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APA (6^th Edition):

McAvoy, K. M. (2012). The Role of the Von Hippel-Lindau Protein in Developmental Cell Death in Sympathetic Neurons. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/19818

Chicago Manual of Style (16^th Edition):

McAvoy, Kathleen M. “The Role of the Von Hippel-Lindau Protein in Developmental Cell Death in Sympathetic Neurons.” 2012. Doctoral Dissertation, University of Rochester. Accessed January 24, 2021. http://hdl.handle.net/1802/19818.

MLA Handbook (7^th Edition):

McAvoy, Kathleen M. “The Role of the Von Hippel-Lindau Protein in Developmental Cell Death in Sympathetic Neurons.” 2012. Web. 24 Jan 2021.

Vancouver:

McAvoy KM. The Role of the Von Hippel-Lindau Protein in Developmental Cell Death in Sympathetic Neurons. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1802/19818.

Council of Science Editors:

McAvoy KM. The Role of the Von Hippel-Lindau Protein in Developmental Cell Death in Sympathetic Neurons. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/19818

Cape Peninsula University of Technology

2. Solomon, Wendy Lynn. The leukocyte apoptosis assay : a clinical predictor of radiosensitivity? .

Degree: 2009, Cape Peninsula University of Technology

URL: http://etd.cput.ac.za/handle/20.500.11838/2246

► The main objective of radiotherapy is to completely eradicate tumours while preserving the integrity of the normal surrounding tissue. The severity of normal tissue reactions… (more)

Subjects/Keywords: Apoptosis; Leucocytes

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APA (6^th Edition):

Solomon, W. L. (2009). The leukocyte apoptosis assay : a clinical predictor of radiosensitivity? . (Thesis). Cape Peninsula University of Technology. Retrieved from http://etd.cput.ac.za/handle/20.500.11838/2246

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):

Solomon, Wendy Lynn. “The leukocyte apoptosis assay : a clinical predictor of radiosensitivity? .” 2009. Thesis, Cape Peninsula University of Technology. Accessed January 24, 2021. http://etd.cput.ac.za/handle/20.500.11838/2246.

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

MLA Handbook (7^th Edition):

Solomon, Wendy Lynn. “The leukocyte apoptosis assay : a clinical predictor of radiosensitivity? .” 2009. Web. 24 Jan 2021.

Vancouver:

Solomon WL. The leukocyte apoptosis assay : a clinical predictor of radiosensitivity? . [Internet] [Thesis]. Cape Peninsula University of Technology; 2009. [cited 2021 Jan 24]. Available from: http://etd.cput.ac.za/handle/20.500.11838/2246.

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

Council of Science Editors:

Solomon WL. The leukocyte apoptosis assay : a clinical predictor of radiosensitivity? . [Thesis]. Cape Peninsula University of Technology; 2009. Available from: http://etd.cput.ac.za/handle/20.500.11838/2246

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

University of Alberta

3. Campbell, Stephanie D. Investigation of the Anti-apoptotic Function and Regulation of Vaccinia Virus F1L.

Degree: PhD, Department of Medical Microbiology and Immunology, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/n296x054h

► Apoptosis, an evolutionarily conserved cell death programme, is a potent barrier against virus infection. Central to this process are mitochondria, which harbour cytochrome c and… (more)

▼ Apoptosis, an evolutionarily conserved cell death programme, is a potent barrier against virus infection. Central to this process are mitochondria, which harbour cytochrome c and other apoptosis-inducing factors. Once released, these factors activate a caspase cascade that culminates in cell death. Mitochondrial integrity is tightly regulated by the Bcl-2 family of proteins, which are united by the presence of one or more conserved Bcl-2 homology, or BH, domains that are critical for protein interactions and function. Bak and Bax are the key pro-apoptotic members that engage the mitochondrial death machinery to release cytochrome c. These proteins are activated by pro-apoptotic BH3-only proteins and inhibited by anti-apoptotic family members, such as Mcl-1. Due to the importance of Bak and Bax, many viruses, including poxviruses, have adapted strategies to interfere with the activation of these two proteins. In the prototypic poxvirus vaccinia virus, this is accomplished by a unique anti-apoptotic protein, F1L. F1L localizes to mitochondria and prevents apoptosis induced by a variety of stimuli. This is achieved by direct binding to Bak, while Bax inhibition is believed to occur by the binding of F1L to the BH3-only protein, BimL. However, the way in which F1L binds Bak and BimL is unknown, since F1L lacks sequence homology to Bcl-2 proteins. Here, we show that F1L functions in a manner that resembles Mcl-1, the major cellular regulator of Bak. Moreover, we have identified divergent BH domains within F1L that are critical for Bak binding and anti-apoptotic activity. Given the importance of the Bcl-2 family of proteins, many members are regulated by ubiquitination, which targets the proteins for proteasomal degradation. Similarly, we have discovered that F1L is tightly regulated by the ubiquitin-proteasome system. Our studies on F1L ubiquitination have also revealed a potential role for F1L in the regulation of mitochondrial morphology. Thus, despite divergence at the sequence level, F1L interacts with Bak in a manner nearly identical to cellular Bcl-2 family members, and, additionally, F1L is governed by the same regulatory mechanisms that control members of the Bcl-2 family.

Subjects/Keywords: Poxvirus; Apoptosis

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APA (6^th Edition):

Campbell, S. D. (2012). Investigation of the Anti-apoptotic Function and Regulation of Vaccinia Virus F1L. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/n296x054h

Chicago Manual of Style (16^th Edition):

Campbell, Stephanie D. “Investigation of the Anti-apoptotic Function and Regulation of Vaccinia Virus F1L.” 2012. Doctoral Dissertation, University of Alberta. Accessed January 24, 2021. https://era.library.ualberta.ca/files/n296x054h.

MLA Handbook (7^th Edition):

Campbell, Stephanie D. “Investigation of the Anti-apoptotic Function and Regulation of Vaccinia Virus F1L.” 2012. Web. 24 Jan 2021.

Vancouver:

Campbell SD. Investigation of the Anti-apoptotic Function and Regulation of Vaccinia Virus F1L. [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2021 Jan 24]. Available from: https://era.library.ualberta.ca/files/n296x054h.

Council of Science Editors:

Campbell SD. Investigation of the Anti-apoptotic Function and Regulation of Vaccinia Virus F1L. [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/n296x054h

4. Bennett, Ailsa. Exploiting mitosis to improve anti-cancer strategies.

Degree: 2017, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:306798

► Antimitotics are used in cancer chemotherapy for the treatment of cancers such as breast, ovarian, lung and prostate. Despite the success of agents such as… (more)

▼ Antimitotics are used in cancer chemotherapy for the treatment of cancers such as breast, ovarian, lung and prostate. Despite the success of agents such as Taxol, problems have emerged such as side effects, resistance and the lack of ability to predict patient responsiveness. As a result, a class of second-generation inhibitors have been developed with the aim to overcome or improve these issues. Such inhibitors target proteins and kinases involved in the control of mitosis and the cell cycle. However, these have yet to be clinically successful and therefore, this highlights the requirement for an increased understanding of the mitotic process and how antimitotics truly elicit their action. Reasons for the lack of efficacy may be due to the absence of biomarkers to stratify patients into those likely to respond to treatment. It may also be possible that other targets are required. Our understanding of the action of antimitotics is therefore paramount to improving cancer chemotherapy. By exploiting mitosis and understanding what happens when mitosis goes wrong, this thesis aims to explore new and improved methods of targeting, but also proposes to improve our understanding of the consequences of aberrant mitoses through the use of small molecule inhibitors. In the first case the thesis investigated the targeting of the spindle checkpoint protein Bub1 with 2OH-BNPP1, where previously inhibitors against the kinase were not acknowledged. However the inhibitor used was not effective in cells and therefore further experimentation was not possible. Secondly, to explore the consequences of mitotic perturbation, an assay to explore aneuploidy was established. To do this a Cenp-E inhibitor GSK923295 was synthesised, which was subsequently used in assays with the Mps1 inhibitor AZ3146 to generate aneuploidy progeny. The Cenp-E inhibitor was then used as an antimitotic agent in the final chapter to explore the mechanism of action of mitotic blockers and drivers often used in cell biology and clinical settings. Evidence suggests that the intrinsic apoptotic pathway is activated upon exposure to these agents. With focus on this pathway, the importance of Bcl-xL on cell survival was considered, revealing particular importance in the post-mitotic response. Ultimately, this thesis should contribute to devising new and improved anti-cancer strategies. Advisors/Committee Members: JACKSON, DEAN DA, Jackson, Dean, Taylor, Stephen.

Subjects/Keywords: mitosis; apoptosis

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APA (6^th Edition):

Bennett, A. (2017). Exploiting mitosis to improve anti-cancer strategies. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:306798

Chicago Manual of Style (16^th Edition):

Bennett, Ailsa. “Exploiting mitosis to improve anti-cancer strategies.” 2017. Doctoral Dissertation, University of Manchester. Accessed January 24, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:306798.

MLA Handbook (7^th Edition):

Bennett, Ailsa. “Exploiting mitosis to improve anti-cancer strategies.” 2017. Web. 24 Jan 2021.

Vancouver:

Bennett A. Exploiting mitosis to improve anti-cancer strategies. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2021 Jan 24]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:306798.

Council of Science Editors:

Bennett A. Exploiting mitosis to improve anti-cancer strategies. [Doctoral Dissertation]. University of Manchester; 2017. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:306798

5. Canussanun Jirachotikoon. Effect of penaeus merguiensis-translationally controlled tumor protein on TPT1 expression of heat-treated human pulp cells .

