subject:( Ferroptosis)

Deakin University

1. Masaldan, Shashank. Investigating metal aberrations in cellular senescence.

Degree: School of Life and Environmental Sciences, 2017, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30103501

► This study explored perturbations in iron and copper homeostasis in senescent cells that contribute to age-associated disease and dysfunction. Altered metal regulation was associated with… (more)

Subjects/Keywords: ageing; autophagy; healthspan; senescence; ferritin; ferritinophagy; ferroptosis

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APA (6^th Edition):

Masaldan, S. (2017). Investigating metal aberrations in cellular senescence. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30103501

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):

Masaldan, Shashank. “Investigating metal aberrations in cellular senescence.” 2017. Thesis, Deakin University. Accessed December 12, 2019. http://hdl.handle.net/10536/DRO/DU:30103501.

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

MLA Handbook (7^th Edition):

Masaldan, Shashank. “Investigating metal aberrations in cellular senescence.” 2017. Web. 12 Dec 2019.

Vancouver:

Masaldan S. Investigating metal aberrations in cellular senescence. [Internet] [Thesis]. Deakin University; 2017. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/10536/DRO/DU:30103501.

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

Council of Science Editors:

Masaldan S. Investigating metal aberrations in cellular senescence. [Thesis]. Deakin University; 2017. Available from: http://hdl.handle.net/10536/DRO/DU:30103501

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

University of Arizona

2. Kerins, Michael John. Ironing Out Roles and Regulation of NRF2 in a Hereditary Cancer Syndrome .

Degree: 2019, University of Arizona

URL: http://hdl.handle.net/10150/633229

► The deadly kidney cancers associated with hereditary leiomyomatosis and renal cell cancer (HLRCC) show activation of the nuclear factor (erythroid 2)-like 2 (NFE2L2, NRF2) transcription… (more)

Subjects/Keywords: Cancer; ferroptosis; HLRCC; iron; NRF2; signaling

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APA (6^th Edition):

Kerins, M. J. (2019). Ironing Out Roles and Regulation of NRF2 in a Hereditary Cancer Syndrome . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/633229

Chicago Manual of Style (16^th Edition):

Kerins, Michael John. “Ironing Out Roles and Regulation of NRF2 in a Hereditary Cancer Syndrome .” 2019. Doctoral Dissertation, University of Arizona. Accessed December 12, 2019. http://hdl.handle.net/10150/633229.

MLA Handbook (7^th Edition):

Kerins, Michael John. “Ironing Out Roles and Regulation of NRF2 in a Hereditary Cancer Syndrome .” 2019. Web. 12 Dec 2019.

Vancouver:

Kerins MJ. Ironing Out Roles and Regulation of NRF2 in a Hereditary Cancer Syndrome . [Internet] [Doctoral dissertation]. University of Arizona; 2019. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/10150/633229.

Council of Science Editors:

Kerins MJ. Ironing Out Roles and Regulation of NRF2 in a Hereditary Cancer Syndrome . [Doctoral Dissertation]. University of Arizona; 2019. Available from: http://hdl.handle.net/10150/633229

University of Ottawa

3. Shah, Ronak. Autoxidation and its Inhibition in Both Industrial and Biological Contexts: New Molecules, Methods & Mechanisms .

Degree: 2019, University of Ottawa

URL: http://hdl.handle.net/10393/39838

► Autoxidation, a radical chain reaction, is largely responsible for the degradation of most man-made and biological materials. These include chemical products such as lubricants, plastics… (more)

