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Al-Lawati, Sabah Ali Redha. "Differential gene expression in schizophrenia." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420028.
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Sweeney, Glen E. "Differential gene expression in Physarum." Thesis, University of Leicester, 1987. http://hdl.handle.net/2381/35166.
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Physarum polycephalum has a life-cycle that encompasses two very distinct vegetatively growing cell-types; uninucleate microscopic amoebae, and multinucleate macroscopic plasmodia. cDNA libraries have been prepared from both amoebae and plasmodia using the M13 vector mp8. Clones from the two libraries were screened using a differential hybridisation procedure that identifies clones derived from mRNAs much more abundant in one cell-type than in the other. For both the amoebal library and the plasmodial library it was found that about 5% of the clones represented genes preferentially expressed in the cell-type from which the library was prepared. Some of the cell-type-specific clones obtained were used to probe northern blots of amoebal and plasmodial RNA. Two of the plasmodial-specific clones were found to be derived from highly abundant mRNAs, constituting between 0.5% and 2% of total plasmodial mRNA. Selected clones were then used to look at changes in mRNA concentrations during development by probing northern blots of RNA from amoebae, plasmodia and intermediate cell-types. It was found that the plasmodial-specific mRNAs examined fell into two classes; those expressed early in development, and those expressed late in development. The amoebal-specific clones analysed constituted a single group, with each of the probes used detecting an mRNA whose concentration declined markedly in early development. Some of the changes in gene expression were examined more quantitatively by dot blotting. It was found that the difference in concentration of cell-type-specific mRNAs between amoebae and plasmodia varied from between 10 fold to greater than 100 fold. Analysis of the pattern of gene expression was begun in two mutant strains of Physarum which are unable to complete development. Results obtained from a strain which is arrested late in development (RA612) suggest that the developmentally arrested cells express the plasmodial-specific genes which are activated early in development, but not those that become active late in development. A few of the clones have been sequenced, but no homologies with genes sequenced in other systems were detected.
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Fung, Lai-fan. "Differential gene expression in nasopharyngeal carcinoma /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20604609.
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Liebermeister, Wolfram. "Analysis of optimal differential gene expression." Doctoral thesis, [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=97257347X.
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馮麗芬 and Lai-fan Fung. "Differential gene expression in nasopharyngeal carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31220824.
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方佩儀 and Pui-yee Fong. "Differential gene expression in gestational trophoblastic disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224362.
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Hu, Yanmin. "Differential gene expression in dormant mycobacterium tuberculosis." Thesis, St George's, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325140.
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Ghate, Aditée. "The opioid system and differential gene expression." Université Louis Pasteur (Strasbourg) (1971-2008), 2006. http://www.theses.fr/2006STR13019.
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Le système opioïde consiste en trois sous-types de récepteurs opioïdes (delta, mu et kappa) appartenant à la famille des récepteurs couplés aux protéines G, qui sont activés soit par une famille de peptides endogènes, soit par des ligands exogènes. Les récepteurs opioïdes médient les propriétés renforçantes de la morphine et de ses dérivés. L’administration répétée d’opiacés modifie le niveau de transcription de certains gènes dans certaines régions du cerveau de rongeurs, un effet qui serait une des bases moléculaires possibles de la plasticité neuronale associée au comportement addictif. La technologie des « microarrays » ou « puces » permet d’obtenir une image générale de l’expression de l’ensemble des transcrits dans une cellule. Nous avons observé que les souris déficientes en récepteurs mu ne répondent pas aux effets renforçants ou addictifs de la morphine. Des études ont montré que ces animaux mutantes ne montrent aucune préférence pour l’alcool, le THC et la nicotine. Notre hypothèse est que le récepteur mu serait un élément clé dans la mise en place du comportement addictif. Les souris déficientes en récepteur mu représentent un outil unique pour identifier des phénomènes adaptatifs communs à l’ensemble des drogues d’abus. Nous proposons d’utiliser cette lignée pour identifier une collection de gènes dépendants du système opioïde endogène, et dont l’expression est communément dérégulée par l’administration chronique de drogues par la technique des puces. Au cours de ma thèse, j’ai