Degree: คณะวิทยาศาสตร์ สาขาวิชาชีววิทยาโมเลกุลและชีวสารสนเทศ, 2014, Prince of Songkla University

URL: http://kb.psu.ac.th/psukb/handle/2010/9906

Subjects/Keywords: Apoptosis

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APA (6^th Edition):

Jirachotikoon, C. (2014). Effect of penaeus merguiensis-translationally controlled tumor protein on TPT1 expression of heat-treated human pulp cells . (Thesis). Prince of Songkla University. Retrieved from http://kb.psu.ac.th/psukb/handle/2010/9906

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):

Jirachotikoon, Canussanun. “Effect of penaeus merguiensis-translationally controlled tumor protein on TPT1 expression of heat-treated human pulp cells .” 2014. Thesis, Prince of Songkla University. Accessed January 24, 2021. http://kb.psu.ac.th/psukb/handle/2010/9906.

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

MLA Handbook (7^th Edition):

Jirachotikoon, Canussanun. “Effect of penaeus merguiensis-translationally controlled tumor protein on TPT1 expression of heat-treated human pulp cells .” 2014. Web. 24 Jan 2021.

Vancouver:

Jirachotikoon C. Effect of penaeus merguiensis-translationally controlled tumor protein on TPT1 expression of heat-treated human pulp cells . [Internet] [Thesis]. Prince of Songkla University; 2014. [cited 2021 Jan 24]. Available from: http://kb.psu.ac.th/psukb/handle/2010/9906.

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

Council of Science Editors:

Jirachotikoon C. Effect of penaeus merguiensis-translationally controlled tumor protein on TPT1 expression of heat-treated human pulp cells . [Thesis]. Prince of Songkla University; 2014. Available from: http://kb.psu.ac.th/psukb/handle/2010/9906

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

6. Poranki, Deepika. Keratin Biomaterial Treatments For Burn Injury And Mechanisms Of Tissue Survival.

Degree: 2012, Wake Forest University

URL: http://hdl.handle.net/10339/37431

► Thermal burns typically display an injury pattern dictated by the transfer of the thermal energy into the skin and underlying tissues. There are often three… (more)

▼ Thermal burns typically display an injury pattern dictated by the transfer of the thermal energy into the skin and underlying tissues. There are often three zones of injury represented by a necrotic zone of disrupted cells and tissue, an intermediate zone of injured and dying cells, and a distant zone of stressed cells that will recover with proper treatment. There are currently no approved clinical therapies that target the zone of stasis and can reduce the need for excision and grafting by salvaging potentially viable cells and tissue and thereby contributing to spontaneous healing. In this project, we endeavored to investigate the potential of keratin biomaterials to mediate such healing. Pilot studies testing treatment of chemical (mouse model) and thermal (swine model) burns showed that a native mixture (termed "crude keratose" throughout this thesis) of keratose was able to promote wound healing by stabilizing the size of the burn, suggesting that cell survival was being facilitated in the zone of stasis. These results led us to hypothesize that the interaction of the keratose biomaterial with cells and tissue promoted survival and reduced the total body surface area burned. As crude keratose is a heterogeneous mixture of proteins representing alpha and gamma protein fractions, we determined the differential activity on cell survival associated with these fractions by using an in vitro thermal stress model and showed that gamma keratose contributed to cell survival while alpha keratose did not. In additional studies, the specific mechanism of cell survival associated with the gamma keratose fraction was investigated. These results showed that gamma keratose was able to down regulate the genes involved in cell death pathways. Later, an in vivo porcine deep partial thickness burn model was developed to study the wound healing properties of a modified keratose hydrogel (MKH) that contained a reduced amount of gamma keratose, reflecting the same concentrations used in in vitro thermal stress model. The MKH showed a faster re-epithelialization rate and wound closure compared to other treatments. Finally, to investigate the potential clinical relevance to actual burn treatment, a delayed treatment thermal burn study was performed. These results showed that MKH was able to promote faster wound healing compared to other treatments but not with the same efficacy compared to more immediate post-burn treatment. This work suggested the potential benefit of using keratin biomaterial in burn therapy and provided informative data for developing second generation keratin biomaterial treatments.

Subjects/Keywords: Apoptosis

…x28;TBSA) burned is the increase in cell death after the thermal insult. Apoptosis and… …biochemical changes associated with apoptosis. The death receptors usually belong to the tumor… …intrinsic pathway of apoptosis. Once the initiator caspases are activated, they cleave and… …Schultz DZ, Apoptosis: Programmed cell death at a molecular level. Semin Arthritis Rheum. 2003… …inhibitory proteins) [101]. The members of BCL2 family proteins regulate apoptosis…

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APA (6^th Edition):

Poranki, D. (2012). Keratin Biomaterial Treatments For Burn Injury And Mechanisms Of Tissue Survival. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/37431

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):

Poranki, Deepika. “Keratin Biomaterial Treatments For Burn Injury And Mechanisms Of Tissue Survival.” 2012. Thesis, Wake Forest University. Accessed January 24, 2021. http://hdl.handle.net/10339/37431.

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

MLA Handbook (7^th Edition):

Poranki, Deepika. “Keratin Biomaterial Treatments For Burn Injury And Mechanisms Of Tissue Survival.” 2012. Web. 24 Jan 2021.

Vancouver:

Poranki D. Keratin Biomaterial Treatments For Burn Injury And Mechanisms Of Tissue Survival. [Internet] [Thesis]. Wake Forest University; 2012. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10339/37431.

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

Council of Science Editors:

Poranki D. Keratin Biomaterial Treatments For Burn Injury And Mechanisms Of Tissue Survival. [Thesis]. Wake Forest University; 2012. Available from: http://hdl.handle.net/10339/37431

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

7. Lyons, Erica Lynn. Cannabinoid Receptor Signaling in Human SH-SY5Y Neuroblastoma Cell Viability, Proliferation Rate, and Extension Length.

Degree: 2019, Wake Forest University

URL: http://hdl.handle.net/10339/93988

► We created clonal cell lines that stably overexpress either CB1 (CB1XS) or CB2 receptor (CB2XS) in human neuroblastoma SH-SY5Y as a model to investigate the… (more)

▼ We created clonal cell lines that stably overexpress either CB1 (CB1XS) or CB2 receptor (CB2XS) in human neuroblastoma SH-SY5Y as a model to investigate the role of cannabinoid signaling in neurite extension, proliferation, apoptosis, and cell viability. The mRNA of the enzymatic components of the endogenous cannabinoid system diacylglycerol lipase, monoacylglycerol lipase, alpha/beta-hydrolase domain containing 6, alpha/beta-hydrolase domain containing 12, N-acyl phosphatidylethanolamine phospholipase D, and fatty acid amide hydrolase are present in SH-SY5Y cells. Activity of these enzymes produced endocannabinoid ligands, resulting in a steady state concentration of 2-arachidonoylglycerol of 135 pmol per gram of protein and anandamide of 0.82 pmol per gram protein. Application of tetrahydrolipstatin, an inhibitor of diacylglycerol lipase activity, decreased 2-arachidonoylglycerol concentration to 15 pmol per gram of protein while anandamide remained at 0.79 pmol per gram of protein. Oxotremorine M, an agonist of Gq coupled muscarinic acetylcholine receptors, mobilized calcium from intracellular stores to stimulate diacylglycerol lipase, increasing 2-arachidonoylglycerol concentration to 564 pmol per gram of protein. A 2-arachidonoylglycerol hydrolysis enzyme inhibitor cocktail increased 2-arachidonoylglycerol to 2,140 pmol per gram protein. Transfection resulted in a stable increase of CB1 receptor mRNA by 11 fold increase in abundance in the CB1XS cell line and of CB2 receptor mRNA by 14 fold increase in abundance in the CB2XS cell line. Cannabinoid receptor overexpression did not alter the mRNA abundance of the enzyme components of the endogenous cannabinoid system in SH-SY5Y cells. Parental SH-SY5Y cells had an average neurite length per nuclei of 0.7 μm per nuclei. Stable increased expression of CB2 receptor in three clonal cell lines did not consistently change extension length, and resulted in a maximal neurite length per nuclei increase to 1.69 μm. Stable increased expression of CB1 receptor increased the abundance of one soma long neuritic extensions from 0.7 to 6.0 micrometers per nuclei per field. This CB1 stimulated increase in neurite length was not constitutive receptor activity as it was halved by tetrahydrolipstatin inhibition of diacylglycerol lipase enzymatic production of the endogenous cannabinoid ligand 2-arachidonoylglycerol. Neurite extension length was halved with a p of 0.07 by gallein inhibition of G protein beta gamma dependent signaling. Stable increased expression of CB1 receptor increased the mRNA abundance of growth cone associated protein 43 and ST8 Alpha-N-Acetyl-Neuraminide Alpha-2,8-Sialyltransferase 2 mRNA and decreased integrin alpha 1 mRNA. Stable increased expression of CB2 receptor increased neural cell adhesion molecule and synaptotagmin 1 mRNA. We identified the endogenous cannabinoid enzyme monoacylglycerol lipase as a novel target of retinoic acid mRNA transcription in the SH-SY5Y neuroblastoma model of neuron differentiation and neurite extension. …

Subjects/Keywords: apoptosis

…Cannabinoid Receptors Does not Alter SH-SY5Y Viability or Promote Apoptosis… …Cannabinoid Receptors Does Not Alter Apoptosis in Human SH-SY5Y Neuroblastoma Cells… …Not Alter Apoptosis in Human SH-SY5Y Neuroblastoma Cells.... �� ..118 Figure 4.5… …Figure 6.2 Effect of CB1 and CB2 Cannabinoid Receptors Extension Length, Apoptosis… …apoptosis, and cell viability. The mRNA of the enzymatic components of the endogenous cannabinoid…

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APA (6^th Edition):

Lyons, E. L. (2019). Cannabinoid Receptor Signaling in Human SH-SY5Y Neuroblastoma Cell Viability, Proliferation Rate, and Extension Length. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/93988

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):

Lyons, Erica Lynn. “Cannabinoid Receptor Signaling in Human SH-SY5Y Neuroblastoma Cell Viability, Proliferation Rate, and Extension Length.” 2019. Thesis, Wake Forest University. Accessed January 24, 2021. http://hdl.handle.net/10339/93988.