▼ Autoxidation, a radical chain reaction, is largely responsible for the degradation of most man-made and biological materials. These include chemical products such as lubricants, plastics and rubber; as well as biological molecules and membranes within our bodies. The development of means to hinder this process has been a major focus of the petroleum, chemical, pharmaceutical and biotechnology industry over the past century. The two most common strategies to emerge from these efforts have been the use of compounds that either prevent the initiation of autoxidation or trap the propagating radicals, so-called radical-trapping antioxidants (RTAs). Herein, we describe our efforts towards the design and development of extremely potent heterocyclic diarylamine RTAs, and their activity in a variety of applications ranging from isotropic organic solution to mammalian cells. We have elucidated the important structural motifs and mechanistic considerations necessary for the development of next-generation arylamine RTAs. Some of the substituted heterocyclic diarylamines analogs we disclose are among the best inhibitors of high temperature autoxidations described to date. Alongside, we developed novel analytical tools to facilitate the studies and acquisition of results for characterizing RTA activity in organic solutions and lipid bilayers. These fluorescent probes are highly relevant and allow for the determination of hydroperoxide and acid concentrations rapidly, as well as screen (or counter-screen) RTAs in liposomal membranes. Our methodologies address numerous drawbacks from frequently used ‘plug-and-play’ assays and we anticipate they will fill a current unmet need in both industrial and academic laboratories worldwide. Moreover, the recent characterization of ferroptosis – a novel regulated necrotic-like cell-death pathway associated with the accumulation of lipid hydroperoxides – has paved a way forward for studying oxidation induced damage in a biological context. Utilizing our expertise in lipid peroxidation and inhibition, we elucidated the prominent role of autoxidation in the execution of ferroptotic cell death. Alongside, our analytical tools and RTAs have also enabled the identification and characterization of novel ferroptosis inhibitors. Furthermore, this has prompted the development of a correlation to predict anti-ferroptosis activity of small-molecules using simple spectrophotometric assays.

Subjects/Keywords: Ferroptosis; Autoxidation; Antioxidant; Lipoxygenase; Antioxidant Assay; Diarylamines

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APA (6^th Edition):

Shah, R. (2019). Autoxidation and its Inhibition in Both Industrial and Biological Contexts: New Molecules, Methods & Mechanisms . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/39838

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):

Shah, Ronak. “Autoxidation and its Inhibition in Both Industrial and Biological Contexts: New Molecules, Methods & Mechanisms .” 2019. Thesis, University of Ottawa. Accessed December 12, 2019. http://hdl.handle.net/10393/39838.

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

MLA Handbook (7^th Edition):

Shah, Ronak. “Autoxidation and its Inhibition in Both Industrial and Biological Contexts: New Molecules, Methods & Mechanisms .” 2019. Web. 12 Dec 2019.

Vancouver:

Shah R. Autoxidation and its Inhibition in Both Industrial and Biological Contexts: New Molecules, Methods & Mechanisms . [Internet] [Thesis]. University of Ottawa; 2019. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/10393/39838.

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

Council of Science Editors:

Shah R. Autoxidation and its Inhibition in Both Industrial and Biological Contexts: New Molecules, Methods & Mechanisms . [Thesis]. University of Ottawa; 2019. Available from: http://hdl.handle.net/10393/39838

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

Duke University

4. Ding, Chien-Kuang Cornelia. Regulation of Ferroptosis by a novel NADPH phosphatase MESH1 .

Degree: 2019, Duke University

URL: http://hdl.handle.net/10161/18658

► Ferroptosis is a form of regulated cell death featured by lipid peroxidation and breakage of cell membrane. However, the molecular mediators and regulators are… (more)

Subjects/Keywords: Biochemistry; Molecular biology; Ferroptosis; HDDC3; MESH1; NADPH

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APA (6^th Edition):

Ding, C. C. (2019). Regulation of Ferroptosis by a novel NADPH phosphatase MESH1 . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/18658

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):

Ding, Chien-Kuang Cornelia. “Regulation of Ferroptosis by a novel NADPH phosphatase MESH1 .” 2019. Thesis, Duke University. Accessed December 12, 2019. http://hdl.handle.net/10161/18658.

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

MLA Handbook (7^th Edition):

Ding, Chien-Kuang Cornelia. “Regulation of Ferroptosis by a novel NADPH phosphatase MESH1 .” 2019. Web. 12 Dec 2019.

Vancouver:

Ding CC. Regulation of Ferroptosis by a novel NADPH phosphatase MESH1 . [Internet] [Thesis]. Duke University; 2019. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/10161/18658.

