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You searched for +publisher:"Dalhousie University" +contributor:("Dr. Melanie Dobson"). Showing records 1 – 3 of 3 total matches.

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Dalhousie University

1. Tse, Brenda. IDENTIFICATION AND CHARACTERIZATION OF PROMYELOCYTIC LEUKEMIA (PML)-ISOFORM 1 SPECIFIC PROTEIN-PROTEIN INTERACTIONS.

Degree: MS, Department of Pathology, 2012, Dalhousie University

URL: http://hdl.handle.net/10222/15493 

Loss of the promyelocytic leukemia (PML) protein is associated with genomic instability/cancer. There are several isoforms of the PML protein that localize in PML nuclear bodies (PML NBs). How each individual isoform contributes to the functions of PML NBs is unknown. The objective of this study was to identify and characterize PML isoform-I (PML-I) specific protein-protein interactions. Using yeast two-hybrid screens, several interacting partners of PML-I were identified that play roles in translational regulation, including eukaryotic initiation factor 3 subunit K (eIF3K). Our studies demonstrated that eIF3K interacts with PML-I in vitro and in vivo. Through its interaction with eIF3K, overexpression of PML-I resulted in the concomitant increase in eIF3K protein levels in mammalian cells. This suggests that PML-I may be involved in regulating eIF3K protein translation or stability, which in turn could affect translation of specific mRNAs or global translation in cancer cells with reduced expression of PML-I. Advisors/Committee Members: Dr. Catherine Too (external-examiner), Dr. Wenda Greer (graduate-coordinator), Dr. Melanie Dobson (thesis-reader), Dr. David Waisman (thesis-reader), Dr. Graham Dellaire (thesis-supervisor), Not Applicable (ethics-approval), Not Applicable (manuscripts), Not Applicable (copyright-release).

Subjects/Keywords: PML and PML isoforms; PML nuclear bodies; eIF3K; Translation initiation; Yeast two-hybrid screen

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

APA (6th Edition):

Tse, B. (2012). IDENTIFICATION AND CHARACTERIZATION OF PROMYELOCYTIC LEUKEMIA (PML)-ISOFORM 1 SPECIFIC PROTEIN-PROTEIN INTERACTIONS. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15493

Chicago Manual of Style (16th Edition):

Tse, Brenda. “IDENTIFICATION AND CHARACTERIZATION OF PROMYELOCYTIC LEUKEMIA (PML)-ISOFORM 1 SPECIFIC PROTEIN-PROTEIN INTERACTIONS.” 2012. Masters Thesis, Dalhousie University. Accessed January 19, 2021. http://hdl.handle.net/10222/15493.

MLA Handbook (7th Edition):

Tse, Brenda. “IDENTIFICATION AND CHARACTERIZATION OF PROMYELOCYTIC LEUKEMIA (PML)-ISOFORM 1 SPECIFIC PROTEIN-PROTEIN INTERACTIONS.” 2012. Web. 19 Jan 2021.

Vancouver:

Tse B. IDENTIFICATION AND CHARACTERIZATION OF PROMYELOCYTIC LEUKEMIA (PML)-ISOFORM 1 SPECIFIC PROTEIN-PROTEIN INTERACTIONS. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/10222/15493.

Council of Science Editors:

Tse B. IDENTIFICATION AND CHARACTERIZATION OF PROMYELOCYTIC LEUKEMIA (PML)-ISOFORM 1 SPECIFIC PROTEIN-PROTEIN INTERACTIONS. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15493


Dalhousie University

2. Racine, Trina. THE AVIAN REOVIRUS TRICISTRONIC S1 mRNA: NEW INSIGHTS INTO CONTROL OF TRANSLATION INITIATION.

Degree: PhD, Department of Microbiology & Immunology, 2010, Dalhousie University

URL: http://hdl.handle.net/10222/12842 

The S1 genome segment of avian reovirus is functionally tricistronic, encoding three independent protein products (named p10, p17 and ?C) from three sequential, partially overlapping open reading frames (ORFs). The dogma of translation initiation, the cap-dependent scanning model, suggests that ribosomes would normally only translate the 5?-proximal ORF. Four alternate mechanisms of translation initiation could account for translation of the downstream ?C ORF; an IRES element, reinitiation, ribosome shunting, and leaky scanning. The objective of my doctoral research was to investigate the translation initiation mechanisms that are operative on the S1 mRNA. Translation of the p10 and p17 ORFs was revealed to be coordinated via standard leaky scanning, while none of the known mechanisms of translation initiation could account for expression of the ?C ORF. Further investigation determined that two alternate cap-dependent mechanisms contribute to translation initiation at the ?C AUG codon. The first mechanism involves a modified version of enhanced leaky scanning. Although insertion of upstream elements known to impede scanning ribosomal subunits dramatically inhibited translation of the downstream ORF in the context of other mRNAs, the same elements only marginally reduced ?C translation. Specific features of the S1 mRNA therefore function to promote leaky scanning and translation of the ?C ORF. The inability to eliminate ?C expression beyond a threshold retention level of ~20-30%, despite the presence of eight upstream start codons that should eliminate leaky scanning, strongly suggests that ribosomes must also utilize a scanning-independent means to access the internal ?C start site. This mechanism for ?C translation initiation, which I termed ribosome handoff, allows ribosomes to bypass upstream elements, and requires a sequence-dependent translation enhancer element present within S1 nucleotides 366-392 that may function to mediate handoff via complementarity with 18S ribosomal RNA. Translation initiation at the ?C start site is therefore made possible by two alternative mechanisms, enhanced leaky scanning and ribosome handoff from the 5?-cap. The novelty of these two mechanisms highlights the complexity of the translation initiation process and the potential heterogeneity of cellular ribosomes, which raises the possibility that internal initiation may be far more common than currently appreciated. Advisors/Committee Members: Dr. John Patton (external-examiner), Dr. Brent Johnston (graduate-coordinator), Dr. Christine Barnes (thesis-reader), Dr. Melanie Dobson (thesis-reader), Dr. Patrick Lee (thesis-reader), Dr. Roy Duncan (thesis-supervisor), Not Applicable (ethics-approval), Not Applicable (manuscripts), Not Applicable (copyright-release).