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

MLA Handbook (7^th Edition):

Lyons, Erica Lynn. “Cannabinoid Receptor Signaling in Human SH-SY5Y Neuroblastoma Cell Viability, Proliferation Rate, and Extension Length.” 2019. Web. 24 Jan 2021.

Vancouver:

Lyons EL. Cannabinoid Receptor Signaling in Human SH-SY5Y Neuroblastoma Cell Viability, Proliferation Rate, and Extension Length. [Internet] [Thesis]. Wake Forest University; 2019. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10339/93988.

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

Council of Science Editors:

Lyons EL. Cannabinoid Receptor Signaling in Human SH-SY5Y Neuroblastoma Cell Viability, Proliferation Rate, and Extension Length. [Thesis]. Wake Forest University; 2019. Available from: http://hdl.handle.net/10339/93988

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

University of Debrecen

8. Djeribi Ep Zaidi, Salima. Comparison of the uptake of apoptotic and necrotic cells by macrophages .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/242181

► macrophages recognise and engulf apoptotic and necrotic cell via the same mechanisms including PS and Rac1 dependency. Apoptotic and necrotic cell compete with each other… (more)

Subjects/Keywords: apoptosis

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APA (6^th Edition):

Djeribi Ep Zaidi, S. (n.d.). Comparison of the uptake of apoptotic and necrotic cells by macrophages . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/242181

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Djeribi Ep Zaidi, Salima. “Comparison of the uptake of apoptotic and necrotic cells by macrophages .” Thesis, University of Debrecen. Accessed January 24, 2021. http://hdl.handle.net/2437/242181.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Djeribi Ep Zaidi, Salima. “Comparison of the uptake of apoptotic and necrotic cells by macrophages .” Web. 24 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Djeribi Ep Zaidi S. Comparison of the uptake of apoptotic and necrotic cells by macrophages . [Internet] [Thesis]. University of Debrecen; [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2437/242181.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Djeribi Ep Zaidi S. Comparison of the uptake of apoptotic and necrotic cells by macrophages . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/242181

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Adelaide

9. Harvey, Natasha Lynn. The biochemical and cellular analysis of caspase-2 activation during apoptosis / by Natasha Harvey.

Degree: 1998, University of Adelaide

URL: http://hdl.handle.net/2440/19306

► Apoptosis, or programmed cell death, is a fundamental process during both embryonic development and adult homeostasis. Aberrant apoptosis has been associated with a number of… (more)

Subjects/Keywords: Apoptosis.

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APA (6^th Edition):

Harvey, N. L. (1998). The biochemical and cellular analysis of caspase-2 activation during apoptosis / by Natasha Harvey. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/19306

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):

Harvey, Natasha Lynn. “The biochemical and cellular analysis of caspase-2 activation during apoptosis / by Natasha Harvey.” 1998. Thesis, University of Adelaide. Accessed January 24, 2021. http://hdl.handle.net/2440/19306.

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

MLA Handbook (7^th Edition):

Harvey, Natasha Lynn. “The biochemical and cellular analysis of caspase-2 activation during apoptosis / by Natasha Harvey.” 1998. Web. 24 Jan 2021.

Vancouver:

Harvey NL. The biochemical and cellular analysis of caspase-2 activation during apoptosis / by Natasha Harvey. [Internet] [Thesis]. University of Adelaide; 1998. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2440/19306.

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

Council of Science Editors:

Harvey NL. The biochemical and cellular analysis of caspase-2 activation during apoptosis / by Natasha Harvey. [Thesis]. University of Adelaide; 1998. Available from: http://hdl.handle.net/2440/19306

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

10. García-Riart Monzón, Beatriz Inmaculada. Análisis del perfil de microRNA en la eliminación de los progenitores esqueléticos de los espacios interdigitales embrionarios.

Degree: 2017, Universidad de Cantabria

URL: http://hdl.handle.net/10902/11505

► RESUMEN: El análisis de secuenciación masiva de RNA de pequeño tamaño, en combinación con diversos análisis por qPCR, pusieron de manifiesto la implicación de los… (more)

Subjects/Keywords: Apoptosis

…implicados en la tenogénesis 30 3.3. MicroRNA implicados en senescencia y apoptosis durante el… …en el control de la división celular, proliferación, diferenciación, apoptosis y también en… …apoptosis celular. Mientras que la desregulación de su producción puede alterar la fisiología… …articular. 2. Proliferar, diferenciarse a condrocitos hipertróficos entrando en apoptosis en el… …condrocitos hipertróficos diferenciados mueren por apoptosis o pueden sufrir también…

10 more images…

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APA (6^th Edition):

García-Riart Monzón, B. I. (2017). Análisis del perfil de microRNA en la eliminación de los progenitores esqueléticos de los espacios interdigitales embrionarios. (Doctoral Dissertation). Universidad de Cantabria. Retrieved from http://hdl.handle.net/10902/11505

Chicago Manual of Style (16^th Edition):

García-Riart Monzón, Beatriz Inmaculada. “Análisis del perfil de microRNA en la eliminación de los progenitores esqueléticos de los espacios interdigitales embrionarios.” 2017. Doctoral Dissertation, Universidad de Cantabria. Accessed January 24, 2021. http://hdl.handle.net/10902/11505.

MLA Handbook (7^th Edition):

García-Riart Monzón, Beatriz Inmaculada. “Análisis del perfil de microRNA en la eliminación de los progenitores esqueléticos de los espacios interdigitales embrionarios.” 2017. Web. 24 Jan 2021.

Vancouver:

García-Riart Monzón BI. Análisis del perfil de microRNA en la eliminación de los progenitores esqueléticos de los espacios interdigitales embrionarios. [Internet] [Doctoral dissertation]. Universidad de Cantabria; 2017. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10902/11505.

Council of Science Editors:

García-Riart Monzón BI. Análisis del perfil de microRNA en la eliminación de los progenitores esqueléticos de los espacios interdigitales embrionarios. [Doctoral Dissertation]. Universidad de Cantabria; 2017. Available from: http://hdl.handle.net/10902/11505

University of Hong Kong

11. 卢盈颖. Mechanistic study on the inhibition of the late stage of basal autophagy progression by a natural compound (NAADP) and a synthetic small chemical (vacuolin-1).

Degree: 2014, University of Hong Kong

URL: http://hdl.handle.net/10722/207179

► Autophagy is a catabolic lysosomal degradation process essential for cellular homeostasis and cell survival. Dysfunctional autophagy has been associated with wide ranges of human diseases,… (more)

▼ Autophagy is a catabolic lysosomal degradation process essential for cellular homeostasis and cell survival. Dysfunctional autophagy has been associated with wide ranges of human diseases, e.g. cancer and neurodegenerative diseases. Although enormous progress has been made on the core molecular machineries of autophagy, mechanisms of autophagy induction, autophagosome maturation, and autophagosomal-lysosomal fusion still remain elusive in mammalian cells. 　　The two pore channel 2 (TPC2) is a new member of the superfamily of voltage-gated Na+/Ca2+ channels located on lysosomes. Accumulating evidence indicates that nicotinic acid adenine dinucleotide phosphate (NAADP), one of the most potent Ca2+ mobilizing nucleotides, elicits Ca2+ release from lysosomes via TPC2 in many cell types. Herein, we first studied the role and mechanism of NAADP/TPC2/Ca2+ signaling in regulation of autophagy in mammalian cells. We found that overexpression TPC2 in Hela cells or mouse embryonic stem (ES) cells inhibited autophagosomal-lysosomal fusion, thereby resulting in the accumulation of autophagosomes. Treatment of TPC2 expressing cells with NAADP-AM, a cell-permeant NAADP agonist, further induced the accumulation, whereas Ned-19, a NAADP antagonist, reversed it. Interestingly, inhibiting MTOR activity failed to increase TPC2-induced autophagosome accumulation, but ATG5 knockdown markedly blocked it. Importantly, overexpression of TPC2 alkalinized lysosomal pH, whereas lysosomal re-acidification abolished TPC2-induced autophagosome accumulation. In addition, TPC2 overexpression had no effect on general endosomal-lysosomal degradation but prevented the recruitment of Rab-7 to autophagosomes. Taken together, our data demonstrate that NAADP/TPC2/Ca2+ signaling alkalinizes lysosomal pH to specifically inhibit the later stage of basal autophagy progression. Development of agonists or antagonists of NAADP should provide a novel approach to specifically manipulate autophagy. 　　Along this line, a large number of small chemicals that modulate autophagy have actually been widely used to dissect this process and some of them, e.g. chloroquine (CQ), might be ultimately applied to treat a variety of autophagy-associated human diseases. Yet most of the autophagy chemical modulators lack specificity, or potency, or both. Therefore we screened a panel of small chemicals that are commercially available and have been previously shown to affect vesicle trafficking or organelle morphology on autophagy regulation. We found that vacuolin-1, a cell permeable small molecule, potently and reversibly inhibited autophagosomal-lysosomal fusion in mammalian cells, thereby inducing the accumulation of autophagosomes. Vacuolin-1 treatment also blocked the fusion between endosomes and lysosomes, resulting in a defect in general endosomal-lysosomal degradation. Interestingly, treatment of cells with vacuolin-1 alkalinized lysosomal pH and decreased lysosomal Ca2+ content. Besides marginally inhibiting vacuolar ATPase activity, vacuolin-1 treatment markedly… Advisors/Committee Members: Yue, J (advisor), Tang, F (advisor).

Subjects/Keywords: Apoptosis

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APA (6^th Edition):

卢盈颖. (2014). Mechanistic study on the inhibition of the late stage of basal autophagy progression by a natural compound (NAADP) and a synthetic small chemical (vacuolin-1). (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/207179

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

Chicago Manual of Style (16^th Edition):

卢盈颖. “Mechanistic study on the inhibition of the late stage of basal autophagy progression by a natural compound (NAADP) and a synthetic small chemical (vacuolin-1).” 2014. Thesis, University of Hong Kong. Accessed January 24, 2021. http://hdl.handle.net/10722/207179.