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

Council of Science Editors:

Ding CC. Regulation of Ferroptosis by a novel NADPH phosphatase MESH1 . [Thesis]. Duke University; 2019. Available from: http://hdl.handle.net/10161/18658

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

University of Ottawa

5. Zilka, Omkar. On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death & Targeting Tetrahydronaphthyridinols to the Mitochondria .

Degree: 2018, University of Ottawa

URL: http://hdl.handle.net/10393/37343

► Lipid peroxidation is well established to contribute to the etiology of many deteriorative conditions including neurodegeneration, cardiovascular disease, cancer, aging, and recently in ferroptosis—a regulated,… (more)

Subjects/Keywords: lipid autoxidation; ferroptosis; oxidative stress; mitochondria; radical trapping antioxidant

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APA (6^th Edition):

Zilka, O. (2018). On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death & Targeting Tetrahydronaphthyridinols to the Mitochondria . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/37343

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):

Zilka, Omkar. “On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death & Targeting Tetrahydronaphthyridinols to the Mitochondria .” 2018. Thesis, University of Ottawa. Accessed December 12, 2019. http://hdl.handle.net/10393/37343.

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

MLA Handbook (7^th Edition):

Zilka, Omkar. “On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death & Targeting Tetrahydronaphthyridinols to the Mitochondria .” 2018. Web. 12 Dec 2019.

Vancouver:

Zilka O. On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death & Targeting Tetrahydronaphthyridinols to the Mitochondria . [Internet] [Thesis]. University of Ottawa; 2018. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/10393/37343.

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

Council of Science Editors:

Zilka O. On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death & Targeting Tetrahydronaphthyridinols to the Mitochondria . [Thesis]. University of Ottawa; 2018. Available from: http://hdl.handle.net/10393/37343

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

University of Manitoba

6. Blankstein, Anna R. Siramesine and lapatinib induce synergic cell death via a ferroptotic mechanism in lung adenocarcinoma and glioblastoma cells.

Degree: Biochemistry and Medical Genetics, 2017, University of Manitoba

URL: http://hdl.handle.net/1993/32404

► In cancer cells, the most common forms of cell death are often actively inhibited, contributing to the development of drug resistance. Identifying and exploiting alternative… (more)

Subjects/Keywords: Cell death; Ferroptosis; Glioblastoma; Lung adenocarcinoma; Drug synergy; Drug repurposing

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APA (6^th Edition):

Blankstein, A. R. (2017). Siramesine and lapatinib induce synergic cell death via a ferroptotic mechanism in lung adenocarcinoma and glioblastoma cells. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/32404

Chicago Manual of Style (16^th Edition):

Blankstein, Anna R. “Siramesine and lapatinib induce synergic cell death via a ferroptotic mechanism in lung adenocarcinoma and glioblastoma cells.” 2017. Masters Thesis, University of Manitoba. Accessed December 12, 2019. http://hdl.handle.net/1993/32404.

MLA Handbook (7^th Edition):

Blankstein, Anna R. “Siramesine and lapatinib induce synergic cell death via a ferroptotic mechanism in lung adenocarcinoma and glioblastoma cells.” 2017. Web. 12 Dec 2019.

Vancouver:

Blankstein AR. Siramesine and lapatinib induce synergic cell death via a ferroptotic mechanism in lung adenocarcinoma and glioblastoma cells. [Internet] [Masters thesis]. University of Manitoba; 2017. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/1993/32404.

Council of Science Editors:

Blankstein AR. Siramesine and lapatinib induce synergic cell death via a ferroptotic mechanism in lung adenocarcinoma and glioblastoma cells. [Masters Thesis]. University of Manitoba; 2017. Available from: http://hdl.handle.net/1993/32404

University of Ottawa

7. Schaefer, Emily Lydia. On the Formation of Cholesterol Autoxidation Products in Lipid Bilayers and Electrophilic Secosterols Derived Therefrom .

