subject:(Mitochondria)

University of Alberta

1. Dromparis, Peter R. Mitochondria in Vascular Health and Disease.

Degree: PhD, Department of Medicine, 2013, University of Alberta

URL: https://era.library.ualberta.ca/files/0z708x22n

► Mitochondria generate reactive oxygen species (mROS) and metabolic substrates like alpha-ketogluterate (αKG), in proportion to oxygen, which target extra-mitochondrial effectors to coordinate a cellular response.… (more)

▼ Mitochondria generate reactive oxygen species (mROS) and metabolic substrates like alpha-ketogluterate (αKG), in proportion to oxygen, which target extra-mitochondrial effectors to coordinate a cellular response. For example, acute hypoxia decreases mROS, resulting in pulmonary artery smooth muscle cell (PASMC) contraction and hypoxic pulmonary vasoconstriction. Metabolic suppression can mimic the hypoxic effects, even in normoxia. In cancer, which has suppressed mitochondrial glucose oxidation (GO), reduced mitochondrial-derived signals including mROS and αKG stabilize hypoxia inducible factor 1α (HIF1α), resulting in normoxic activation that contributes to apoptosis resistance and angiogenesis. This metabolic suppression is shared with hyperproliferative and anti-apoptotic cells in the distal pulmonary artery (PA) wall, and is the hallmark of pulmonary arterial hypertension (PHT). Recently, we proposed that endoplasmic reticulum (ER)-stress-induced disruption of an ‘ER-mitochondrial unit’ as a PHT trigger, since the ER provides Ca2+ that is required for many of the key mitochondrial metabolic enzymes like pyruvate dehydrogenase (PDH) and Krebs cycle enzymes like isocitrate dehydrogenase (IDH; produces αKG). We show that like ER-stress, loss of uncoupling protein-2 (UCP2), reduces mitochondrial calcium (Ca2+m) in PASMCs. This suppresses PDH activity, Krebs cycle function and mROS production, activating HIF1α and contributing to apoptosis resistance in vitro. Mice lacking UCP2 spontaneously develop PHT with distal PA remodeling similar to hypoxic wildtype mice (a standard PHT model). This is the first description of UCP2 influencing oxygen sensing and may open a new window for biomarker or therapeutic strategies. We also show targeting ER-stress is a viable therapeutic strategy in PHT. 4-phenylbutyric acid (PBA), a FDA approved chemical chaperone that facilitates protein folding and attenuates ER-stress. PBA prevented and reversed pulmonary vascular remodeling and PHT in chronic hypoxia and monocrotaline rodents. In isolated PASMCs, PBA, and a second chemical chaperone tauroursodeoxycholate maintained Ca2+m, normalizing PDH activity and mROS/αKG, reducing proliferation and inducing apoptosis in hypoxia (an ER-stress inducer). Thus, pathobiology linked with the functional dysregulation between mitochondria and other organelles can be therapeutically targeted. Finally, we show that mitochondrial activation with thiazolidinediones can impair HIF1α signaling in a hindlimb ischemia model, potentially explaining some of the adverse cardiovascular events in some patients with these drugs.

Subjects/Keywords: mitochondria

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APA (6^th Edition):

Dromparis, P. R. (2013). Mitochondria in Vascular Health and Disease. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/0z708x22n

Chicago Manual of Style (16^th Edition):

Dromparis, Peter R. “Mitochondria in Vascular Health and Disease.” 2013. Doctoral Dissertation, University of Alberta. Accessed March 02, 2021. https://era.library.ualberta.ca/files/0z708x22n.

MLA Handbook (7^th Edition):

Dromparis, Peter R. “Mitochondria in Vascular Health and Disease.” 2013. Web. 02 Mar 2021.

Vancouver:

Dromparis PR. Mitochondria in Vascular Health and Disease. [Internet] [Doctoral dissertation]. University of Alberta; 2013. [cited 2021 Mar 02]. Available from: https://era.library.ualberta.ca/files/0z708x22n.

Council of Science Editors:

Dromparis PR. Mitochondria in Vascular Health and Disease. [Doctoral Dissertation]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/0z708x22n

2. Ford, Kara Alexandra. The Role of C-Terminal Src Kinase on Mitochondrial Function.

Degree: Department of Molecular Pharmacology, Physiology and Biotechnology, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:733329/

► The role of C-Terminal Src Kinase (CSK) in mitochondrial function was evaluated in this thesis. CSK is mainly found in the cytosol and involved in… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Ford, K. A. (2017). The Role of C-Terminal Src Kinase on Mitochondrial Function. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:733329/

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):

Ford, Kara Alexandra. “The Role of C-Terminal Src Kinase on Mitochondrial Function.” 2017. Thesis, Brown University. Accessed March 02, 2021. https://repository.library.brown.edu/studio/item/bdr:733329/.

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

MLA Handbook (7^th Edition):

Ford, Kara Alexandra. “The Role of C-Terminal Src Kinase on Mitochondrial Function.” 2017. Web. 02 Mar 2021.

Vancouver:

Ford KA. The Role of C-Terminal Src Kinase on Mitochondrial Function. [Internet] [Thesis]. Brown University; 2017. [cited 2021 Mar 02]. Available from: https://repository.library.brown.edu/studio/item/bdr:733329/.

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

Council of Science Editors:

Ford KA. The Role of C-Terminal Src Kinase on Mitochondrial Function. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:733329/

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

Oregon State University

3. Gregg, Charles Thornton. Oxidative phosphorylation and respiratory control in insect mitochondria.

Degree: PhD, Chemistry, 1959, Oregon State University

URL: http://hdl.handle.net/1957/50766

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Gregg, C. T. (1959). Oxidative phosphorylation and respiratory control in insect mitochondria. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/50766

Chicago Manual of Style (16^th Edition):

Gregg, Charles Thornton. “Oxidative phosphorylation and respiratory control in insect mitochondria.” 1959. Doctoral Dissertation, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/50766.

MLA Handbook (7^th Edition):

Gregg, Charles Thornton. “Oxidative phosphorylation and respiratory control in insect mitochondria.” 1959. Web. 02 Mar 2021.

Vancouver:

Gregg CT. Oxidative phosphorylation and respiratory control in insect mitochondria. [Internet] [Doctoral dissertation]. Oregon State University; 1959. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/50766.

Council of Science Editors:

Gregg CT. Oxidative phosphorylation and respiratory control in insect mitochondria. [Doctoral Dissertation]. Oregon State University; 1959. Available from: http://hdl.handle.net/1957/50766

Oregon State University

4. Mahlum, Lisa Michelle. Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl.

Degree: MS, Animal Science, 2001, Oregon State University

URL: http://hdl.handle.net/1957/32425

► Sperm mobility denotes the net movement of a sperm population. Previous work implicated mitochondrial function as a basis underlying phenotypic variation in this quantitative trait.… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Mahlum, L. M. (2001). Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/32425

Chicago Manual of Style (16^th Edition):

Mahlum, Lisa Michelle. “Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl.” 2001. Masters Thesis, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/32425.