développé l’utilisation, des puces à ADNc et à oligonucléotides pour mes différents projets : l’analyse de la variation d'expression de gènes lors de l’activation de récepteurs opioïdes; l’identification de gènes dont l’expression est restreinte à une structure du cerveau impliquée dans l’addiction ; et l’étude du phénotype obèse de souris déficientes pour les trois récepteurs opioïdesThe opioid system consists of three G-protein coupled receptors, mu, delta, and kappa, which are stimulated by a family of endogenous opioid peptides like beta-endorphin and exogenous ligands such as morphine. It is believed that the repeated opiate administration alters gene expression in different brain regions of rodents, an effect which may contribute to plastic changes associated with addictive behaviour. Oligonucleotide and cDNA microarrays are the two most commonly used methods to profile the expression of thousands of genes in parallel. Gene expression studies performed by microarray analysis or by parallel measurements of the mRNA of multiple candidate genes have become a powerful tool to screen gene expression in the brain after application of drugs of abuse. Studies have shown that the reinforcing properties of morphine, alcohol, cannabinoids and nicotine are abolished or diminished in mice lacking the mu-opioid receptor. The genetic approach therefore highlights mu opioid receptors as convergent molecular switches which mediate reinforcement following direct (eg: morphine) or indirect activation (non-opioid drugs). Use of the mu-opioid receptor knockout mice would therefore help in identifying the genes, downstream of the mu-opioid receptor, that are commonly dysregulated following long term exposure to drugs of abuse. My thesis work involved establishment and use of cDNA and oligonucleotide microarrays screening tools in our laboratory to identify the transcriptional adaptations that occur on activation or in absence of the opioid receptors. I have also characterised obese phenotype observed in the triple opioid receptor knockout mice. Our laboratory is also interested in performing region-specific deletions of the opioid system and is therefore in the process of developing transgenic mice under region-specific promoters. A part of my thesis work also involved searching for region-specific markers for brain areas relevant in drug addiction
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Fong, Pui-yee. "Differential gene expression in gestational trophoblastic disease /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23440132.
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Andersson, Tove. "Approaches to differential gene expression analysis in atherosclerosis." Doctoral thesis, KTH, Biotechnology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-3400.
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Todays rapid development of powerful tools for geneexpression analysis provides unprecedented resources forelucidating complex molecular events.
The objective of this workhas been to apply, combine andevaluate tools for analysis of differential gene expressionusing atherosclerosis as a model system. First, an optimisedsolid-phase protocol for representational difference analysis(RDA) was applied to twoin vitromodel systems. Initially, The RDA enrichmentprocedure was investigated by shotgun cloning and sequencing ofsuccessive difference products. In the subsequent steps,combinations of RDA and microarray analysis were used tocombine the selectivity and sensitivity of RDA with thehigh-throughput nature of microarrays. This was achieved byimmobilization of RDA clones onto microarrays dedicated forgene expression analysis in atherosclerosis as well ashybridisation of labelled RDA products onto global microarrayscontaining more than 32,000 human clones. Finally, RDA wasapplied for the investigation of the focal localisation ofatherosclerotic plaques in mice usingin vivotissue samples as starting material.
A large number of differentially expressed clones wereisolated and confirmed by real time PCR. A very diverse rangeof gene fragments was identified in the RDA products especiallywhen they were screened with global microarrays. However, themicroarray data also seem to contain some noise which is ageneral problem using microarrays and should be compensated forby careful verification of the results.
Quite a large number of candidate genes related to theatherosclerotic process were found by these studies. Inparticular several nuclear receptors with altered expression inresponse to oxidized LDL were identified and deserve furtherinvestigation. Extended functional annotation does not liewithin the scope of this thesis but raw data in the form ofnovel sequences and accession numbers of known sequences havebeen made publicly available in GenBank. Parts of the data arealso available for interactive exploration on-line through aninteractive software tool. The data generated thus constitute abase for new hypotheses to be tested in the field ofatherosclerosis.
Keywords:representational difference analysis, geneexpression profiling, microarray analysis, atherosclerosis,foam cell formation
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De, las Heras Rachel, and n/a. "Neuronal Differentiation: A Study Into Differential Gene Expression." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040225.161725.