Degree: 2019, University of Ottawa

URL: http://hdl.handle.net/10393/39568

► Lipid peroxidation is believed to play a key role in the onset and progression of degenerative disease. Interestingly, although cholesterol is the most abundant lipid… (more)

▼ Lipid peroxidation is believed to play a key role in the onset and progression of degenerative disease. Interestingly, although cholesterol is the most abundant lipid in the human body, our understanding of its autoxidation and subsequent decomposition is relatively limited. In fact, until recently, cholesterol-7-hydroperoxide was accepted as the only primary product of cholesterol autoxidation in organic solution, however, our group exhibited that the 4-, 5-, and 6-hydroperoxides are also formed. Although this work facilitated thorough investigation of the complexities of both H-atom abstraction and addition in cholesterol autoxidation in organic solution, it did not account for the dynamic environment of a cell membrane. Herein, we report on the product distribution of these primary autoxidation products in lipid bilayers and how antioxidant supplementation, H-bonding interactions, and concentration of polyunsaturated fatty acid (PUFA) substrate influence both the product distribution and efficiency of autoxidation. Indeed, not only does H-bonding of the 3β-OH of cholesterol appear to shut-down C4 H-atom abstraction, the absence of kinetic chol-5α-OOH product is likely due to the poor potency of α- tocopherol (α-TOH), also as a result of H-bonding with phosphate head group of lipid membrane phospholipids. Therefore, within a lipid membrane the 7-hydroperoxide products predominate, consistent with literature precedent, however the factors involved are more complex than previously understood. Moreover, with the authentic cholesterol hydroperoxides in hand, we sought to determine if the different regioisomers exhibit different cytotoxicity. Glutathione peroxidases (GPXs) are cytoprotective enzymes that reduce harmful hydroperoxides to benign alcohols in vivo. Using RSL3, a small-molecule inhibitor for GPX4, we were able to sensitize mammalian cells to ferroptotic cell death via administration of our exogenously prepared chol-OOHs. Surprisingly, we found that the toxicities of each of 7α-OOH, 6β-OOH and 5α-OOH were only marginally augmented by RSL3 treatment, suggesting that they do not substantially sensitize cells to ferroptosis, perhaps because their decomposition to lipid peroxidation chain-initiating species (i.e. alkoxyl radicals) is not particularly efficient. Instead their cytotoxicities may derive from other mechanisms, such as the induction of apoptosis. This inspired our investigation of the fate of lipid hydroperoxides in vivo, namely the secondary products of the predominant 7-hydroperoxide species. Acid-catalyzed Hock fragmentation, known for the industrial synthesis of phenol and acetone from cumene or implication in the generation of 4-hydroxynonenal (4-HNE), of 5α- and 6β-OOH has been shown by our group to produce highly electrophilic secosterol species; we sought to investigate the same decomposition mechanism for 7α-OOH in light of our investigations in the lipid membrane. Interestingly, we found that Hock fragmentation of 7α-OOH does not exhibit products resulting from the anticipated O-vinyl…

Subjects/Keywords: Cholesterol autoxidation; Lipid peroxidation; Secosterols; Ferroptosis; Atherosclerosis; Antioxidants

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APA (6^th Edition):

Schaefer, E. L. (2019). On the Formation of Cholesterol Autoxidation Products in Lipid Bilayers and Electrophilic Secosterols Derived Therefrom . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/39568

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):

Schaefer, Emily Lydia. “On the Formation of Cholesterol Autoxidation Products in Lipid Bilayers and Electrophilic Secosterols Derived Therefrom .” 2019. Thesis, University of Ottawa. Accessed December 12, 2019. http://hdl.handle.net/10393/39568.

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

MLA Handbook (7^th Edition):

Schaefer, Emily Lydia. “On the Formation of Cholesterol Autoxidation Products in Lipid Bilayers and Electrophilic Secosterols Derived Therefrom .” 2019. Web. 12 Dec 2019.

Vancouver:

Schaefer EL. On the Formation of Cholesterol Autoxidation Products in Lipid Bilayers and Electrophilic Secosterols Derived Therefrom . [Internet] [Thesis]. University of Ottawa; 2019. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/10393/39568.