MLA Handbook (7^th Edition):

Mahlum, Lisa Michelle. “Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl.” 2001. Web. 02 Mar 2021.

Vancouver:

Mahlum LM. Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl. [Internet] [Masters thesis]. Oregon State University; 2001. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/32425.

Council of Science Editors:

Mahlum LM. Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl. [Masters Thesis]. Oregon State University; 2001. Available from: http://hdl.handle.net/1957/32425

Oregon State University

5. Will, Yvonne. Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death.

Degree: PhD, Biochemistry and Biophysics, 1999, Oregon State University

URL: http://hdl.handle.net/1957/32950

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Will, Y. (1999). Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/32950

Chicago Manual of Style (16^th Edition):

Will, Yvonne. “Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death.” 1999. Doctoral Dissertation, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/32950.

MLA Handbook (7^th Edition):

Will, Yvonne. “Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death.” 1999. Web. 02 Mar 2021.

Vancouver:

Will Y. Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. [Internet] [Doctoral dissertation]. Oregon State University; 1999. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/32950.

Council of Science Editors:

Will Y. Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. [Doctoral Dissertation]. Oregon State University; 1999. Available from: http://hdl.handle.net/1957/32950

Oregon State University

6. Savage, Melani K. Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate.

Degree: PhD, Toxicology, 1994, Oregon State University

URL: http://hdl.handle.net/1957/35585

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Savage, M. K. (1994). Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/35585

Chicago Manual of Style (16^th Edition):

Savage, Melani K. “Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate.” 1994. Doctoral Dissertation, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/35585.

MLA Handbook (7^th Edition):

Savage, Melani K. “Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate.” 1994. Web. 02 Mar 2021.

Vancouver:

Savage MK. Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate. [Internet] [Doctoral dissertation]. Oregon State University; 1994. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/35585.

Council of Science Editors:

Savage MK. Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate. [Doctoral Dissertation]. Oregon State University; 1994. Available from: http://hdl.handle.net/1957/35585

Oregon State University

7. Meegungwan, Chongchit. Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina.

Degree: MS, General Science, 1964, Oregon State University

URL: http://hdl.handle.net/1957/48070

► A large number of experiments were done to detect and identify one or more intermediates involved in coupling ATP synthesis to electron transport. Using mitochondria… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Meegungwan, C. (1964). Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/48070

Chicago Manual of Style (16^th Edition):

Meegungwan, Chongchit. “Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina.” 1964. Masters Thesis, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/48070.

MLA Handbook (7^th Edition):

Meegungwan, Chongchit. “Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina.” 1964. Web. 02 Mar 2021.

Vancouver:

Meegungwan C. Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina. [Internet] [Masters thesis]. Oregon State University; 1964. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/48070.

Council of Science Editors:

Meegungwan C. Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina. [Masters Thesis]. Oregon State University; 1964. Available from: http://hdl.handle.net/1957/48070

Oregon State University

8. Petersen, Thomas Gordon. The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea.

Degree: MA, Chemistry, 1963, Oregon State University

URL: http://hdl.handle.net/1957/48921

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Petersen, T. G. (1963). The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/48921

Chicago Manual of Style (16^th Edition):

Petersen, Thomas Gordon. “The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea.” 1963. Masters Thesis, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/48921.

MLA Handbook (7^th Edition):

Petersen, Thomas Gordon. “The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea.” 1963. Web. 02 Mar 2021.

Vancouver:

Petersen TG. The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea. [Internet] [Masters thesis]. Oregon State University; 1963. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/48921.

Council of Science Editors:

Petersen TG. The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea. [Masters Thesis]. Oregon State University; 1963. Available from: http://hdl.handle.net/1957/48921

Oregon State University

9. Smith, Karin Ann. The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides.

Degree: MA, Chemistry, 1962, Oregon State University

URL: http://hdl.handle.net/1957/48841

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Smith, K. A. (1962). The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/48841

Chicago Manual of Style (16^th Edition):

Smith, Karin Ann. “The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides.” 1962. Masters Thesis, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/48841.

MLA Handbook (7^th Edition):

Smith, Karin Ann. “The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides.” 1962. Web. 02 Mar 2021.

Vancouver:

Smith KA. The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides. [Internet] [Masters thesis]. Oregon State University; 1962. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/48841.

Council of Science Editors:

Smith KA. The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides. [Masters Thesis]. Oregon State University; 1962. Available from: http://hdl.handle.net/1957/48841

Oregon State University

10. Tripp, Martha June. Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns.

Degree: MS, General Science, 1967, Oregon State University

URL: http://hdl.handle.net/1957/47315

► Characterization of the enzymatic activity of the ionocyte (mitochondria-rich cell) in the gill epithelium of Oncorhynchus tshawytscha was explored. 1. A method for estimating the… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Tripp, M. J. (1967). Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/47315

Chicago Manual of Style (16^th Edition):

Tripp, Martha June. “Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns.” 1967. Masters Thesis, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/47315.

MLA Handbook (7^th Edition):

Tripp, Martha June. “Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns.” 1967. Web. 02 Mar 2021.

Vancouver:

Tripp MJ. Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns. [Internet] [Masters thesis]. Oregon State University; 1967. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/47315.

Council of Science Editors:

Tripp MJ. Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns. [Masters Thesis]. Oregon State University; 1967. Available from: http://hdl.handle.net/1957/47315

University of Ottawa

11. Mazier, Hannah. Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin .

Degree: 2016, University of Ottawa

URL: http://hdl.handle.net/10393/35572

► Polycystic ovarian syndrome (PCOS) is a multi-factorial infertility disorder whose etiology and pathogenesis is not completely understood. Although there is an association between dysregulation of… (more)

Subjects/Keywords: Reproduction; Mitochondria

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APA (6^th Edition):

Mazier, H. (2016). Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/35572

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):

Mazier, Hannah. “Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin .” 2016. Thesis, University of Ottawa. Accessed March 02, 2021. http://hdl.handle.net/10393/35572.

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

MLA Handbook (7^th Edition):

Mazier, Hannah. “Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin .” 2016. Web. 02 Mar 2021.

Vancouver:

Mazier H. Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin . [Internet] [Thesis]. University of Ottawa; 2016. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10393/35572.