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Neuronal differentiation encompasses an elaborate developmental program which until recently was difficult to study in vitro. The advent of several cell lines able to differentiate in culture proved to be the turning point for gaining an understanding of molecular neuroscience. In particular the olfactory epithelium provides an attractive tool with which to investigate fundamental questions relating to neuronal differentiation, as it displays a unique capacity to regenerate and to retain a neurogenetic potential from its genesis and throughout adult life. The coordinated regulation of gene expression is fundamental to the control of neuronal differentiation. In order to reveal active processes at the molecular level and to dissect key components of molecular pathways, differential gene expression studies provide a foundation for the elucidation of dynamic molecular mechanisms. This thesis identified genes involved in neuronal differentiation by utilising a clonal olfactory receptor neuronal cell line (OLF442). Gene expression levels were identified using differential display and oligonucleotide array technology before and after serum deprivation. Differential display revealed two kinases whose expression levels were elevated during the differentiation of OLF442, identified as focal adhesion kinase (FAK) related non-kinase (FRNK) and mammalian ste20 like (MST)2 kinase. Furthermore, analysis of the oligonucleotide array data confirmed the expression of genes involved in altering presentation of extracellular matrix molecules, in mediating cytoskeletal rearrangements, and in ceasing the cell cycle, supporting the use of OLF442 as a model for studying differentiation. The differentiation of OLF442 results from the synchronisation of multiple transduction cascades and cellular responses as evidenced by the microarray data. A protein that can synchronise such signalling is the non-receptor protein tyrosine kinase, FAK. Thus the finding of the endogenous FAK inhibitor FRNK by differential display was intriguing as there was no difference in the expression level of FAK induced by differentiation, contrasting that of FRNK. This induced FRNK expression was derived autonomously as it was not responsive to the caspase-3 inhibitor, DEVD-CHO. This is particularly pertinent since the primary role of FRNK is to act as an inhibitor of FAK by competing with its substrates and reducing the phosphorylation of both FAK and its associated proteins. Differential display also revealed the upregulation of another kinase, which had 90% homology with rat MST2 kinase within the 3' UTR. Both mouse MST2 kinase (sequence submitted to GenBank, accession number AY058922) and the closely related family member MST1 kinase were sequenced and cloned. Moreover, evidence to support an autonomously expressed carboxyl-terminal domain of MST2 kinase is presented in Chapter 3 and provides a unique way in which MST2 may regulate its own activity. To further understand the role of MST in neuronal differentiation, a series of stable OLF442 transfections (with mutant and wild-type MST constructs) were carried out. MST was localised with cytoplasmic structures that may represent actin stress fibres, indicating a potential cytoskeletal role during neuronal differentiation. This indicated that MST1 may play a role in the morphological processes involved in neuronal differentiation. The identification of two kinases by differential display provided the motivation to understand the cellular context of OLF442 and to determine the phosphorylation status of the mitogen-activated protein kinase (MAPK) signalling cascades. Differentiation of OLF442 induced high-level phosphorylation of a putative B-Raf isoform, MEK2 and ERK1/2. Interestingly, there was a switch between preferential phosphorylation of MEK1 in undifferentiated OLF442 to preferential phosphorylation of MEK2 following differentiation. SAPK/JNK was also phosphorylated, as was the transcription factor c-Jun, which is a common substrate of both the ERK and SAPK/JNK signalling modules. The mapping of the cellular context of differentiating OLF442 has identified a promising model of a novel MAPK module. This consists of FAK signalling through Rap1 to ERK providing sustained activation, which is buffered or terminated by the expression of the endogenous FAK inhibitor FRNK. Furthermore, MST kinase could potentially play a role in regulating the cytoskeletal re-arrangements that are necessary for neuronal differentiation. MST kinase may signal transiently via the SAPK pathway to provide concomitant activation of c-Jun that is required for neuronal differentiation. An understanding of the gene expression pattern of the normal neuronal differentiation program allows a greater understanding of potential developmental aberrations. This could provide an opportunity for therapies to be conceived, while understanding the complexity of neuronal determination could also provide opportunities for stem cell transplantation.
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Bjork, Kathe Elizabeth. "Robust identification of differential gene expression and discrimination /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.
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Thesis (Ph.D. in Biostatistics) -- University of Colorado at Denver and Health Sciences Center, 2006.Typescript. Includes bibliographical references (leaves 237-239). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Neutze, Dana Michelle. "Differential gene expression and progression in cervical neoplasia." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614883.
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Chae, Taylor. "SEX-LINKED DIFFERENTIAL GENE EXPRESSION IN CARICA PAPAYA." Miami University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=miami1533049471465913.