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

MLA Handbook (7^th Edition):

卢盈颖. “Mechanistic study on the inhibition of the late stage of basal autophagy progression by a natural compound (NAADP) and a synthetic small chemical (vacuolin-1).” 2014. Web. 24 Jan 2021.

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

Vancouver:

卢盈颖. Mechanistic study on the inhibition of the late stage of basal autophagy progression by a natural compound (NAADP) and a synthetic small chemical (vacuolin-1). [Internet] [Thesis]. University of Hong Kong; 2014. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10722/207179.

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

Council of Science Editors:

卢盈颖. Mechanistic study on the inhibition of the late stage of basal autophagy progression by a natural compound (NAADP) and a synthetic small chemical (vacuolin-1). [Thesis]. University of Hong Kong; 2014. Available from: http://hdl.handle.net/10722/207179

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

Massey University

12. Haywood, Annika Fleur Margo. In vitro systems to study the relationship between apoptosis in multicellular organisms and yeast.

Degree: MS, Biochemistry, 2000, Massey University

URL: http://hdl.handle.net/10179/12688

► Apoptosis is a distinct form of cell death that is characterised by specific morphological and biochemical markers, such as chromatin condensation and internucleosomal DNA cleavage.… (more)

▼ Apoptosis is a distinct form of cell death that is characterised by specific morphological and biochemical markers, such as chromatin condensation and internucleosomal DNA cleavage. This type of cell death is evolutionarily conserved in higher eukaryotes. Homologues of the main apoptosis regulators, such as the Bcl-2 family of proteins and caspases, have been found in multicellular organisms. However, homologues of these proteins have not been found in the unicellular organism Saccharomyces cerevisiae, although in certain circumstances S. cerevisiae will exhibit features of apoptosis. In this project, we developed in vitro systems to explore the relationship between mammalian apoptosis and any similar mechanism that may be present in yeast. Components derived from yeast and mammalian cells were incubated together in vitro and assessed for the activation of apoptosis. Rat cytochrome c activates apoptosis in mammalian cell-free extracts (human neuroblastoma SY5Y cells). Internucleosomal DNA cleavage was observed in S. cerevisiae spheroplasts when they were incubated in mammalian cell-free extracts activated by rat cytochrome c. Although yeast cytochrome c is similar to rat cytochrome c, it failed to induce apoptosis in mammalian cell-free extracts. Yeast cytosol caused internucleosomal DNA cleavage in PCl2 nuclei. This cleavage was enhanced by rat cytochrome c and was mostly inhibited by the caspase inhibitor DEVD-CHO, but only in the presence of rat cytochrome c. Yeast cytosol did not cause chromatin condensation in PCl2 nuclei or cleavage of Parp (a downstream caspase substrate). Yeast cytosol was therefore unable to induce apoptosis in PCl2 nuclei. Mitochondria play a central role in most forms of mammalian apoptosis. We developed a cell-free system in which we could examine the role of mitochondria in apoptosis. We attempted to activate apoptosis in SY5Y cytosol by the addition of mitochondria subjected to rupture-inducing treatment, with limited success. However, we found that mitochondria purified from healthy SY5Y cells protected PCl2 nuclei from undergoing apoptosis in vitro.

Subjects/Keywords: Apoptosis

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

APA (6^th Edition):

Haywood, A. F. M. (2000). In vitro systems to study the relationship between apoptosis in multicellular organisms and yeast. (Masters Thesis). Massey University. Retrieved from http://hdl.handle.net/10179/12688

Chicago Manual of Style (16^th Edition):

Haywood, Annika Fleur Margo. “In vitro systems to study the relationship between apoptosis in multicellular organisms and yeast.” 2000. Masters Thesis, Massey University. Accessed January 24, 2021. http://hdl.handle.net/10179/12688.

MLA Handbook (7^th Edition):

Haywood, Annika Fleur Margo. “In vitro systems to study the relationship between apoptosis in multicellular organisms and yeast.” 2000. Web. 24 Jan 2021.

Vancouver:

Haywood AFM. In vitro systems to study the relationship between apoptosis in multicellular organisms and yeast. [Internet] [Masters thesis]. Massey University; 2000. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10179/12688.

Council of Science Editors:

Haywood AFM. In vitro systems to study the relationship between apoptosis in multicellular organisms and yeast. [Masters Thesis]. Massey University; 2000. Available from: http://hdl.handle.net/10179/12688

University of Texas – Austin

13. Cohn, Jesse Aaron. Characterizing transcriptional and morphological consequences of long-term activity in a tonic C. elegans sensory neuron.

Degree: PhD, Cell and Molecular Biology, 2019, University of Texas – Austin

URL: http://dx.doi.org/10.26153/tsw/2093

► Two ways that long-term neural activity can affect a neuron are by altering the genes that the cell expresses, and by reshaping cellular architecture. These… (more)

▼ Two ways that long-term neural activity can affect a neuron are by altering the genes that the cell expresses, and by reshaping cellular architecture. These basic changes are imperative for neurons to continue to properly engage with their environment and with other cells. This dissertation outlines the use of the roundworm Caenorhabditis elegans as a tool to interrogate the effects of long-term activity on a tonic sensory neuron, specifically the primary oxygen-sensing neuron pair in the worm termed URXL/R. Described here are two cell-autonomous consequences of this prolonged sensory activity: the novel non-apoptotic transcription of a gene that typically causes cell death, and the growth of branches at the sensory ending of the neuron pair. Each of these projects sets the foundation for future work toward understanding the consequences of and genes that underlie these changes. Chapter Two focuses on the novel transcription of the pro-apoptotic gene egl-1 in URX in adults. EGL-1 is a member of the BH3-only family of proteins known for their role in inducing cell death. In C. elegans, egl-1 is normally transcribed in cells fated to die during development. Through the use of a forward genetic screen and environmental manipulations, we show that egl-1 is also transcribed in the URX neuron pair in adults as a result of prolonged oxygen sensation, and that this transcription does not induce cell death. We show that egl-1 transcription does not appear to contribute to any known URX function, and that its transcription is controlled by at least three pathways: one an unknown oxygen-dependent pathway, the other two comprised of the conserved protein kinases Protein Kinase G (PKG) and Salt-Inducible Kinase (SIK). Several BH3-only proteins in humans are expressed in the post-developmental nervous system without causing apoptosis, though their roles in these cells are largely mysterious, thus URX might provide a useful system for understanding aspects of non-apoptotic expression of BH3-only proteins in adult animals. In Chapter Three, we report that long-term exposure to surface-level oxygen (21%) causes the URX neuron pair to grow complex branching at its sensory dendritic ending. By studying mutants, we show that the oxygen sensory pathway is necessary for branch growth, and that the secondary messengers cGMP and calcium are both involved in this process. We also find that these dendritic branches are likely microtubule based, but do not contain a primary component of the oxygen sensation pathway. Accordingly, we also show that branch length and complexity do not correlate with changes in the cellular physiological or organismal behavioral response to oxygen. Therefore, though branches are grown in response to long-term oxygen exposure, they are unlikely to be involved in oxygen sensation per se. Finally, in Chapter Four, I suggest interesting future directions for each project and summarize my final thoughts. Advisors/Committee Members: Pierce-Shimomura, Jonathan T. (advisor), Atkinson, Nigel (committee member), Mihic, John (committee member), Bratton, Shawn (committee member), Eberhart, Johann (committee member).

Subjects/Keywords: Apoptosis; Plasticity

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APA (6^th Edition):

Cohn, J. A. (2019). Characterizing transcriptional and morphological consequences of long-term activity in a tonic C. elegans sensory neuron. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/2093

Chicago Manual of Style (16^th Edition):

Cohn, Jesse Aaron. “Characterizing transcriptional and morphological consequences of long-term activity in a tonic C. elegans sensory neuron.” 2019. Doctoral Dissertation, University of Texas – Austin. Accessed January 24, 2021. http://dx.doi.org/10.26153/tsw/2093.

MLA Handbook (7^th Edition):

Cohn, Jesse Aaron. “Characterizing transcriptional and morphological consequences of long-term activity in a tonic C. elegans sensory neuron.” 2019. Web. 24 Jan 2021.

Vancouver:

Cohn JA. Characterizing transcriptional and morphological consequences of long-term activity in a tonic C. elegans sensory neuron. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2019. [cited 2021 Jan 24]. Available from: http://dx.doi.org/10.26153/tsw/2093.

Council of Science Editors:

Cohn JA. Characterizing transcriptional and morphological consequences of long-term activity in a tonic C. elegans sensory neuron. [Doctoral Dissertation]. University of Texas – Austin; 2019. Available from: http://dx.doi.org/10.26153/tsw/2093

14. Tagawa, Tsuyoshi. Sevoflurane in combination with propofol， not thiopental， induces a more robust neuroapoptosis than sevoflurane alone in the neonatal mouse brain.

Degree: 博士 (医学), 2017, Mie University / 三重大学

URL: http://hdl.handle.net/10076/14716

►

Purpose Sevoflurane is the most widely used volatile anesthetic of general anesthesia. In children and neonates, it is commonly used alone or in combination with… (more)

Subjects/Keywords: Sevoflurane; Apoptosis; Children

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APA (6^th Edition):

Tagawa, T. (2017). Sevoflurane in combination with propofol， not thiopental， induces a more robust neuroapoptosis than sevoflurane alone in the neonatal mouse brain. (Thesis). Mie University / 三重大学. Retrieved from http://hdl.handle.net/10076/14716

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):

Tagawa, Tsuyoshi. “Sevoflurane in combination with propofol， not thiopental， induces a more robust neuroapoptosis than sevoflurane alone in the neonatal mouse brain.” 2017. Thesis, Mie University / 三重大学. Accessed January 24, 2021. http://hdl.handle.net/10076/14716.