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

Council of Science Editors:

Mazier H. Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin . [Thesis]. University of Ottawa; 2016. Available from: http://hdl.handle.net/10393/35572

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

University of Adelaide

12. Day, David Alexander. Oxidative pathways of isolated plant mitochrondria.

Degree: 1975, University of Adelaide

URL: http://hdl.handle.net/2440/20040

Subjects/Keywords: Mitochondria.

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APA (6^th Edition):

Day, D. A. (1975). Oxidative pathways of isolated plant mitochrondria. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/20040

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):

Day, David Alexander. “Oxidative pathways of isolated plant mitochrondria.” 1975. Thesis, University of Adelaide. Accessed March 02, 2021. http://hdl.handle.net/2440/20040.

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

MLA Handbook (7^th Edition):

Day, David Alexander. “Oxidative pathways of isolated plant mitochrondria.” 1975. Web. 02 Mar 2021.

Vancouver:

Day DA. Oxidative pathways of isolated plant mitochrondria. [Internet] [Thesis]. University of Adelaide; 1975. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2440/20040.

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

Council of Science Editors:

Day DA. Oxidative pathways of isolated plant mitochrondria. [Thesis]. University of Adelaide; 1975. Available from: http://hdl.handle.net/2440/20040

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

Harvard University

13. Roach, Allie M. An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease.

Degree: ALM, 2018, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192

►

The mitochondrial permeability transition pore (mPTP) contributes to pathological outcomes in various contexts of tissue injury and disease involving mitochondrial perturbation, including in the kidneys.… (more)

Subjects/Keywords: Nephrology; Mitochondria

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APA (6^th Edition):

Roach, A. M. (2018). An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease. (Masters Thesis). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192

Chicago Manual of Style (16^th Edition):

Roach, Allie M. “An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease.” 2018. Masters Thesis, Harvard University. Accessed March 02, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192.

MLA Handbook (7^th Edition):

Roach, Allie M. “An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease.” 2018. Web. 02 Mar 2021.

Vancouver:

Roach AM. An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease. [Internet] [Masters thesis]. Harvard University; 2018. [cited 2021 Mar 02]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192.

Council of Science Editors:

Roach AM. An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease. [Masters Thesis]. Harvard University; 2018. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192

14. Vusse, Ger. The role of mitochondria in testicular steroid production.

Degree: 1975, Erasmus University Medical Center

URL: http://hdl.handle.net/1765/31391

► textabstractThe testicular gland is the main androgen producing organ in male animals. The production of androgens is regulated by LH, secreted by the pituitary. The… (more)

Subjects/Keywords: mitochondria

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APA (6^th Edition):

Vusse, G. (1975). The role of mitochondria in testicular steroid production. (Doctoral Dissertation). Erasmus University Medical Center. Retrieved from http://hdl.handle.net/1765/31391

Chicago Manual of Style (16^th Edition):

Vusse, Ger. “The role of mitochondria in testicular steroid production.” 1975. Doctoral Dissertation, Erasmus University Medical Center. Accessed March 02, 2021. http://hdl.handle.net/1765/31391.

MLA Handbook (7^th Edition):

Vusse, Ger. “The role of mitochondria in testicular steroid production.” 1975. Web. 02 Mar 2021.

Vancouver:

Vusse G. The role of mitochondria in testicular steroid production. [Internet] [Doctoral dissertation]. Erasmus University Medical Center; 1975. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1765/31391.

Council of Science Editors:

Vusse G. The role of mitochondria in testicular steroid production. [Doctoral Dissertation]. Erasmus University Medical Center; 1975. Available from: http://hdl.handle.net/1765/31391

University of Arizona

15. Brown, Daniel Robert. GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES.

Degree: 1987, University of Arizona

URL: http://hdl.handle.net/10150/184046

► Comparative studies documented relationships between mitochondrial respiration and phenotype among genetically divergent animals. Broiler chickens' mitochondria ranked higher than layer chickens' for state 3 respiration… (more)

▼ Comparative studies documented relationships between mitochondrial respiration and phenotype among genetically divergent animals. Broiler chickens' mitochondria ranked higher than layer chickens' for state 3 respiration (16.1 ± 0.4 μM O₂/mg protein/min), respiratory control ratio (3.5 ± 0.1) and ADP:O ratio (1.05 ± 0.01 μM ADP/μA O) utilizing succinate. Broilers yielded more (P < .05) mitochondrial protein than did layers (7.8 vs. 6.2 ± 0.2 mg/g hepatic tissue). Within-breed mitochondrial activity had no associations with chicken weight or egg production. C57BL/6J mice mitochondria had higher (P < .05) respiratory control ratios (4.06 vs. 3.78 ± 0.09), and C57BL/6J females higher state 3 respiration rates utilizing succinate (strain by sex interaction P < .01), than A/J or BALB/cJ mice mitochondria. BALB/cJ mitochondria had higher (P < .05) ADP:O ratios utilizing pyruvate than C57BL/6J mitochondria (1.58 vs. 1.46 ± 0.04 μM ADP/μA O). Rapid ATP synthesis rates of C57BL/6J female mice were associated generally with reproductive superiority. Inbred mouse body weight was not associated with mitochondrial respiration. Original data confirmed CB6F₁, but not CAF₁, hybrid mice were heterotic for postweaning growth. Hybridization increased (P < .05) mitochondrial mass, but did not enhance respiration. No association existed between growth heterosis and mitochondrial function in hybrid mice. Unexpected sexual dimorphism in mitochondrial respiration existed across mouse strains. Testosterone administration and orchiectomy confirmed female mice exhibited superior organelle activity. Mitochondrial ATP synthesis rates of Holstein cows correlated (+.30 to +.48) with milk production traits of cows and their dams suggested maternal breeding values for milk yield might be improved by considering mitochondrial effects. No breed differences in state 3 respiration (17.7 ± 0.6 μM O2/mg protein/min) or ADP:O ratio with succinate (1.17 ± 0.01 μM ADP/μA O) existed among Angus, Brangus and Hereford cows. Regression analyses of growth traits of cows and their relatives on mitochondrial parameters revealed mainly nonsignificant mitochondrial effects. Significant regression coefficients (-0.43 to -1.05) were found for some cattle growth traits regressed on ADP:O ratios. No mitochondrial complementation occurred between neutrally-combining animal strains. Complementation occurred in mitochondrial mixtures from females of mouse strains with positive combining ability exclusively. Cow mitochondrial mixtures had lower (P < .05) state 3 rates than predicted. Advisors/Committee Members: DeNise, S. K (advisor), Allen, Ronald E. (committeemember), Ray, Donald E. (committeemember), Reid, B. L. (committeemember), McDaniel, Robert G. (committeemember).

Subjects/Keywords: Mitochondria.