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De, las Heras Rachel. "Neuronal Differentiation: A Study Into Differential Gene Expression." Thesis, Griffith University, 2003. http://hdl.handle.net/10072/367735.
Full textAbstract:
Neuronal differentiation encompasses an elaborate developmental program which until recently was difficult to study in vitro. The advent of several cell lines able to differentiate in culture proved to be the turning point for gaining an understanding of molecular neuroscience. In particular the olfactory epithelium provides an attractive tool with which to investigate fundamental questions relating to neuronal differentiation, as it displays a unique capacity to regenerate and to retain a neurogenetic potential from its genesis and throughout adult life. The coordinated regulation of gene expression is fundamental to the control of neuronal differentiation. In order to reveal active processes at the molecular level and to dissect key components of molecular pathways, differential gene expression studies provide a foundation for the elucidation of dynamic molecular mechanisms. This thesis identified genes involved in neuronal differentiation by utilising a clonal olfactory receptor neuronal cell line (OLF442). Gene expression levels were identified using differential display and oligonucleotide array technology before and after serum deprivation. Differential display revealed two kinases whose expression levels were elevated during the differentiation of OLF442, identified as focal adhesion kinase (FAK) related non-kinase (FRNK) and mammalian ste20 like (MST)2 kinase. Furthermore, analysis of the oligonucleotide array data confirmed the expression of genes involved in altering presentation of extracellular matrix molecules, in mediating cytoskeletal rearrangements, and in ceasing the cell cycle, supporting the use of OLF442 as a model for studying differentiation. The differentiation of OLF442 results from the synchronisation of multiple transduction cascades and cellular responses as evidenced by the microarray data. A protein that can synchronise such signalling is the non-receptor protein tyrosine kinase, FAK. Thus the finding of the endogenous FAK inhibitor FRNK by differential display was intriguing as there was no difference in the expression level of FAK induced by differentiation, contrasting that of FRNK. This induced FRNK expression was derived autonomously as it was not responsive to the caspase-3 inhibitor, DEVD-CHO. This is particularly pertinent since the primary role of FRNK is to act as an inhibitor of FAK by competing with its substrates and reducing the phosphorylation of both FAK and its associated proteins. Differential display also revealed the upregulation of another kinase, which had 90% homology with rat MST2 kinase within the 3 ΠUTR. Both mouse MST2 kinase (sequence submitted to GenBank, accession number AY058922) and the closely related family member MST1 kinase were sequenced and cloned. Moreover, evidence to support an autonomously expressed carboxyl-terminal domain of MST2 kinase is presented in Chapter 3 and provides a unique way in which MST2 may regulate its own activity. To further understand the role of MST in neuronal differentiation, a series of stable OLF442 transfections (with mutant and wild-type MST constructs) were carried out. MST was localised with cytoplasmic structures that may represent actin stress fibres, indicating a potential cytoskeletal role during neuronal differentiation. This indicated that MST1 may play a role in the morphological processes involved in neuronal differentiation. The identification of two kinases by differential display provided the motivation to understand the cellular context of OLF442 and to determine the phosphorylation status of the mitogen-activated protein kinase (MAPK) signalling cascades. Differentiation of OLF442 induced high-level phosphorylation of a putative B-Raf isoform, MEK2 and ERK1/2. Interestingly, there was a switch between preferential phosphorylation of MEK1 in undifferentiated OLF442 to preferential phosphorylation of MEK2 following differentiation. SAPK/JNK was also phosphorylated, as was the transcription factor c-Jun, which is a common substrate of both the ERK and SAPK/JNK signalling modules. The mapping of the cellular context of differentiating OLF442 has identified a promising model of a novel MAPK module. This consists of FAK signalling through Rap1 to ERK providing sustained activation, which is buffered or terminated by the expression of the endogenous FAK inhibitor FRNK. Furthermore, MST kinase could potentially play a role in regulating the cytoskeletal re-arrangements that are necessary for neuronal differentiation. MST kinase may signal transiently via the SAPK pathway to provide concomitant activation of c-Jun that is required for neuronal differentiation. An understanding of the gene expression pattern of the normal neuronal differentiation program allows a greater understanding of potential developmental aberrations. This could provide an opportunity for therapies to be conceived, while understanding the complexity of neuronal determination could also provide opportunities for stem cell transplantationThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Morgan, Daniel Colin. "A Gene Co-Expression Network Mining Approach for Differential Expression Analysis." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1416989632.