Subjects/Keywords: Translation Initiation; Avian Reovirus; S1 mRNA

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

APA (6th Edition):

Racine, T. (2010). THE AVIAN REOVIRUS TRICISTRONIC S1 mRNA: NEW INSIGHTS INTO CONTROL OF TRANSLATION INITIATION. (Doctoral Dissertation). Dalhousie University. Retrieved from http://hdl.handle.net/10222/12842

Chicago Manual of Style (16th Edition):

Racine, Trina. “THE AVIAN REOVIRUS TRICISTRONIC S1 mRNA: NEW INSIGHTS INTO CONTROL OF TRANSLATION INITIATION.” 2010. Doctoral Dissertation, Dalhousie University. Accessed January 19, 2021. http://hdl.handle.net/10222/12842.

MLA Handbook (7th Edition):

Racine, Trina. “THE AVIAN REOVIRUS TRICISTRONIC S1 mRNA: NEW INSIGHTS INTO CONTROL OF TRANSLATION INITIATION.” 2010. Web. 19 Jan 2021.

Vancouver:

Racine T. THE AVIAN REOVIRUS TRICISTRONIC S1 mRNA: NEW INSIGHTS INTO CONTROL OF TRANSLATION INITIATION. [Internet] [Doctoral dissertation]. Dalhousie University; 2010. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/10222/12842.

Council of Science Editors:

Racine T. THE AVIAN REOVIRUS TRICISTRONIC S1 mRNA: NEW INSIGHTS INTO CONTROL OF TRANSLATION INITIATION. [Doctoral Dissertation]. Dalhousie University; 2010. Available from: http://hdl.handle.net/10222/12842


Dalhousie University

3. Holloway, Ryan. MACROPHAGE AEBP1 CONTRIBUTES TO MAMMARY EPITHELIAL CELL HYPERPLASIA AS A NOVEL REGULATOR OF SONIC HEDGEHOG SIGNALLING.

Degree: MS, Department of Biochemistry & Molecular Biology, 2012, Dalhousie University

URL: http://hdl.handle.net/10222/15828 

Chronic inflammation stimulates mammary tumourigenesis by disrupting signalling interactions between the epithelial ducts and the surrounding stromal microenvironment. Adipocyte enhancer-binding protein 1 (AEBP1) promotes mammary epithelial cell hyperplasia as a stromal factor that enhances activity of the proinflammatory transcription factor Nuclear Factor-?B (NF-?B) in macrophages. Aberrant NF-?B activity in macrophages elevates production of proinflammatory signals and the ligand sonic hedgehog (Shh), a significant contributor to tumourigenesis. In this study, Shh expression was elevated in macrophages isolated from transgenic mice (AEBP1TG) that overexpress AEBP1. Transient overexpression of AEBP1 in a macrophage cell line resulted in increased Shh expression. Furthermore, hedgehog target genes Gli1 and Bmi1 were up-regulated in mammary epithelium of AEBP1TG mice and HC11 mammary epithelial cells co-cultured with AEBP1TG macrophages. Growth of HC11 cells and mammary tumours was enhanced in response to AEBP1TG macrophages. These findings suggest that macrophage AEBP1 overexpression contributes to mammary hyperplasia through enhanced hedgehog signalling. Advisors/Committee Members: n/a (external-examiner), Dr. Richard Singer (graduate-coordinator), Dr. Melanie Dobson (thesis-reader), Dr. Graham Dellaire (thesis-reader), Dr. Paola Marignani (thesis-reader), Dr. Hyo-Sung Ro (thesis-supervisor), Received (ethics-approval), Yes (manuscripts), Yes (copyright-release).

Subjects/Keywords: hyperplasia; Sonic hedgehog; mammary gland; macrophage; AEBP1

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

APA (6th Edition):

Holloway, R. (2012). MACROPHAGE AEBP1 CONTRIBUTES TO MAMMARY EPITHELIAL CELL HYPERPLASIA AS A NOVEL REGULATOR OF SONIC HEDGEHOG SIGNALLING. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15828

Chicago Manual of Style (16th Edition):

Holloway, Ryan. “MACROPHAGE AEBP1 CONTRIBUTES TO MAMMARY EPITHELIAL CELL HYPERPLASIA AS A NOVEL REGULATOR OF SONIC HEDGEHOG SIGNALLING.” 2012. Masters Thesis, Dalhousie University. Accessed January 19, 2021. http://hdl.handle.net/10222/15828.

MLA Handbook (7th Edition):

Holloway, Ryan. “MACROPHAGE AEBP1 CONTRIBUTES TO MAMMARY EPITHELIAL CELL HYPERPLASIA AS A NOVEL REGULATOR OF SONIC HEDGEHOG SIGNALLING.” 2012. Web. 19 Jan 2021.

Vancouver:

Holloway R. MACROPHAGE AEBP1 CONTRIBUTES TO MAMMARY EPITHELIAL CELL HYPERPLASIA AS A NOVEL REGULATOR OF SONIC HEDGEHOG SIGNALLING. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/10222/15828.

Council of Science Editors:

Holloway R. MACROPHAGE AEBP1 CONTRIBUTES TO MAMMARY EPITHELIAL CELL HYPERPLASIA AS A NOVEL REGULATOR OF SONIC HEDGEHOG SIGNALLING. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15828

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