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APA (6^th Edition):

Brown, D. R. (1987). GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/184046

Chicago Manual of Style (16^th Edition):

Brown, Daniel Robert. “GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. ” 1987. Doctoral Dissertation, University of Arizona. Accessed March 02, 2021. http://hdl.handle.net/10150/184046.

MLA Handbook (7^th Edition):

Brown, Daniel Robert. “GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. ” 1987. Web. 02 Mar 2021.

Vancouver:

Brown DR. GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. [Internet] [Doctoral dissertation]. University of Arizona; 1987. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10150/184046.

Council of Science Editors:

Brown DR. GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. [Doctoral Dissertation]. University of Arizona; 1987. Available from: http://hdl.handle.net/10150/184046

Rice University

16. Tjahjono, Elissa. ESRE Network Activation and Regulation Provide Insight into Mitochondrial Surveillance.

Degree: PhD, Natural Sciences, 2020, Rice University

URL: http://hdl.handle.net/1911/108354

► All living organisms exist in a precarious state of homeostasis that requires constant maintenance. A wide variety of stresses, including hypoxia, heat, and infection by… (more)

▼ All living organisms exist in a precarious state of homeostasis that requires constant maintenance. A wide variety of stresses, including hypoxia, heat, and infection by pathogens perpetually threaten to imbalance this state. Organisms use a battery of defenses to mitigate damage and restore normal function. In a pyoverdine-dependent Caenorhabditis elegans-Pseudomonas aeruginosa assay, C. elegans’ defense response utilizes the phylogenetically conserved ESRE (Ethanol and Stress Response Element) network, which has previously been shown to mitigate damage from a variety of abiotic stresses. It is intriguing that this network is involved in innate immunity; it indicates that host innate immune responses overlap with responses to abiotic stresses. I further investigated the ESRE defense network following exposure to P. aeruginosa and showed that mitochondrial damage leads to ESRE activation both in C. elegans and in mammals. Mitochondrial dysfunction contributes to a wide variety of pathologies, including neurodegenerative diseases, cancer, metabolic diseases, and aging. Mitochondrial status is actively surveilled by several different systems to ensure the preservation of cellular viability. I characterized the ESRE pathway, a novel mitochondrial surveillance system, and showed that it is robustly activated in response to increased superoxide radical. This differentiates ESRE from other existing mitochondrial surveillance pathways, such as the mitochondrial unfolded protein response (UPRmt) that monitors disruption of mitochondrial protein import and the mitochondrial MAPK (MAPKmt) pathway that responds to mitochondrial bioenergetic disruption. I also observed multiple interactions between the ESRE, UPRmt, and MAPKmt pathways. Understanding mitochondrial surveillance and the interplay that occurs among these pathways is crucial for the advancement and understanding of cell biology. Considering that the ESRE motif and its role in response to mitochondrial damage is conserved in humans, modulation of mitochondrial pathways could confer resistance to stress and improve health span, leading to a direct benefit to human health. Advisors/Committee Members: Bartel, Bonnie (advisor), Kirienko, Natalia V (advisor).

Subjects/Keywords: Mitochondria; ESRE

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APA (6^th Edition):

Tjahjono, E. (2020). ESRE Network Activation and Regulation Provide Insight into Mitochondrial Surveillance. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/108354

Chicago Manual of Style (16^th Edition):

Tjahjono, Elissa. “ESRE Network Activation and Regulation Provide Insight into Mitochondrial Surveillance.” 2020. Doctoral Dissertation, Rice University. Accessed March 02, 2021. http://hdl.handle.net/1911/108354.

MLA Handbook (7^th Edition):

Tjahjono, Elissa. “ESRE Network Activation and Regulation Provide Insight into Mitochondrial Surveillance.” 2020. Web. 02 Mar 2021.

Vancouver:

Tjahjono E. ESRE Network Activation and Regulation Provide Insight into Mitochondrial Surveillance. [Internet] [Doctoral dissertation]. Rice University; 2020. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1911/108354.

Council of Science Editors:

Tjahjono E. ESRE Network Activation and Regulation Provide Insight into Mitochondrial Surveillance. [Doctoral Dissertation]. Rice University; 2020. Available from: http://hdl.handle.net/1911/108354

Columbia University

17. Garcia, Christian Joel. The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles.

Degree: 2020, Columbia University

URL: https://doi.org/10.7916/d8-sg7a-7m23

► Mitochondrial Complex I (CI) is composed of 44 distinct subunits that are assembled with eight Fe- S clusters and a single flavin mononucleotide. Mitochondria is… (more)

Subjects/Keywords: Physiology; Biochemistry; Drosophila melanogaster; Mitochondria; Mitochondria – Formation

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APA (6^th Edition):

Garcia, C. J. (2020). The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-sg7a-7m23

Chicago Manual of Style (16^th Edition):

Garcia, Christian Joel. “The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles.” 2020. Doctoral Dissertation, Columbia University. Accessed March 02, 2021. https://doi.org/10.7916/d8-sg7a-7m23.

MLA Handbook (7^th Edition):

Garcia, Christian Joel. “The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles.” 2020. Web. 02 Mar 2021.

Vancouver:

Garcia CJ. The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles. [Internet] [Doctoral dissertation]. Columbia University; 2020. [cited 2021 Mar 02]. Available from: https://doi.org/10.7916/d8-sg7a-7m23.

Council of Science Editors:

Garcia CJ. The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles. [Doctoral Dissertation]. Columbia University; 2020. Available from: https://doi.org/10.7916/d8-sg7a-7m23

University of Rochester

18. Shum, Laura C. Mitochondrial Metabolism in Bone Physiology and Pathology.

Degree: PhD, 2020, University of Rochester

URL: http://hdl.handle.net/1802/35499

► Worldwide, 1 in 3 women and 1 in 5 men over age 50 will experience fractures due to a decline in bone quality. Elucidating the… (more)

Subjects/Keywords: Bone; Mitochondria; Metabolism

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APA (6^th Edition):

Shum, L. C. (2020). Mitochondrial Metabolism in Bone Physiology and Pathology. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/35499

Chicago Manual of Style (16^th Edition):

Shum, Laura C. “Mitochondrial Metabolism in Bone Physiology and Pathology.” 2020. Doctoral Dissertation, University of Rochester. Accessed March 02, 2021. http://hdl.handle.net/1802/35499.

MLA Handbook (7^th Edition):

Shum, Laura C. “Mitochondrial Metabolism in Bone Physiology and Pathology.” 2020. Web. 02 Mar 2021.

Vancouver:

Shum LC. Mitochondrial Metabolism in Bone Physiology and Pathology. [Internet] [Doctoral dissertation]. University of Rochester; 2020. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1802/35499.