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

MLA Handbook (7^th Edition):

Tagawa, Tsuyoshi. “Sevoflurane in combination with propofol， not thiopental， induces a more robust neuroapoptosis than sevoflurane alone in the neonatal mouse brain.” 2017. Web. 24 Jan 2021.

Vancouver:

Tagawa T. Sevoflurane in combination with propofol， not thiopental， induces a more robust neuroapoptosis than sevoflurane alone in the neonatal mouse brain. [Internet] [Thesis]. Mie University / 三重大学; 2017. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10076/14716.

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

Council of Science Editors:

Tagawa T. Sevoflurane in combination with propofol， not thiopental， induces a more robust neuroapoptosis than sevoflurane alone in the neonatal mouse brain. [Thesis]. Mie University / 三重大学; 2017. Available from: http://hdl.handle.net/10076/14716

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

15. Nicholls, Samantha Elizabeth Bernard. Development and Characterization of Caspase Activatable GFP and a Family of Fluorescent Reporters.

Degree: PhD, Chemistry, 2013, U of Massachusetts : PhD

URL: https://scholarworks.umass.edu/open_access_dissertations/721

► The cellular process of programmed cell death, or apoptosis, is critical in homeostasis and development. In addition it's misfunction is implicated in an array… (more)

Subjects/Keywords: apoptosis; GFP; Chemistry

12 more images…

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APA (6^th Edition):

Nicholls, S. E. B. (2013). Development and Characterization of Caspase Activatable GFP and a Family of Fluorescent Reporters. (Doctoral Dissertation). U of Massachusetts : PhD. Retrieved from https://scholarworks.umass.edu/open_access_dissertations/721

Chicago Manual of Style (16^th Edition):

Nicholls, Samantha Elizabeth Bernard. “Development and Characterization of Caspase Activatable GFP and a Family of Fluorescent Reporters.” 2013. Doctoral Dissertation, U of Massachusetts : PhD. Accessed January 24, 2021. https://scholarworks.umass.edu/open_access_dissertations/721.

MLA Handbook (7^th Edition):

Nicholls, Samantha Elizabeth Bernard. “Development and Characterization of Caspase Activatable GFP and a Family of Fluorescent Reporters.” 2013. Web. 24 Jan 2021.

Vancouver:

Nicholls SEB. Development and Characterization of Caspase Activatable GFP and a Family of Fluorescent Reporters. [Internet] [Doctoral dissertation]. U of Massachusetts : PhD; 2013. [cited 2021 Jan 24]. Available from: https://scholarworks.umass.edu/open_access_dissertations/721.

Council of Science Editors:

Nicholls SEB. Development and Characterization of Caspase Activatable GFP and a Family of Fluorescent Reporters. [Doctoral Dissertation]. U of Massachusetts : PhD; 2013. Available from: https://scholarworks.umass.edu/open_access_dissertations/721

University of Alberta

16. Kapty, Janice S. Evaluation of Phosphatidylserine-Binding Peptides Radiolabeled with Fluorine 18 for in vivo Imaging of Apoptosis.

Degree: PhD, Department of Oncology, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/bc386j75x

► We currently do not have a clinical method to directly assess apoptosis induced by cancer therapies. Phosphatidylserine (PS) is an attractive target for imaging apoptosis… (more)

▼ We currently do not have a clinical method to directly assess apoptosis induced by cancer therapies. Phosphatidylserine (PS) is an attractive target for imaging apoptosis since it is on the exterior of the apoptotic cells and PS externalization is an early marker of apoptosis. PS-binding peptides are an attractive option for developing an imaging probe to detect apoptosis using positron emission tomography. In this study we evaluated binding characteristics of PS-binding peptides for ability to bind to PS, radiolabeled PS-binding peptides with fluorine-18, and performed in vitro and in vivo analysis of 18F radiolabeled PS-binding peptides including biodistribution analysis and dynamic PET imaging in a murine tumor model of apoptosis. Four peptides were evaluated for PS binding characteristics using a plate based assay system, a liposome mimic of cell membrane PS presentation, and a cell assay of apoptosis. The results indicate that all four peptides bind to PS and are specific to apoptotic cells. The widely used 18F prosthetic group N-succinimidyl-4-[18F]fluorobenzoate ([18F]SFB) and the recently developed N-[6-(4-[18F]fluorobenzylidene) aminooxyhexyl]maleimide ([18F]FBAM) were investigated for radiolabeling of two representative phosphatidylserine-binding peptides. The prosthetic groups were compared with respect to required reaction conditions for optimum labeling, radiolabeling yield and chemoselectivity. The N-terminus labeled product produced by reaction of [18F]SFB with binding peptide LIKKPF was produced in 18% radiochemical yield while no N-terminus labeled product could be isolated following [18F]SFB reaction with PDGLSR. When the peptides were modified by addition of a cysteine residue at the N-terminus they provided almost quantitative radiochemical yields with [18F]FBAM. Results indicate that for the peptides in this study, [18F]FBAM is a more useful prosthetic group compared to [18F]SFB due to its excellent chemo-selectivity and high radiochemical yield. We report the first experiments where PS-binding peptides were radiolabeled with 18F and evaluated as possible radiotracers for imaging apoptosis. We investigated two radio-peptides ([18F]FBAM-CLIKKPF and [18F]FBAM-CPGDLSR) in vitro and in vivo as possible radiotracers able to bind to apoptotic cells and to image chemotherapy induced apoptosis.

Subjects/Keywords: phosphatidylserine; apoptosis; peptides

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

APA (6^th Edition):

Kapty, J. S. (2012). Evaluation of Phosphatidylserine-Binding Peptides Radiolabeled with Fluorine 18 for in vivo Imaging of Apoptosis. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/bc386j75x

Chicago Manual of Style (16^th Edition):

Kapty, Janice S. “Evaluation of Phosphatidylserine-Binding Peptides Radiolabeled with Fluorine 18 for in vivo Imaging of Apoptosis.” 2012. Doctoral Dissertation, University of Alberta. Accessed January 24, 2021. https://era.library.ualberta.ca/files/bc386j75x.

MLA Handbook (7^th Edition):

Kapty, Janice S. “Evaluation of Phosphatidylserine-Binding Peptides Radiolabeled with Fluorine 18 for in vivo Imaging of Apoptosis.” 2012. Web. 24 Jan 2021.

Vancouver:

Kapty JS. Evaluation of Phosphatidylserine-Binding Peptides Radiolabeled with Fluorine 18 for in vivo Imaging of Apoptosis. [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2021 Jan 24]. Available from: https://era.library.ualberta.ca/files/bc386j75x.

Council of Science Editors:

Kapty JS. Evaluation of Phosphatidylserine-Binding Peptides Radiolabeled with Fluorine 18 for in vivo Imaging of Apoptosis. [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/bc386j75x

17. Tamura, Akihiro. Accelerated apoptosis of peripheral blood monocytes in Cebpb-deficient mice : Cebpb欠損マウスの末梢血における単球アポトーシスの亢進.

Degree: 博士(医学), 2016, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/215389 ; http://dx.doi.org/10.14989/doctor.k19563

Final publication is available at http://www.sciencedirect.com/science/article/pii/S0006291X1530276X

新制・課程博士

甲第19563号

医博第4070号

Subjects/Keywords: Cebpb; monocytes; apoptosis

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APA (6^th Edition):

Tamura, A. (2016). Accelerated apoptosis of peripheral blood monocytes in Cebpb-deficient mice : Cebpb欠損マウスの末梢血における単球アポトーシスの亢進. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/215389 ; http://dx.doi.org/10.14989/doctor.k19563

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):

Tamura, Akihiro. “Accelerated apoptosis of peripheral blood monocytes in Cebpb-deficient mice : Cebpb欠損マウスの末梢血における単球アポトーシスの亢進.” 2016. Thesis, Kyoto University / 京都大学. Accessed January 24, 2021. http://hdl.handle.net/2433/215389 ; http://dx.doi.org/10.14989/doctor.k19563.

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

MLA Handbook (7^th Edition):

Tamura, Akihiro. “Accelerated apoptosis of peripheral blood monocytes in Cebpb-deficient mice : Cebpb欠損マウスの末梢血における単球アポトーシスの亢進.” 2016. Web. 24 Jan 2021.

Vancouver:

Tamura A. Accelerated apoptosis of peripheral blood monocytes in Cebpb-deficient mice : Cebpb欠損マウスの末梢血における単球アポトーシスの亢進. [Internet] [Thesis]. Kyoto University / 京都大学; 2016. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2433/215389 ; http://dx.doi.org/10.14989/doctor.k19563.

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

Council of Science Editors:

Tamura A. Accelerated apoptosis of peripheral blood monocytes in Cebpb-deficient mice : Cebpb欠損マウスの末梢血における単球アポトーシスの亢進. [Thesis]. Kyoto University / 京都大学; 2016. Available from: http://hdl.handle.net/2433/215389 ; http://dx.doi.org/10.14989/doctor.k19563

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

University of Manchester

18. King, Louise. Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity.

Degree: 2019, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:322785

► Apoptotic sensitivity between individual cells within a population is varied and the molecular basis of this variation is unclear. Bcl-2 family proteins are the central… (more)

Subjects/Keywords: Apoptosis; Bcl-2

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APA (6^th Edition):

King, L. (2019). Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:322785

Chicago Manual of Style (16^th Edition):

King, Louise. “Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity.” 2019. Doctoral Dissertation, University of Manchester. Accessed January 24, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:322785.

MLA Handbook (7^th Edition):

King, Louise. “Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity.” 2019. Web. 24 Jan 2021.

Vancouver:

King L. Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity. [Internet] [Doctoral dissertation]. University of Manchester; 2019. [cited 2021 Jan 24]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:322785.