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Owens, Sarah Marie. "Differential expression of recent gene duplicates in developmental tissues of Arabidopsis thaliana." Oxford, Ohio : Miami University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1250185890.
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Crampton, Matthew S., and n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.
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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.
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Brownlie, Laura. "Differential gene expression studies in non-melanoma skin cancer." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323449.
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Crampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.
Full textAbstract:
Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Lam, T. H. Jason. "Differential gene expression associated with phenotypic virulence of mycobacterium tuberculosis." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37769005.
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Saul, Katherine E. "Differential gene expression in Danio rerio during optic nerve regeneration /." View online, 2008. http://ecommons.txstate.edu/bioltad/13.
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Lam, T. H. Jason, and 林梓軒. "Differential gene expression associated with phenotypic virulence of mycobacterium tuberculosis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37769005.
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Di, Capua Daniele-Mario. "Differential gene expression patterns of the vasculature in scleroderma biopsies." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:8881/R/?func=dbin-jump-full&object_id=92385.
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Liu, Zhiping. "Differential mucosal gene expression modulates the development of murine colitis." [Ames, Iowa : Iowa State University], 2008.
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McKenna, Louise Agnes. "Differential gene expression in normal and diseased human articular cartilage." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369207.
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Carter, Deborah. "Analysis of differential gene expression patterns in non-Hodgkin's lymphoma." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301273.
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Benvenuti, Silvia. "Differential gene expression in rodent embryo fibroblasts upon replicative senescence." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271477.
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Sharp, Matthew George Frederick. "Differential gene expression in benign and malignant human breast tumours." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/35146.
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Metastasis is a complex process involving the dissemination of tumour cells from the site of the primary tumour and their subsequent growth at a distant site. Metastasis is the major cause of death in breast cancer patients, and so the elucidation of molecular mechanisms of metastasis is a major goal in cancer research today. Two types of tumour which differ in their metastatic capacities were compared in an attempt to identify those genes which are associated with the malignant phenotype. Differential screening of cDNA libraries from fibroadenomas (benign) and carcinomas (malignant) of the breast was used to identify sequences corresponding to genes expressed at different levels in these two tissues. Expression of the sequences identified was predominantly in the epithelium of the tumour samples, as shown by in situ hybridisation, and the sequences fell into three groups. A number of transcripts of the mitochondrial genome were found to be more abundant in carcinoma samples, including subunit 2 of cytochrome c oxidase, subunits 2 and 4 of NADH dehydrogenase, and subunit 6 of F0F1ATPase, although the abundances of the latter three sequences were not significantly different when a larger panel was examined. Conversely, a group of translation-associated transcripts were found to be more abundant in fibroadenomas. The mRNAs corresponding to elongation factor 1? and the ribosomal protein P2 were more abundant in the benign tissue studied. This finding correlates positively with the higher levels of expression in fibroadenomas of another ribosomal protein (HUBCEP80) in the panel of tumours studied here. Similarly, differential screening indicates that the third group of sequences are more abundant in fibroadenomas relative to carcinomas. This group contains interspersed repetitive elements of the Alu family.
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Adam, Emma N. "DIFFERENTIAL GENE EXPRESSION IN EQUINE CARTILAGINOUS TISSUES AND INDUCED CHONDROCYTES." UKnowledge, 2016. http://uknowledge.uky.edu/gluck_etds/25.
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Degenerative joint disease, or osteoarthritis, is a major cause of lameness and morbidity in horses, humans, and dogs. There are no truly satisfactory cures for this widespread problem and current treatments all have limitations or unwanted side effects.
New cell-based strategies to repair joint surface lesions have generated a high level of interest, but have yet to achieve the full restoration of articular cartilage structure and function. Currently used therapy cells include autologous chondrocytes and adult mesenchymal cells such as bone marrow derived cells and adipose derived cells. Unfortunately, the resultant repair tissue is biomechanically inferior fibrocartilage. A critical gap in knowledge in this regard is a limited understanding of the specific cellular phenotype of normal, robust articular chondrocytes.