Council of Science Editors:

Shum LC. Mitochondrial Metabolism in Bone Physiology and Pathology. [Doctoral Dissertation]. University of Rochester; 2020. Available from: http://hdl.handle.net/1802/35499

Oregon State University

19. Wernick, Riana I. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.

Degree: PhD, Zoology, 2016, Oregon State University

URL: http://hdl.handle.net/1957/59186

► Understanding the impact of mitochondrial dysfunction on genome evolution has the potential not only to provide new insights on the basic evolutionary processes influencing mitochondrial… (more)

▼ Understanding the impact of mitochondrial dysfunction on genome evolution has the potential not only to provide new insights on the basic evolutionary processes influencing mitochondrial and nuclear genomes, but may also reveal novel avenues for evolutionary adaptive recovery from harmful mutations. Aberrant mitochondrial activity is fundamental to the pathology of mitochondrial diseases in addition to neurodegenerative disorders. While the effects of mitochondrial dysfunction have received much attention, less is known about their impact on genome evolution and potential target mechanisms for ameliorating the harmful effects of mitochondrial impairment. Characterizing genome modifications in animal populations predisposed to mitochondrial dysfunction may identify novel genes, mechanisms, and physiological pathways to target for recovery and provides a genome-wide perspective on the impact of aberrant mitochondrial activity. This dissertation research investigates how mitochondrial and nuclear genomes evolve in organisms genetically predisposed to mitochondrial dysfunction and contrasts genomic evolution in large and small population sizes. This work furthers understanding of the impact of evolutionary forces which influence genome evolution in population with reduced fitness, and reveals new insights into genomic responses to mitochondrial dysfunction. Chapters 2 and 3 of this dissertation focus on genome evolution using a set of mitochondrial respiratory chain mutant (gas-1¬ strain) and wild-type (N2 strain) Caenorhabditis elegans mutation-accumulation (MA) lines that experienced single-worm bottlenecking. The N2 MA lines, derived from a previous experiment, were bottlenecked for 250 generations. The gas-1 MA lines were created for this research, and bottlenecked in the laboratory for a maximum of 50 generations. Chapter 2 investigates mitogenomic evolution and heteroplasmic inheritance patterns evolving under extreme drift in gas-1 and N2 MA lines. Chapter 3 analyzes nuclear genome evolution using this same set of gas-1 and N2 MA lines. In contrast, Chapter 4 provides a complementary perspective, analyzing mitochondrial and nuclear genome evolution in twenty-four gas-1 'recovery line' (RC) populations, evolved in large population sizes for sixty generations. Bioinformatic methods and computational simulations were applied to characterize and evaluate genome evolution and provide a comprehensive investigation of the impact of mitochondrial dysfunction within a population genetics framework. In Chapter 2 our results of inherited mitochondrial DNA (mtDNA) heteroplasmy are in alignment with predictions of theories where a small subset of mtDNA molecules from the parental generation repopulates the mitochondrial genome pool for the progeny. Comparisons between Chapter 2 and 4 suggest that in both gas-1 and N2 strains organelle genome copy number is elevated in an environment characterized with extreme genetic drift but is less impacted throughout evolution in large populations when the force of genetic drift is… Advisors/Committee Members: Denver, Dee R. (advisor), Perez, Viviana (committee member).

Subjects/Keywords: Mitochondria; Caenorhabditis elegans

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APA (6^th Edition):

Wernick, R. I. (2016). Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/59186

Chicago Manual of Style (16^th Edition):

Wernick, Riana I. “Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.” 2016. Doctoral Dissertation, Oregon State University. Accessed March 02, 2021. http://hdl.handle.net/1957/59186.

MLA Handbook (7^th Edition):

Wernick, Riana I. “Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.” 2016. Web. 02 Mar 2021.

Vancouver:

Wernick RI. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Oregon State University; 2016. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1957/59186.

Council of Science Editors:

Wernick RI. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. [Doctoral Dissertation]. Oregon State University; 2016. Available from: http://hdl.handle.net/1957/59186

University of Waterloo

20. Dubinski, Alicia. The Effects of Copper Availability on Mitochondrial Function in Saccharomyces cerevisiae.

Degree: 2019, University of Waterloo

URL: http://hdl.handle.net/10012/14684

► Copper (Cu) is crucial for cell function and survival and plays important roles in enzyme-catalyzed metabolic processes, transport of cargo through cellular membranes, and protein… (more)

▼ Copper (Cu) is crucial for cell function and survival and plays important roles in enzyme-catalyzed metabolic processes, transport of cargo through cellular membranes, and protein breakdown. The mitochondria are home to two important Cu-containing enzymes: cytochrome c oxidase (COX) and superoxide dismutase 1 (Sod1). Delivery of Cu to COX, the terminal electron acceptor in the respiratory chain, is suggested to happen in a bucket brigade fashion via the proteins Cox17, Sco1, and Cox11. Sod1, the other major mitochondrial cuproprotein, is thought to obtain Cu from its chaperone, Ccs1. Because the mitochondria are a central player in Cu storage and regulation, our goal in this study is to analyze how changes in extracellular Cu concentration impact mitochondrial function in Saccharomyces cerevisiae. Our results showed that Cox17, Sco1, and Cox11 responded differently to excess and limiting Cu, suggesting alternate functions for these proteins in mitochondria unrelated to COX assembly. During Cu deficient conditions we noticed an interesting redistribution of mitochondrial Cu: retention of Cu in mitochondrial Sod1 is accompanied by a complete loss of COX activity. This phenotype suggests a regulatory mechanism where Cu is preferentially donated to mitochondrial Sod1 instead of COX when Cu is limited. Interestingly, we also find that Cu redistribution in the mitochondria is affected when we change the primary carbon source from glucose to galactose. We propose that Cu distribution in mitochondria is controlled by an affinity gradient. Analysis of cell cycle progression showed that in excess Cu, yeast displayed a cell cycle defect while Cu deficient conditions did not affect cell cycle progression. Strikingly, changing the primary carbon source to galactose led to a cell cycle defect in the presence of a Cu specific chelator. Overall, we suggest that the presence of mitochondrial Sod1 is essential for cell cycle progression. The protein machinery responsible for Cu homeostasis has been well characterized, however the transport of Cu to cellular compartments and regulatory mechanisms involved in Cu import and export are not fully understood. We now demonstrate a novel phenotype that provides insight into regulation of Cu within the mitochondria. Additionally, we find that mitochondrial Cu distribution is affected by carbon source, and is associated with changes in cell cycle progression. These findings further our understanding of Cu homeostasis in yeast, and will likely have implications on Cu-related disorders, such as Menkes disease.