Council of Science Editors:

King L. Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity. [Doctoral Dissertation]. University of Manchester; 2019. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:322785

Wake Forest University

19. ZHANG, KAILONG. SUSCEPTIBILITY OF GLIOBLASTOMA CELLS TO ONCOLYTIC VESICULAR STOMATITIS VIRUS.

Degree: 2020, Wake Forest University

URL: http://hdl.handle.net/10339/96816

► Glioblastoma (GBM) is the deadliest type of brain tumor with very poor survival rates. Thus, GBM patients are candidates for novel therapies such as oncolytic… (more)

Subjects/Keywords: Apoptosis-regulating genes

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APA (6^th Edition):

ZHANG, K. (2020). SUSCEPTIBILITY OF GLIOBLASTOMA CELLS TO ONCOLYTIC VESICULAR STOMATITIS VIRUS. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/96816

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):

ZHANG, KAILONG. “SUSCEPTIBILITY OF GLIOBLASTOMA CELLS TO ONCOLYTIC VESICULAR STOMATITIS VIRUS.” 2020. Thesis, Wake Forest University. Accessed January 24, 2021. http://hdl.handle.net/10339/96816.

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

MLA Handbook (7^th Edition):

ZHANG, KAILONG. “SUSCEPTIBILITY OF GLIOBLASTOMA CELLS TO ONCOLYTIC VESICULAR STOMATITIS VIRUS.” 2020. Web. 24 Jan 2021.

Vancouver:

ZHANG K. SUSCEPTIBILITY OF GLIOBLASTOMA CELLS TO ONCOLYTIC VESICULAR STOMATITIS VIRUS. [Internet] [Thesis]. Wake Forest University; 2020. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10339/96816.

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

Council of Science Editors:

ZHANG K. SUSCEPTIBILITY OF GLIOBLASTOMA CELLS TO ONCOLYTIC VESICULAR STOMATITIS VIRUS. [Thesis]. Wake Forest University; 2020. Available from: http://hdl.handle.net/10339/96816

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

20. Bennett, Ailsa. Exploiting mitosis to improve anti-cancer strategies.

Degree: PhD, 2017, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/exploiting-mitosis-to-improve-anticancer-strategies(b29182a1-2f37-47cb-8dc5-cbef76786dd2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703036

► Antimitotics are used in cancer chemotherapy for the treatment of cancers such as breast, ovarian, lung and prostate. Despite the success of agents such as… (more)

▼ Antimitotics are used in cancer chemotherapy for the treatment of cancers such as breast, ovarian, lung and prostate. Despite the success of agents such as Taxol, problems have emerged such as side effects, resistance and the lack of ability to predict patient responsiveness. As a result, a class of second-generation inhibitors have been developed with the aim to overcome or improve these issues. Such inhibitors target proteins and kinases involved in the control of mitosis and the cell cycle. However, these have yet to be clinically successful and therefore, this highlights the requirement for an increased understanding of the mitotic process and how antimitotics truly elicit their action. Reasons for the lack of efficacy may be due to the absence of biomarkers to stratify patients into those likely to respond to treatment. It may also be possible that other targets are required. Our understanding of the action of antimitotics is therefore paramount to improving cancer chemotherapy. By exploiting mitosis and understanding what happens when mitosis goes wrong, this thesis aims to explore new and improved methods of targeting, but also proposes to improve our understanding of the consequences of aberrant mitoses through the use of small molecule inhibitors. In the first case the thesis investigated the targeting of the spindle checkpoint protein Bub1 with 2OH-BNPP1, where previously inhibitors against the kinase were not acknowledged. However the inhibitor used was not effective in cells and therefore further experimentation was not possible. Secondly, to explore the consequences of mitotic perturbation, an assay to explore aneuploidy was established. To do this a Cenp-E inhibitor GSK923295 was synthesised, which was subsequently used in assays with the Mps1 inhibitor AZ3146 to generate aneuploidy progeny. The Cenp-E inhibitor was then used as an antimitotic agent in the final chapter to explore the mechanism of action of mitotic blockers and drivers often used in cell biology and clinical settings. Evidence suggests that the intrinsic apoptotic pathway is activated upon exposure to these agents. With focus on this pathway, the importance of Bcl-xL on cell survival was considered, revealing particular importance in the post-mitotic response. Ultimately, this thesis should contribute to devising new and improved anti-cancer strategies.

Subjects/Keywords: 616.99; mitosis; apoptosis

10 more images…

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APA (6^th Edition):

Bennett, A. (2017). Exploiting mitosis to improve anti-cancer strategies. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/exploiting-mitosis-to-improve-anticancer-strategies(b29182a1-2f37-47cb-8dc5-cbef76786dd2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703036

Chicago Manual of Style (16^th Edition):

Bennett, Ailsa. “Exploiting mitosis to improve anti-cancer strategies.” 2017. Doctoral Dissertation, University of Manchester. Accessed January 24, 2021. https://www.research.manchester.ac.uk/portal/en/theses/exploiting-mitosis-to-improve-anticancer-strategies(b29182a1-2f37-47cb-8dc5-cbef76786dd2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703036.

MLA Handbook (7^th Edition):

Bennett, Ailsa. “Exploiting mitosis to improve anti-cancer strategies.” 2017. Web. 24 Jan 2021.

Vancouver:

Bennett A. Exploiting mitosis to improve anti-cancer strategies. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2021 Jan 24]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/exploiting-mitosis-to-improve-anticancer-strategies(b29182a1-2f37-47cb-8dc5-cbef76786dd2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703036.

Council of Science Editors:

Bennett A. Exploiting mitosis to improve anti-cancer strategies. [Doctoral Dissertation]. University of Manchester; 2017. Available from: https://www.research.manchester.ac.uk/portal/en/theses/exploiting-mitosis-to-improve-anticancer-strategies(b29182a1-2f37-47cb-8dc5-cbef76786dd2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703036

Hong Kong University of Science and Technology

21. Wu, Weiwei. S-nitrosylation of XIAP at Cys213 of BIR2 domain impairs XIAP's anti-caspase-3 activity.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-62654 ; https://doi.org/10.14711/thesis-b1254332 ; http://repository.ust.hk/ir/bitstream/1783.1-62654/1/th_redirect.html

► XIAP is the most widely expressed IAP and plays an important role in regulating cell survival. XIAP contains three baculoviral IAP repeats (BIRs) domain and… (more)

Subjects/Keywords: Apoptosis ; Parkinson's disease

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APA (6^th Edition):

Wu, W. (2013). S-nitrosylation of XIAP at Cys213 of BIR2 domain impairs XIAP's anti-caspase-3 activity. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-62654 ; https://doi.org/10.14711/thesis-b1254332 ; http://repository.ust.hk/ir/bitstream/1783.1-62654/1/th_redirect.html

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

Chicago Manual of Style (16^th Edition):

Wu, Weiwei. “S-nitrosylation of XIAP at Cys213 of BIR2 domain impairs XIAP's anti-caspase-3 activity.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed January 24, 2021. http://repository.ust.hk/ir/Record/1783.1-62654 ; https://doi.org/10.14711/thesis-b1254332 ; http://repository.ust.hk/ir/bitstream/1783.1-62654/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Wu, Weiwei. “S-nitrosylation of XIAP at Cys213 of BIR2 domain impairs XIAP's anti-caspase-3 activity.” 2013. Web. 24 Jan 2021.

Vancouver:

Wu W. S-nitrosylation of XIAP at Cys213 of BIR2 domain impairs XIAP's anti-caspase-3 activity. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Jan 24]. Available from: http://repository.ust.hk/ir/Record/1783.1-62654 ; https://doi.org/10.14711/thesis-b1254332 ; http://repository.ust.hk/ir/bitstream/1783.1-62654/1/th_redirect.html.

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

Council of Science Editors:

Wu W. S-nitrosylation of XIAP at Cys213 of BIR2 domain impairs XIAP's anti-caspase-3 activity. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-62654 ; https://doi.org/10.14711/thesis-b1254332 ; http://repository.ust.hk/ir/bitstream/1783.1-62654/1/th_redirect.html

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

22. Doan, Hung 1982-. Studies on Fortilin-Prohibitin Interaction.

Degree: Doctoral, Biochemistry, 2013, The University of Texas Medical Branch at Galveston

URL: http://hdl.handle.net/2152.3/541

► Abstract: Apoptosis, programmed cell death, is a tightly regulated process that occurs in development, in tissue maintenance and turnover, and in regulating the immune system.… (more)

Subjects/Keywords: Apoptosis; protein interactions

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APA (6^th Edition):

Doan, H. 1. (2013). Studies on Fortilin-Prohibitin Interaction. (Doctoral Dissertation). The University of Texas Medical Branch at Galveston. Retrieved from http://hdl.handle.net/2152.3/541

Chicago Manual of Style (16^th Edition):

Doan, Hung 1982-. “Studies on Fortilin-Prohibitin Interaction.” 2013. Doctoral Dissertation, The University of Texas Medical Branch at Galveston. Accessed January 24, 2021. http://hdl.handle.net/2152.3/541.

MLA Handbook (7^th Edition):

Doan, Hung 1982-. “Studies on Fortilin-Prohibitin Interaction.” 2013. Web. 24 Jan 2021.

Vancouver:

Doan H1. Studies on Fortilin-Prohibitin Interaction. [Internet] [Doctoral dissertation]. The University of Texas Medical Branch at Galveston; 2013. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2152.3/541.

Council of Science Editors:

Doan H1. Studies on Fortilin-Prohibitin Interaction. [Doctoral Dissertation]. The University of Texas Medical Branch at Galveston; 2013. Available from: http://hdl.handle.net/2152.3/541

University of Arizona

23. Monasky, Ross Calvin. The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence .

Degree: 2018, University of Arizona

URL: http://hdl.handle.net/10150/628172

► Enteropathogenic Escherichia coli (EPEC) is a leading cause of infantile diarrhea, particularly in developing countries. EPEC belongs to the attaching and effacing (A/E) family of… (more)

Subjects/Keywords: Apoptosis; EPEC; siRNA

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APA (6^th Edition):

Monasky, R. C. (2018). The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence . (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/628172

Chicago Manual of Style (16^th Edition):

Monasky, Ross Calvin. “The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence .” 2018. Masters Thesis, University of Arizona. Accessed January 24, 2021. http://hdl.handle.net/10150/628172.