This thesis examines the global mRNA transcriptome of equine articular cartilage to test the hypothesis that adult articular chondrocytes have a unique gene expression profile. In the first part of the study, RNA-sequencing was used to compare the mRNA transcriptome of normal adult articular cartilage with five other cartilaginous tissues. From these comparisons, locus level gene expression and alternative splicing patterns have been identified that clearly distinguish articular cartilage. In the second part of the study, fetal (interzone, cartilage anlagen chondrocytes, dermal fibroblasts) and adult (bone marrow derived, adipose derived, articular chondrocytes, dermal fibroblasts) primary cells were grown in culture and stimulated to differentiate into chondrocytes. The chondrogenic differentiation potential as assessed by matrix proteoglycan and the expression of cartilage biomarker genes was highly variable among cell types. Together, these results advance our understanding of the specific phenotype of articular chondrocytes and the potential of prospective therapeutic progenitor cells to differentiate into articular chondrocytes. This new knowledge will improve efforts to optimize cell-based therapies for osteoarthritis and the repair of joint cartilage lesions.
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Dimont, Emmanuel. "Methods for the Analysis of Differential Composition of Gene Expression." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226062.
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Modern next-generation sequencing and microarray-based assays have empowered the computational biologist to measure various aspects of biological activity. This has led to the growth of genomics, transcriptomics and proteomics as fields of study of the complete set of DNA, RNA and proteins in living cells respectively. One major challenge in the analysis of this data, however, has been the widespread lack of sufficiently large sample sizes due to the high cost of new emerging technologies, making statistical inference difficult. In addition, due to the hierarchical nature of the various types of data, it is important to correctly integrate them to make meaningful biological discoveries and better informed decisions for the successful treatment of disease. In this dissertation I propose: (1) a novel method for more powerful statistical testing of differential digital gene expression between two conditions, (2) a framework for the integration of multi-level biologic data, demonstrated with the compositional analysis of gene expression and its link to promoter structure, and (3) an extension to a more complex generalized linear modeling framework, demonstrated with the compositional analysis of gene expression and its link to pathway structure adjusted for confounding covariates.
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Chapman, Tajekesa Kudzaishe Pamacheche. "Regulation of PABP1 function by differential post-translational modification." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25875.
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Post-transcriptional control of gene expression is critical for normal cellular function and viability. Poly(A)-binding protein (PABP) 1 is the prototypical member of a family of RNA-binding proteins which are key post-transcriptional regulators. PABP1 is multifunctional, acting as a primary determinant of translation efficiency and mRNA stability, regulating the fate of specific mRNAs, and participating in microRNAmediated regulation and nonsense-mediated mRNA decay. As well as binding various mRNAs, PABP1 achieves its multifunctionality through protein-protein interactions with numerous PABP-interacting motif (PAM)-2 motif-containing protein partners. These have been identified to bind the same site within the C-terminal PABC domain, therefore it is unclear how different PABP1 functions are coordinated. Recently, PABP1 was found to exhibit extensive post-translational modification (PTM), including putative lysine acetylation/methylation switches, which were suggested as a potential mechanism by which interactions with different PAM2 motifcontaining proteins may be regulated. In particular, in silico molecular modelling of the acetylation or dimethylation of the position 606 lysine residue (Lys606) within the PABC domain, using available structures of PABC in complex with PAM2 peptides of eukaryotic release factor (eRF)-3a and PABP-interacting protein (Paip)-2, suggested that modification of this residue, which is critical in PABC-PAM2 interactions, may differentially affect these PABP1 interactions. To examine the role of the Lys606 modification as a molecular switch to dictate PABC-mediated protein-protein interactions, site-specifically acetylated recombinant PABC domain was generated using cutting–edge amber codon suppression recoding technology. Following sequential purification by affinity, ion exchange and size exclusion chromatography, recombinant PABC protein quality was analysed by biophysical approaches such as thermal denaturation assay (TDA), dynamic light scattering (DLS), circular dichroism (CD) and liquid chromatography mass spectrometry (LCMS). Biochemical and biophysical analysis of PABC-PAM2 interactions was subsequently undertaken using GST-pulldown analysis, with the well characterised Paip2 protein, and Surface Plasmon Resonance (SPR) using PAM2 peptides of eRF3, Paip2 and trinucleotide repeat-containing (Tnrc) 6C (or GW182) proteins. These revealed that PABC Lys606 acetylation significantly increased the affinity and increased the association rate for eRF3 peptide. In contrast, effects on Paip2 peptide binding were less suggestive. Furthermore, although approaches to decipher the biological relevance of Lys606 and its modifications within cells are in their infancy, they reflect the complexity of studying PTM function in vitro. Overall, these data provide support for the hypothesis that Lys606 modification status confers selectivity between PABP1 protein partners suggesting a potential mechanism for how its multi-functionality may be coordinated.