Subjects/Keywords: Copper; yeast; mitochondria

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APA (6^th Edition):

Dubinski, A. (2019). The Effects of Copper Availability on Mitochondrial Function in Saccharomyces cerevisiae. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/14684

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):

Dubinski, Alicia. “The Effects of Copper Availability on Mitochondrial Function in Saccharomyces cerevisiae.” 2019. Thesis, University of Waterloo. Accessed March 02, 2021. http://hdl.handle.net/10012/14684.

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

MLA Handbook (7^th Edition):

Dubinski, Alicia. “The Effects of Copper Availability on Mitochondrial Function in Saccharomyces cerevisiae.” 2019. Web. 02 Mar 2021.

Vancouver:

Dubinski A. The Effects of Copper Availability on Mitochondrial Function in Saccharomyces cerevisiae. [Internet] [Thesis]. University of Waterloo; 2019. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10012/14684.

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

Council of Science Editors:

Dubinski A. The Effects of Copper Availability on Mitochondrial Function in Saccharomyces cerevisiae. [Thesis]. University of Waterloo; 2019. Available from: http://hdl.handle.net/10012/14684

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

Texas A&M University

21. Pratt, Anthony Thomas. Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6.

Degree: MS, Biochemistry, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155711

► The mitochondrial respiratory chain (MRC) consists of four multi-protein complexes in the inner membrane of mitochondria and is the main site of cellular respiration. MRC… (more)

Subjects/Keywords: Coa6; yeast; mitochondria

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APA (6^th Edition):

Pratt, A. T. (2015). Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155711

Chicago Manual of Style (16^th Edition):

Pratt, Anthony Thomas. “Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6.” 2015. Masters Thesis, Texas A&M University. Accessed March 02, 2021. http://hdl.handle.net/1969.1/155711.

MLA Handbook (7^th Edition):

Pratt, Anthony Thomas. “Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6.” 2015. Web. 02 Mar 2021.

Vancouver:

Pratt AT. Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6. [Internet] [Masters thesis]. Texas A&M University; 2015. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1969.1/155711.

Council of Science Editors:

Pratt AT. Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6. [Masters Thesis]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155711

22. Poston, Chloe N. Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites.

Degree: PhD, Chemistry, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320610/

► Mass spectrometry has been a long-standing analytical tool for chemists. Tandem mass spectrometry-based proteomics capitalizes on the sensitivity, accuracy, and efficiency of this classic technique… (more)

Subjects/Keywords: Mitochondria-Associated Membranes

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APA (6^th Edition):

Poston, C. N. (2013). Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320610/

Chicago Manual of Style (16^th Edition):

Poston, Chloe N. “Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites.” 2013. Doctoral Dissertation, Brown University. Accessed March 02, 2021. https://repository.library.brown.edu/studio/item/bdr:320610/.

MLA Handbook (7^th Edition):

Poston, Chloe N. “Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites.” 2013. Web. 02 Mar 2021.

Vancouver:

Poston CN. Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2021 Mar 02]. Available from: https://repository.library.brown.edu/studio/item/bdr:320610/.

Council of Science Editors:

Poston CN. Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320610/

Victoria University of Wellington

23. Schneider, Rémy. Intercellular mitochondrial transfer in neural cells.

Degree: 2017, Victoria University of Wellington

URL: http://hdl.handle.net/10063/6977

► Intercellular mitochondrial transfer is the acquisition of exogenous mitochondria by one cell from another cell. The transfer event is generally not stochastic but directed. It… (more)

▼ Intercellular mitochondrial transfer is the acquisition of exogenous mitochondria by one cell from another cell. The transfer event is generally not stochastic but directed. It largely results in a benefit for the recipient cell. In the brain, the support structure astrocytes provide to neurons establishes a framework to investigate mitochondrial transfer between neural cells. During neurodegeneration or brain development, mitochondrial transfer between neural cells may alleviate disease phenotypes or help form the early cytoarchitecture and connectome of the brain. To begin to investigate intercellular mitochondrial transfer in neural cells, co-culture experiments were performed, between two independent, fluorescently labelled cell populations, either in a monolayer or in three-dimensional spheroid culture. Initially, fluorescently labelled mitochondria were co-cultured with neonatal neurons. Although punctate mitochondrial fluorescence was found in neurons, the conventional tools and methods used to label mitochondria and assess their location were found to have limitations, and new methods were developed. Transfer is most often seen in response to injury. Stable mtDNA-depleted (ρ⁰) astrocytes were generated as a mitochondrial specific injury. These astrocytes cannot respire, have impaired biosynthesis and ATP production, fractured mitochondrial networks with swollen mitochondria, and require pyruvate and uridine to meet their bioenergetic demands. When ρ⁰ astrocytes were co-cultured with the appropriate cell type in the absence of pyruvate and uridine, mitochondrial transfer was observed, leading to restoration of an entire mitochondrial network. The mechanism of mitochondrial transfer into ρ⁰ astrocytes was highly suggestive of cell fusion and was donor cell-type specific. This went against the convention in the literature that tunneling nanotubes (TNTs) or extracellular vesicles (EVs) discretely transfer clusters of mitochondria to damaged recipient cells. This PhD dissertation challenges the conventional tools to produce microscopic images proving mitochondrial transfer and suggests cell fusion as the mechanism by which non-native mitochondria exist inside a cell. Advisors/Committee Members: McConnell, Melanie, Berridge, Michael.

Subjects/Keywords: Mitochondria; Transfer; Microscopy

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APA (6^th Edition):

Schneider, R. (2017). Intercellular mitochondrial transfer in neural cells. (Doctoral Dissertation). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/6977

Chicago Manual of Style (16^th Edition):

Schneider, Rémy. “Intercellular mitochondrial transfer in neural cells.” 2017. Doctoral Dissertation, Victoria University of Wellington. Accessed March 02, 2021. http://hdl.handle.net/10063/6977.

MLA Handbook (7^th Edition):

Schneider, Rémy. “Intercellular mitochondrial transfer in neural cells.” 2017. Web. 02 Mar 2021.

Vancouver:

Schneider R. Intercellular mitochondrial transfer in neural cells. [Internet] [Doctoral dissertation]. Victoria University of Wellington; 2017. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10063/6977.

Council of Science Editors:

Schneider R. Intercellular mitochondrial transfer in neural cells. [Doctoral Dissertation]. Victoria University of Wellington; 2017. Available from: http://hdl.handle.net/10063/6977

University of Toronto

24. Sidorova, Elena. Assessing the Cytoprotective Properties and Central Nervous System Expression Profile of Mammalian Sirtuin SIRT3.