MLA Handbook (7^th Edition):

Monasky, Ross Calvin. “The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence .” 2018. Web. 24 Jan 2021.

Vancouver:

Monasky RC. The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence . [Internet] [Masters thesis]. University of Arizona; 2018. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10150/628172.

Council of Science Editors:

Monasky RC. The Role of EspH and Host Cell Proteins in Enteropathogenic Escherichia Coli-Induced Cell Death and Virulence . [Masters Thesis]. University of Arizona; 2018. Available from: http://hdl.handle.net/10150/628172

University of Waterloo

24. Mitchell, Andrew. Morphological and Apoptotic Alterations in Skeletal Muscle of Mice Deficient in Apoptosis Repressor with Caspase Recruitment Domain.

Degree: 2012, University of Waterloo

URL: http://hdl.handle.net/10012/6434

► Altered apoptotic signaling in skeletal muscle has been observed in a number of disease states associated with skeletal muscle atrophy. Therefore, understanding the mechanisms that… (more)

▼ Altered apoptotic signaling in skeletal muscle has been observed in a number of disease states associated with skeletal muscle atrophy. Therefore, understanding the mechanisms that lead to increased skeletal muscle apoptosis may help to prevent the atrophy associated with various diseases. Apoptosis repressor with caspase recruitment domain (ARC) is a potent anti-apoptotic protein that is able to inhibit apoptosis mediated by both the death-receptor and mitochondrial pathways. In addition, ARC has a unique distribution pattern and is highly expressed in terminally differentiated tissue such as skeletal muscle. To characterize the role of ARC in skeletal muscle morphology and apoptosis, soleus and plantaris muscles of 18 week-old ARC-deficient mice were excised and compared to those of age-matched wild-type littermates. While no differences were seen in muscle weights between genotypes, in the ARC KO animals, the cross-sectional area (CSA) of the soleus was smaller, while the CSA of the plantaris was larger. With respect to fiber type distribution, both muscles demonstrated a shift towards a faster myosin heavy chain expression pattern. For example, soleus muscles of ARC KO animals had significantly less type I fibers and more IIa fibers, while plantaris muscles had significantly less type IIa fibers, and more IIb fibers. In ARC KO animals, type I and IIa fibers were significantly smaller in the soleus, while type IIb fibers were larger in the plantaris. DNA fragmentation (a hallmark of apoptosis) was increased in the soleus, but not plantaris muscles of ARC KO animals. Surprisingly, activity of the proteolytic enzymes caspase-2, -3, -8, and -9, as well as calpains, was not different in either soleus or plantaris muscles. To determine whether a lack of ARC protein affects apoptotic signaling in skeletal muscle, the total expression of pro- and anti-apoptotic proteins were also assessed. In the soleus, no changes were observed in whole tissue AIF, cytochrome c, EndoG, and Smac. In the plantaris, there was no change in total muscle AIF; however, there were trends towards decreased cytochrome c, and increased Smac, as well as a significant decrease in EndoG ARC KO animals. No changes were observed in Bcl-2 and XIAP in the soleus; however, there were significant reductions in FLIP(s) and HSP70 content. In the plantaris, no changes were observed in anti-apoptotic protein content. Subcellular fractionation of red quadriceps for ARC KO mice revealed an increased Bax:Bcl-2 ratio in the isolated mitochondrial fractions. Furthermore, in cytosolic fractions of red quadriceps, AIF protein content was significantly increased in ARC KO animals. Conversely, no changes in apoptotic-related protein content were observed in any fractions from white quadriceps between groups. In agreement with these findings, isolated mitochondria from ARC-deficient animals were more susceptible to calcium induced swelling, as well as membrane potential loss compared to controls. Taken together, these results suggest that in slow-oxidative skeletal…

Subjects/Keywords: Skeletal Muscle; Apoptosis

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APA (6^th Edition):

Mitchell, A. (2012). Morphological and Apoptotic Alterations in Skeletal Muscle of Mice Deficient in Apoptosis Repressor with Caspase Recruitment Domain. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/6434

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):

Mitchell, Andrew. “Morphological and Apoptotic Alterations in Skeletal Muscle of Mice Deficient in Apoptosis Repressor with Caspase Recruitment Domain.” 2012. Thesis, University of Waterloo. Accessed January 24, 2021. http://hdl.handle.net/10012/6434.

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

MLA Handbook (7^th Edition):

Mitchell, Andrew. “Morphological and Apoptotic Alterations in Skeletal Muscle of Mice Deficient in Apoptosis Repressor with Caspase Recruitment Domain.” 2012. Web. 24 Jan 2021.

Vancouver:

Mitchell A. Morphological and Apoptotic Alterations in Skeletal Muscle of Mice Deficient in Apoptosis Repressor with Caspase Recruitment Domain. [Internet] [Thesis]. University of Waterloo; 2012. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10012/6434.

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

Council of Science Editors:

Mitchell A. Morphological and Apoptotic Alterations in Skeletal Muscle of Mice Deficient in Apoptosis Repressor with Caspase Recruitment Domain. [Thesis]. University of Waterloo; 2012. Available from: http://hdl.handle.net/10012/6434

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

University of Manchester

25. King, Louise. Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity.

Degree: PhD, 2020, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/understanding-how-the-bcl2-interactome-contributes-to-apoptotic-sensitivity(5883268b-b097-4a40-b7c8-d10f72a6d38b).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799470

► Apoptotic sensitivity between individual cells within a population is varied and the molecular basis of this variation is unclear. Bcl-2 family proteins are the central… (more)

Subjects/Keywords: Apoptosis; Bcl-2

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APA (6^th Edition):

King, L. (2020). Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/understanding-how-the-bcl2-interactome-contributes-to-apoptotic-sensitivity(5883268b-b097-4a40-b7c8-d10f72a6d38b).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799470

Chicago Manual of Style (16^th Edition):

King, Louise. “Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity.” 2020. Doctoral Dissertation, University of Manchester. Accessed January 24, 2021. https://www.research.manchester.ac.uk/portal/en/theses/understanding-how-the-bcl2-interactome-contributes-to-apoptotic-sensitivity(5883268b-b097-4a40-b7c8-d10f72a6d38b).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799470.

MLA Handbook (7^th Edition):

King, Louise. “Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity.” 2020. Web. 24 Jan 2021.

Vancouver:

King L. Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity. [Internet] [Doctoral dissertation]. University of Manchester; 2020. [cited 2021 Jan 24]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/understanding-how-the-bcl2-interactome-contributes-to-apoptotic-sensitivity(5883268b-b097-4a40-b7c8-d10f72a6d38b).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799470.

Council of Science Editors:

King L. Understanding how the Bcl-2 interactome contributes to apoptotic sensitivity. [Doctoral Dissertation]. University of Manchester; 2020. Available from: https://www.research.manchester.ac.uk/portal/en/theses/understanding-how-the-bcl2-interactome-contributes-to-apoptotic-sensitivity(5883268b-b097-4a40-b7c8-d10f72a6d38b).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799470

Loyola University Chicago

26. Figueroa, Iris Teresa. The Role of Pidd Protein in Adenoviral Induction of Apoptosis.

Degree: MS, Microbiology and Immunology, 2015, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_theses/3132

► The Adenovirus E1A gene sensitizes cells to genetic insults and apoptosis, most notably in response to cytotoxic factors from innate immune cells. The mechanisms… (more)

Subjects/Keywords: Adenovirus; Apoptosis; Virology

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APA (6^th Edition):

Figueroa, I. T. (2015). The Role of Pidd Protein in Adenoviral Induction of Apoptosis. (Thesis). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_theses/3132

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):

Figueroa, Iris Teresa. “The Role of Pidd Protein in Adenoviral Induction of Apoptosis.” 2015. Thesis, Loyola University Chicago. Accessed January 24, 2021. https://ecommons.luc.edu/luc_theses/3132.

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

MLA Handbook (7^th Edition):

Figueroa, Iris Teresa. “The Role of Pidd Protein in Adenoviral Induction of Apoptosis.” 2015. Web. 24 Jan 2021.

Vancouver:

Figueroa IT. The Role of Pidd Protein in Adenoviral Induction of Apoptosis. [Internet] [Thesis]. Loyola University Chicago; 2015. [cited 2021 Jan 24]. Available from: https://ecommons.luc.edu/luc_theses/3132.

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

Council of Science Editors:

Figueroa IT. The Role of Pidd Protein in Adenoviral Induction of Apoptosis. [Thesis]. Loyola University Chicago; 2015. Available from: https://ecommons.luc.edu/luc_theses/3132

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

University of Georgia

27. Harrison, Laura. Occurrence of apoptosis in lymphoid tissues from chickens acutely infected with strains of Newcastle disease of varying virulence.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/25479

► Newcastle Disease Virus (NDV) poses many threats to the poultry industry. Virulence of different strains varies widely and creates a wide range of disease manifestations.… (more)

Subjects/Keywords: Apoptosis; Immunohistochemistry; Caspase

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APA (6^th Edition):

Harrison, L. (2014). Occurrence of apoptosis in lymphoid tissues from chickens acutely infected with strains of Newcastle disease of varying virulence. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/25479

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):

Harrison, Laura. “Occurrence of apoptosis in lymphoid tissues from chickens acutely infected with strains of Newcastle disease of varying virulence.” 2014. Thesis, University of Georgia. Accessed January 24, 2021. http://hdl.handle.net/10724/25479.

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

MLA Handbook (7^th Edition):

Harrison, Laura. “Occurrence of apoptosis in lymphoid tissues from chickens acutely infected with strains of Newcastle disease of varying virulence.” 2014. Web. 24 Jan 2021.