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

Council of Science Editors:

Schaefer EL. On the Formation of Cholesterol Autoxidation Products in Lipid Bilayers and Electrophilic Secosterols Derived Therefrom . [Thesis]. University of Ottawa; 2019. Available from: http://hdl.handle.net/10393/39568

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

University of California – San Diego

8. Hoong, Christina. Synthesis, Design, and Cytotoxicity of Organoferrous Anticancer Agents.

Degree: Chemistry, 2017, University of California – San Diego

URL: http://www.escholarship.org/uc/item/4dk1c7nz

► Since the discovery of ferrocene in 1951 and subsequent structure elucidation in the following years, a wealth of literature is available on ferrocene functionalization. The… (more)

Subjects/Keywords: Organic chemistry; anticancer; benzoyl ferrocene derivatives; ferrocenyl agents; ferroptosis; iron homeostasis; small molecule synthesis

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APA (6^th Edition):

Hoong, C. (2017). Synthesis, Design, and Cytotoxicity of Organoferrous Anticancer Agents. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/4dk1c7nz

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):

Hoong, Christina. “Synthesis, Design, and Cytotoxicity of Organoferrous Anticancer Agents.” 2017. Thesis, University of California – San Diego. Accessed December 12, 2019. http://www.escholarship.org/uc/item/4dk1c7nz.

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

MLA Handbook (7^th Edition):

Hoong, Christina. “Synthesis, Design, and Cytotoxicity of Organoferrous Anticancer Agents.” 2017. Web. 12 Dec 2019.

Vancouver:

Hoong C. Synthesis, Design, and Cytotoxicity of Organoferrous Anticancer Agents. [Internet] [Thesis]. University of California – San Diego; 2017. [cited 2019 Dec 12]. Available from: http://www.escholarship.org/uc/item/4dk1c7nz.

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

Council of Science Editors:

Hoong C. Synthesis, Design, and Cytotoxicity of Organoferrous Anticancer Agents. [Thesis]. University of California – San Diego; 2017. Available from: http://www.escholarship.org/uc/item/4dk1c7nz

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

Université de Montréal

9. Saint-Germain, Emmanuelle. Mécanismes moléculaires de régulation de l’interaction SOCS1-p53 et leurs impacts sur la suppression tumorale .

Degree: 2018, Université de Montréal

URL: http://hdl.handle.net/1866/21191

Subjects/Keywords: SOCS1; p53; Senescence; Ferroptose; Phosphorylation; Kinases SRC; Cancer; YES1; SFK; Ferroptosis; Kinases; SFKs; SRC

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APA (6^th Edition):

Saint-Germain, E. (2018). Mécanismes moléculaires de régulation de l’interaction SOCS1-p53 et leurs impacts sur la suppression tumorale . (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/21191

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):

Saint-Germain, Emmanuelle. “Mécanismes moléculaires de régulation de l’interaction SOCS1-p53 et leurs impacts sur la suppression tumorale .” 2018. Thesis, Université de Montréal. Accessed December 12, 2019. http://hdl.handle.net/1866/21191.

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

MLA Handbook (7^th Edition):

Saint-Germain, Emmanuelle. “Mécanismes moléculaires de régulation de l’interaction SOCS1-p53 et leurs impacts sur la suppression tumorale .” 2018. Web. 12 Dec 2019.

Vancouver:

Saint-Germain E. Mécanismes moléculaires de régulation de l’interaction SOCS1-p53 et leurs impacts sur la suppression tumorale . [Internet] [Thesis]. Université de Montréal; 2018. [cited 2019 Dec 12]. Available from: http://hdl.handle.net/1866/21191.

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

Council of Science Editors:

Saint-Germain E. Mécanismes moléculaires de régulation de l’interaction SOCS1-p53 et leurs impacts sur la suppression tumorale . [Thesis]. Université de Montréal; 2018. Available from: http://hdl.handle.net/1866/21191

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

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