Degree: 2011, University of Toronto

URL: http://hdl.handle.net/1807/31443

►

Sirtuins are a family of nicotinamide adenine dinucleotide - dependent enzymes, which have gained recent interest due to their ability to directly or indirectly regulate… (more)

Subjects/Keywords: mitochondria; SIRT3; 0719

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APA (6^th Edition):

Sidorova, E. (2011). Assessing the Cytoprotective Properties and Central Nervous System Expression Profile of Mammalian Sirtuin SIRT3. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/31443

Chicago Manual of Style (16^th Edition):

Sidorova, Elena. “Assessing the Cytoprotective Properties and Central Nervous System Expression Profile of Mammalian Sirtuin SIRT3.” 2011. Masters Thesis, University of Toronto. Accessed March 02, 2021. http://hdl.handle.net/1807/31443.

MLA Handbook (7^th Edition):

Sidorova, Elena. “Assessing the Cytoprotective Properties and Central Nervous System Expression Profile of Mammalian Sirtuin SIRT3.” 2011. Web. 02 Mar 2021.

Vancouver:

Sidorova E. Assessing the Cytoprotective Properties and Central Nervous System Expression Profile of Mammalian Sirtuin SIRT3. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1807/31443.

Council of Science Editors:

Sidorova E. Assessing the Cytoprotective Properties and Central Nervous System Expression Profile of Mammalian Sirtuin SIRT3. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/31443

University of Texas Southwestern Medical Center

25. Carrer, Michele. Regulation of Metabolic Processes by Micrornas and Class I Histone Deacetylases.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1232

► Obesity is a medical condition resulting from accumulation of excess body fat that affects more than 30% of the adult population in the U.S. Obesity-related… (more)

▼ Obesity is a medical condition resulting from accumulation of excess body fat that affects more than 30% of the adult population in the U.S. Obesity-related pathological conditions include heart disease, stroke, type 2 diabetes and certain types of cancer. Despite the high incidence and the elevated social costs, the molecular basis of obesity and associated metabolic syndrome are still poorly understood. Yet, the need for novel therapeutic approaches for the treatment and prevention of obesity remains. In humans and animal model of disease, hallmarks of obesity include dysregulation of genes involved in mitochondrial function, lipid uptake and lipid storage. The dynamic and modifiable regulation of transcriptional pathways that control mitochondrial function and adipogenesis, as well as additional aspects of mammalian metabolism, will provide new approaches for pharmacological intervention in obesity. Thus, the modulation of epigenetic histone modifications and microRNA functions represents a potentially powerful approach for the treatment of metabolic disorders. We show that the Ppargc1b gene, which encodes the PGC-1β protein, also co-transcribes two microRNAs, miR-378 and miR-378*. Mice lacking miR-378/378* are resistant to high fat diet-induced obesity and display enhanced mitochondrial fatty acid metabolism and elevated oxidative capacity of insulin-target tissues. Taken together, our findings reveal that miR-378 and miR-378* function as integral components of the regulatory circuit formed by PGC-1beta and nuclear hormone receptors to control the overall oxidative capacity and energy homeostasis of insulin-target tissues. MiR-378/378* mutant mice do not display overt phenotypes under normal laboratory conditions, whereas their phenotypes become apparent under conditions of stress, in this case in response to excessive caloric intake. Thus, pharmacological modulation of miR-378/378* function might represent an effective approach in the treatment of obesity. In obese humans and mice, the unused caloric energy resulting from excessive net caloric intake is converted to triglycerides and stored in adipocytes for further usage. Lipid accumulation within adipocytes is under the control of a cascade of transcription factors that interact with histone acetyltransferases and deacetylases. We show that histone deacetylase inhibitors efficiently block adipocyte differentiation in vitro. Furthermore, through a loss-of-function approach, we provide evidence that histone deacetylases 1 and 2 play redundant and requisite roles in adipogenesis. In conclusion, we unveiled previously unrecognized roles for miR-378/378* in the control of mitochondrial metabolism and energy homeostasis, and for histone deacetylases in the control of adipocyte differentiation. Advisors/Committee Members: Olson, Eric N..

Subjects/Keywords: Adipocytes; MicroRNAs; Mitochondria

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APA (6^th Edition):

Carrer, M. (2013). Regulation of Metabolic Processes by Micrornas and Class I Histone Deacetylases. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1232

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):

Carrer, Michele. “Regulation of Metabolic Processes by Micrornas and Class I Histone Deacetylases.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed March 02, 2021. http://hdl.handle.net/2152.5/1232.

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

MLA Handbook (7^th Edition):

Carrer, Michele. “Regulation of Metabolic Processes by Micrornas and Class I Histone Deacetylases.” 2013. Web. 02 Mar 2021.

Vancouver:

Carrer M. Regulation of Metabolic Processes by Micrornas and Class I Histone Deacetylases. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2152.5/1232.

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

Council of Science Editors:

Carrer M. Regulation of Metabolic Processes by Micrornas and Class I Histone Deacetylases. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/1232

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

University of Texas Southwestern Medical Center

26. Mullen, Andrew Robbins. Reductive Carboxylation Is a Novel Pathway of Glutamine Metabolism That Supports the Growth of Tumor Cells with Metabolic Defects.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/2726

► In growing cancer cells, oxidative metabolism of glucose and glutamine in the mitochondria provide precursors needed for de novo synthesis of proteins, nucleic acids and… (more)

Subjects/Keywords: Glutamine; Mitochondria; Neoplasms

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

APA (6^th Edition):

Mullen, A. R. (2013). Reductive Carboxylation Is a Novel Pathway of Glutamine Metabolism That Supports the Growth of Tumor Cells with Metabolic Defects. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/2726

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):

Mullen, Andrew Robbins. “Reductive Carboxylation Is a Novel Pathway of Glutamine Metabolism That Supports the Growth of Tumor Cells with Metabolic Defects.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed March 02, 2021. http://hdl.handle.net/2152.5/2726.

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

MLA Handbook (7^th Edition):

Mullen, Andrew Robbins. “Reductive Carboxylation Is a Novel Pathway of Glutamine Metabolism That Supports the Growth of Tumor Cells with Metabolic Defects.” 2013. Web. 02 Mar 2021.

Vancouver:

Mullen AR. Reductive Carboxylation Is a Novel Pathway of Glutamine Metabolism That Supports the Growth of Tumor Cells with Metabolic Defects. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2152.5/2726.