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Stuiver, Ingrid. "Differential gene expression in TPA responsive and non-responsive mouse fibroblasts." Diss., The University of Arizona, 1992. http://hdl.handle.net/10150/185783.
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Our laboratory has previously isolated a 12-O-tetradecanoylphorbol-13-acetate (TPA)-nonresponsive variant line (VT-1) from mouse 3T3-L1 cells. Here the expression of type I collagen pro-α2 (pro-α2(I)) mRNA and production of type I collagen in these two cell lines is examined. In quiescent cells, the pro-α2(I) steady state mRNA levels were 4 times greater in 3T3-L1 cells than in VT-1 cells. TPA addition caused the steady-state levels of pro-α2(I) mRNA to be 6 times greater in 3T3-L1 cells than in VT-1 cells. The pro-α2(I) protein levels in the extracellular matrix or culture media of 3T3-L1 cells were substantially elevated by TPA treatment but no significant increase was detected in VT-1 cells. The correlation of collagen expression with a TPA-mediated mitogenic response suggests a new role for collagen as an early component of mitogenic signal transduction. Expression of protooncogenes and other mitogenically related genes were also examined in 3T3-L1 and VT-1 cells. c-fos, c-myc, c-jun and ornithine decarboxylase were expressed in both cell lines. These findings suggest that expression of these genes may be necessary but not sufficient for a TPA induced mitogenic response. Two of the TPA Inducible Early (TIE) genes selected had no homology with any other known sequence. Here, mRNA expression levels of these novel genes (TIE-10B and TIE-44) are examined in 3T3-L1 and VT-1 cells and in several mouse tissues. Within 30 minutes of TPA treatment, TIE gene mRNA is increased in 3T3-L1 cells; whereas, with the exception of TIE-10B, low levels or delayed mRNA expression is seen in VT-1 cells. The two genes are expressed in most mouse tissues tested. mRNA levels of both TIE genes also increased in response to serum supplemented medium. Typical mRNA expression patterns for protooncogenes c-fos, c-myc, c-jun are seen when cells are treated with TPA or serum-supplemented media. The differential mRNA expression of the TIE genes relative to other growth potentiating genes and in response to mitogens other than TPA is indicative of the complexity and wide range of genes involved in several possible pathways leading to the cells' mitogenic response. (Abstract shortened with permission of author.)
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Zablocki, Destinee Elizabeth. "Differential Expression of Calsarcin Genes in Orthognathic Surgery Patients with ACTN3 R577X Gene Deviations." Master's thesis, Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/405298.
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Oral BiologyM.S.
Objective: Malocclusion is a complex musculoskeletal trait, with muscle playing an integral role in vertical facial development. A single nucleotide polymorphism (SNP) produces the R577XX nonsense mutation in the alpha-actinin-3 (ACTN3) gene, creating a stop codon and loss of its protein. With loss of ACTN3, alpha-actinin-2 (ACTN2) is upregulated. Calsarcins, known inhibitors of calcineurin activation, preferentially bind ACTN2 leading to a surge in free calcineurin. The increase in calcineurin activity produces the phenotypic shift of fast muscle fibers toward the slow myogenic program seen in the ACTN3 null genotype (Seto et al., 2013). Here, we have tested whether calsarcin gene expression is affected by ACTN3 genotypes in human masseter muscle. Methods: Subjects undergoing orthodontic treatment and orthognathic surgery were recruited from the University of Lille, Department of Oral and Maxillofacial Surgery in Northern France. During the bilateral sagittal split osteotomy, masseter muscle samples were collected from the discarded section of deep anterior superficial masseter muscle, snap frozen, and shipped to Dr. Sciote’s lab at Temple University. RNA from masseter muscle samples was isolated from 41 subjects using TRIzolTM reagent. MYOZ gene expression was quantified by RT-PCR using an adult skeletal muscle reference standard (commercially prepared skeletal muscle RNA; Ambion, Inc), and individual primer-probe sets for MYOZ1, MYOZ2, MYOZ3, and HPRT1 (utilized for normalization of data). ANOVA and unpaired t-tests were used to determine the significance of expression differences between MYOZ genes and by ACTN3 R577X genotypes, as well as by malocclusion classes. Pearson analyses were used to determine correlations between MYOZ expression and fiber type mean percent occupancies. Results: The main aim of this project was to determine whether expression of the three calsarcin genes, MYOZ1, 2, and 3, differs between subjects with RR, RX and XX genotypes for the ACTN3 gene, as well as