Vancouver:

Harrison L. Occurrence of apoptosis in lymphoid tissues from chickens acutely infected with strains of Newcastle disease of varying virulence. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10724/25479.

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

Council of Science Editors:

Harrison L. Occurrence of apoptosis in lymphoid tissues from chickens acutely infected with strains of Newcastle disease of varying virulence. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/25479

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

University of Montana

28. Lei, Haotian. Modulation of cytochrome c’s peroxidase activity by Ω-loops C and D in monomers and dimers.

Degree: PhD, 2019, University of Montana

URL: https://scholarworks.umt.edu/etd/11436

► Mitochondrial cytochrome c is a heme containing protein with flexible heme ligation. Cytochrome c in its native state with Met80 bound to the heme… (more)

▼ Mitochondrial cytochrome c is a heme containing protein with flexible heme ligation. Cytochrome c in its native state with Met80 bound to the heme is an electron shuttle in the electron transport chain. Under apoptotic stimuli, cytochrome c oxidizes the mitochondrial lipid cardiolipin, leading to the release of pro-apoptotic factors into the cytoplasm. To oxidize cardiolipin, Met80 in Ω-loop D must be dissociated from the heme iron, which allows cytochrome c to obtain access to alternative conformers. Two segments of cytochrome c, namely Ω-loops C and D, have been suggested to be important in regulating the dissociation of Met80. Unlike most residues in Ω-loop D, positions 81 and 83 have evolve to more sterically demanding residues in higher eukaryotes, leading to a 30-fold decrease in peroxidase activity. We study the effects of evolutionary substitutions at positions 81 and 83 in both human and yeast iso-1 cytochrome c. The side chain volumes at positions 81 and 83 do not fully account for the difference in the peroxidase activity between human and yeast iso-1 cytochrome c, indicating that other segments of cytochrome c contribute significantly to the low intrinsic peroxidase activity of human cytochrome c. All naturally occurring disease-related mutations, namely G41S, Y48H, and A51V, of human cytochrome c, which contain abnormally high peroxidase activity, are located in Ω-loop C, suggesting that Ω-loop C is an important modulator of the peroxidase activity. Investigating the disease mutation, A51V, in human cytochrome c significantly destabilizes Ω-loop D, resulting in enhancement of peroxidase activity. Dimeric cytochrome c with an open heme coordination site has been suggested to mediate the peroxidase activity in the early stage of apoptosis. We have recently solved a structure of human dimeric cytochrome c, demonstrating that the heme ligation in dimeric cytochrome c is pH dependent, providing a pH-inducible switch that controls the peroxidase activity of the human dimer near physiological pH.

Subjects/Keywords: apoptosis; cytochrome c

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

APA (6^th Edition):

Lei, H. (2019). Modulation of cytochrome c’s peroxidase activity by Ω-loops C and D in monomers and dimers. (Doctoral Dissertation). University of Montana. Retrieved from https://scholarworks.umt.edu/etd/11436

Chicago Manual of Style (16^th Edition):

Lei, Haotian. “Modulation of cytochrome c’s peroxidase activity by Ω-loops C and D in monomers and dimers.” 2019. Doctoral Dissertation, University of Montana. Accessed January 24, 2021. https://scholarworks.umt.edu/etd/11436.

MLA Handbook (7^th Edition):

Lei, Haotian. “Modulation of cytochrome c’s peroxidase activity by Ω-loops C and D in monomers and dimers.” 2019. Web. 24 Jan 2021.

Vancouver:

Lei H. Modulation of cytochrome c’s peroxidase activity by Ω-loops C and D in monomers and dimers. [Internet] [Doctoral dissertation]. University of Montana; 2019. [cited 2021 Jan 24]. Available from: https://scholarworks.umt.edu/etd/11436.

Council of Science Editors:

Lei H. Modulation of cytochrome c’s peroxidase activity by Ω-loops C and D in monomers and dimers. [Doctoral Dissertation]. University of Montana; 2019. Available from: https://scholarworks.umt.edu/etd/11436

University of New South Wales

29. Cooley Andrade, Osvaldo. A Study of the Apoptotic Effects of Detergent Sclerosants on Vascular and Circulating Blood Cells.

Degree: Clinical School - St Vincent's Hospital, 2017, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/58361 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:45847/SOURCE02?view=true

► The in vitro effects of detergent sclerosants, sodium tetradecylsulphate (STS) andpolidocanol (POL) on cell activation, cytokine release, apoptosis and oncosis wereinvestigated. The general hypothesis of… (more)

Subjects/Keywords: Oncosis; Sclerosants; Apoptosis

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

APA (6^th Edition):

Cooley Andrade, O. (2017). A Study of the Apoptotic Effects of Detergent Sclerosants on Vascular and Circulating Blood Cells. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/58361 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:45847/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Cooley Andrade, Osvaldo. “A Study of the Apoptotic Effects of Detergent Sclerosants on Vascular and Circulating Blood Cells.” 2017. Doctoral Dissertation, University of New South Wales. Accessed January 24, 2021. http://handle.unsw.edu.au/1959.4/58361 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:45847/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Cooley Andrade, Osvaldo. “A Study of the Apoptotic Effects of Detergent Sclerosants on Vascular and Circulating Blood Cells.” 2017. Web. 24 Jan 2021.

Vancouver:

Cooley Andrade O. A Study of the Apoptotic Effects of Detergent Sclerosants on Vascular and Circulating Blood Cells. [Internet] [Doctoral dissertation]. University of New South Wales; 2017. [cited 2021 Jan 24]. Available from: http://handle.unsw.edu.au/1959.4/58361 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:45847/SOURCE02?view=true.

Council of Science Editors:

Cooley Andrade O. A Study of the Apoptotic Effects of Detergent Sclerosants on Vascular and Circulating Blood Cells. [Doctoral Dissertation]. University of New South Wales; 2017. Available from: http://handle.unsw.edu.au/1959.4/58361 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:45847/SOURCE02?view=true

University of New South Wales

30. Desouza, Melissa. Defined tropomyosin filament populations regulate sensitivity to apoptosis.

Degree: Medical Sciences, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55355 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37346/SOURCE02?view=true

► The actin cytoskeleton acts as both a sensor and mediator of programmed cell death known as apoptosis. Tropomyosins (Tpm) are a family of actin binding… (more)

▼ The actin cytoskeleton acts as both a sensor and mediator of programmed cell death known as apoptosis. Tropomyosins (Tpm) are a family of actin binding proteins that regulate numerous actin functions and limited studies demonstrate a role for defined tropomyosin isoforms in regulating apoptosis. The Tpm2.1 isoform regulates cell detachment-induced apoptosis, known as anoikis, and the Tpm1.1 isoform is implicated in regulating apoptosis induced by oxidative stress. As there are numerous tropomyosins that have not been evaluated for their role in apoptosis the aim of this thesis is to determine whether tropomyosins regulate apoptosis in an isoform- and stimulus-dependent manner. A B35 cell model over-expressing tropomyosin was utilised to evaluate the function of specific isoforms in apoptosis. High throughput characterisation of over-expressing clones showed that tropomyosins regulate the morphological properties and phenotype of cells in an isoform-dependent manner. Furthermore, Tpm2.1 over-expression increased the number of actin filament bundles per cell and induced a parallel re-arrangement of microfilaments. Screening of tropomyosin over-expressing clones for apoptosis sensitivity to different stimuli revealed numerous isoform-specific changes in apoptosis activation. Tpm2.1 over-expression enhanced apoptosis sensitivity to the actin stabilising drug Jasplakinolide and Tpm4.2 over-expression reduced apoptosis sensitivity to the actin destabilising drug Cytochalasin D. Tpm2.1 over-expression sensitised cells to apoptosis via hyper-activation of the intrinsic apoptosis pathway characterised by increased mitochondrial membrane depolarisation and elevated expression of Bak, Mcl-1 and Bcl-2. A second approach was undertaken to perturb tropomyosin function and investigate the mechanism by which tropomyosins regulate apoptosis. Using a novel anti-tropomyosin compound (ATM-4001) the inhibition of tropomyosin function disrupted the actin cytoskeleton of SH-EP neuroblastoma cells resulting in intrinsic apoptosis. A Kinexus antibody microarray further revealed that tropomyosin inhibition impacted the activity of numerous cell signalling pathways (e.g. the MAPK, PI3K/AKT and PKC pathways) which shifted the balance towards apoptosis. Therefore, tropomyosins represent an important link between the actin cytoskeleton, cell signalling pathways and the regulation of apoptosis. As the pathology of many diseases such as cancer and Alzheimer’s disease involve the de-regulation of apoptosis, understanding the role of tropomyosin in regulating apoptosis will provide a unique opportunity to exploit the actin cytoskeleton therapeutically for the treatment of these diseases. Advisors/Committee Members: Gunning, Peter, Faculty of Medicine, UNSW.

Subjects/Keywords: Cancer; Tropomyosin; Apoptosis

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

APA (6^th Edition):

Desouza, M. (2015). Defined tropomyosin filament populations regulate sensitivity to apoptosis. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55355 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37346/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Desouza, Melissa. “Defined tropomyosin filament populations regulate sensitivity to apoptosis.” 2015. Doctoral Dissertation, University of New South Wales. Accessed January 24, 2021. http://handle.unsw.edu.au/1959.4/55355 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37346/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Desouza, Melissa. “Defined tropomyosin filament populations regulate sensitivity to apoptosis.” 2015. Web. 24 Jan 2021.

Vancouver:

Desouza M. Defined tropomyosin filament populations regulate sensitivity to apoptosis. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2021 Jan 24]. Available from: http://handle.unsw.edu.au/1959.4/55355 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37346/SOURCE02?view=true.

Council of Science Editors:

Desouza M. Defined tropomyosin filament populations regulate sensitivity to apoptosis. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55355 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37346/SOURCE02?view=true

Open Access Theses and Dissertations