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

Council of Science Editors:

Mullen AR. Reductive Carboxylation Is a Novel Pathway of Glutamine Metabolism That Supports the Growth of Tumor Cells with Metabolic Defects. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/2726

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

Boston University

27. McLoed, Melissa. THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans.

Degree: 2015, Boston University

URL: http://hdl.handle.net/2144/13983

► Following neuronal injury, calcium signaling plays a critical role in promoting repair processes. Injury produces an initial cytosolic calcium elevation mediated by calcium entry from… (more)

Subjects/Keywords: Neurosciences; Calcium; Mitochondria

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

APA (6^th Edition):

McLoed, M. (2015). THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans. (Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/13983

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):

McLoed, Melissa. “THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans.” 2015. Thesis, Boston University. Accessed March 02, 2021. http://hdl.handle.net/2144/13983.

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

MLA Handbook (7^th Edition):

McLoed, Melissa. “THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans.” 2015. Web. 02 Mar 2021.

Vancouver:

McLoed M. THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans. [Internet] [Thesis]. Boston University; 2015. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2144/13983.

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

Council of Science Editors:

McLoed M. THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans. [Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/13983

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

University of Minnesota

28. Visweswaran, Ramjay. The importance of calcium cycling and mitochondria in the local onset of alternans in the heart.

Degree: PhD, Biomedical Engineering, 2014, University of Minnesota

URL: http://hdl.handle.net/11299/165107

► Action potential duration (APD) alternans can be accompanied by alternans in intracellular calcium, leading to electromechanical alternans. Electromechanical alternans is considered a substrate for ventricular… (more)

▼ Action potential duration (APD) alternans can be accompanied by alternans in intracellular calcium, leading to electromechanical alternans. Electromechanical alternans is considered a substrate for ventricular fibrillation, especially during pathophysiological conditions such as ischemia. The work in thesis seeks to elucidate the spatio-temporal evolution of alternans and to investigate the potential pathways through which they occur. High resolution mapping was used to simultaneously map membrane voltage and intracellular calcium in normal rabbit hearts. By mapping both parameters simultaneously in the same region of the heart, we were able to reveal that instability in calcium cycling plays a primary role in the development of EM alternans in the whole heart. Further, we were able to apply a special restitution portrait analysis to predict the onset of both calcium and APD alternans before it occurs. We also wanted to elucidate the mechanisms behind the increased incidences of arrhythmias during ischemia. By simulating ischemic and mitochondrial dysfunction in isolated rabbit hearts, we were able to show that mitochondrial stress caused by uncoupling of the mitochondria is responsible for early occurrence of both APD and calcium alternans in the heart, which in turn creates a substrate to ventricular arrhythmias. Thus, uncoupling of the mitochondrial network that occurs during ischemia might be the primary reason for increased incidences of arrhythmias in the heart during ischemia. Overall, this study improves our knowledge of alternans and their basic underlying mechanism which can be used in the development of better treatment and/or prevention strategies. Development of techniques to predict alternans before it occurs would be a valuable clinical tool, especially for use in implantable pacemakers paving the way for pre-emptive interventions. In addition, elucidating the mechanism or pathways of alternans formation would lead to targeted drug treatments to prevent alternans and thus, VF and sudden cardiac death.

Subjects/Keywords: Alternans; Calcium; Mitochondria

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

APA (6^th Edition):

Visweswaran, R. (2014). The importance of calcium cycling and mitochondria in the local onset of alternans in the heart. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/165107

Chicago Manual of Style (16^th Edition):

Visweswaran, Ramjay. “The importance of calcium cycling and mitochondria in the local onset of alternans in the heart.” 2014. Doctoral Dissertation, University of Minnesota. Accessed March 02, 2021. http://hdl.handle.net/11299/165107.

MLA Handbook (7^th Edition):

Visweswaran, Ramjay. “The importance of calcium cycling and mitochondria in the local onset of alternans in the heart.” 2014. Web. 02 Mar 2021.

Vancouver:

Visweswaran R. The importance of calcium cycling and mitochondria in the local onset of alternans in the heart. [Internet] [Doctoral dissertation]. University of Minnesota; 2014. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/11299/165107.

Council of Science Editors:

Visweswaran R. The importance of calcium cycling and mitochondria in the local onset of alternans in the heart. [Doctoral Dissertation]. University of Minnesota; 2014. Available from: http://hdl.handle.net/11299/165107

University of Hawaii – Manoa

29. Brucks, Eric Snodgrass. Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes.

Degree: 2015, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/100300

►

M.S. University of Hawaii at Manoa 2014.

The free-living marine bacterial clade known as SAR11 is thought to be one of the most abundant lineages… (more)

Subjects/Keywords: marine; mitochondria; bacteria

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

APA (6^th Edition):

Brucks, E. S. (2015). Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100300

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):

Brucks, Eric Snodgrass. “Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes.” 2015. Thesis, University of Hawaii – Manoa. Accessed March 02, 2021. http://hdl.handle.net/10125/100300.

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

MLA Handbook (7^th Edition):

Brucks, Eric Snodgrass. “Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes.” 2015. Web. 02 Mar 2021.

Vancouver:

Brucks ES. Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes. [Internet] [Thesis]. University of Hawaii – Manoa; 2015. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10125/100300.

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

Council of Science Editors:

Brucks ES. Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes. [Thesis]. University of Hawaii – Manoa; 2015. Available from: http://hdl.handle.net/10125/100300

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

Latrobe University

30. Palmer, Catherine Sarah. MiD49 and MiD51 : new mediators of mitochondrial division.

Degree: PhD, 2012, Latrobe University

URL: http://hdl.handle.net/1959.9/530588

►

Thesis (Ph.D.) - La Trobe University, 2012

Submission note: "A thesis submitted in total fulfilment of the requirement for the degree of Doctor of Philosophy… (more)

Subjects/Keywords: Mitochondria.; Microbiology.; Proteins.

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

APA (6^th Edition):

Palmer, C. S. (2012). MiD49 and MiD51 : new mediators of mitochondrial division. (Doctoral Dissertation). Latrobe University. Retrieved from http://hdl.handle.net/1959.9/530588

Chicago Manual of Style (16^th Edition):

Palmer, Catherine Sarah. “MiD49 and MiD51 : new mediators of mitochondrial division.” 2012. Doctoral Dissertation, Latrobe University. Accessed March 02, 2021. http://hdl.handle.net/1959.9/530588.

MLA Handbook (7^th Edition):

Palmer, Catherine Sarah. “MiD49 and MiD51 : new mediators of mitochondrial division.” 2012. Web. 02 Mar 2021.

Vancouver:

Palmer CS. MiD49 and MiD51 : new mediators of mitochondrial division. [Internet] [Doctoral dissertation]. Latrobe University; 2012. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1959.9/530588.

Council of Science Editors:

Palmer CS. MiD49 and MiD51 : new mediators of mitochondrial division. [Doctoral Dissertation]. Latrobe University; 2012. Available from: http://hdl.handle.net/1959.9/530588

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