between sagittal and vertical classes of malocclusion, asymmetries and TMD. Differences were found for MYOZ3 expression where relative quantities in males, but not females, decreased progressively from the ACTN3 RR, to RX, and XX genotypes. Among subjects with the RX genotype, expression differed significantly between males and females by an unpaired t-test. A statistically significant difference was detected between MYOZ2 and Class II, Class III malocclusions (p=0.05). Sagittal differences were compared further by ANOVA analyses with a statistically significant difference detected for MYOZ3 with a probability of 0.02. Correlation analyses comparing fiber type mean % occupancy with calsarcin gene expression revealed a significant positive relationship between MYOZ2 and type I (slow-twitch) fibers. Correspondingly, a significant correlation of MYOZ2 expression with type IIA and IIX (fast-twitch) fibers was negative. Conclusions: The greatest relative quantity of RNA for the three calsarcin genes was found in MYOZ3, suggesting more calsarcin-3 may be needed in masticatory muscle structure and function than other calsarcin isoforms. Alternatively, high expression of MYOZ3 in the masseter samples may indicate that there are relatively greater amounts of that isoform in cranial muscle than in the limb skeletal muscle standard used in these studies. Also, relative quantities of MYOZ3 expression in males decreased progressively from the ACTN3 RR, to RX, and XX genotypes. While this data may suggest that the ACTN3 R577X polymorphism may affect MYOZ3 expression in males of the malocclusion patient population, an increased sample of male subjects would be needed to determine if this trend has true significance. Expression of MYOZ2 (calsarcin-1) was strongly correlated with slow fiber-type occupancy in masseter muscle of our patient population. The muscle-specific expression of each calsarcin may lend to the understanding of this result. MYOZ2 is the only isoform found in both cardiac muscle and slow-twitch skeletal muscle, while MYOZ1 and MYOZ3 are both found in skeletal muscle with a predilection towards fast-twitch skeletal muscle (Frey et al., 2004).
Temple University--Theses
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Lavery, William Lindsay. "Investigation of changes in gene expression during ageing of the liver." Thesis, University of Sunderland, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288934.
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Shen, Shixue. "Differential gene expression in innate immunity between commercial broilers and layers." [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1848.
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Mutlu, Pelin. "Differential Gene Expression Analysis In Drug Resistant Multiple Myeloma Cell Lines." Phd thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/3/12610970/index.pdf.
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The emergence of drug-resistance of tumor cells is a major complication for succesful chemotherapy. In this study, the molecular mechanisms of resistance to prednisone, vincristine and melphalan in multiple myeloma cell lines, RPMI-8226 and U-266 were investigated. Drug resistance was induced by application of the drugs by stepwise dose increments and confirmed by XTT cytotoxicity assay.
Gene expression analysis demostrated that MDR1 gene is one of the most important factor causing the multidrug resistance phenotype in prednisone, vincristine and melphalan resistant multiple myeloma cell lines. According to microarray analysis alterations in laminin, integrin and collagen genes were detected. Additionally, upregulation of some oncogenes and growth factors (Rho family of GTPases, YES1, ACT2, TGFBR, EPS15, PDGF) was shown to have a role in MDR in multiple myeloma. Significant downregulation of suppressors of cytokine signalling gene expressions and upregulation of different types of interleukine and interferon gene expressions (IL3 and interferon-gamma receptor) which are related to JAK-STAT signalling pathay was shown. Alterations in expression levels of genes related to ceramide metabolism were shown especially for melphalan resistance in multiple myeloma.
The data from vincristine/prednisone and vincristine/melphalan drug combination studies were shown that the usage of vincristine on prednisone and melphalan resistant multiple myeloma cell lines increase the efficacy of the chemotherapy. On the other hand the cross-resistance development of prednisone and melphalan resistant sublines to irradiation was detected.
These results may help to understand the molecular mechanisms of prednisone, vincristine and melphalan resistance in multiple myeloma model cell lines RPMI-8226 and U-266.
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Illing, Nicola. "The control of differential gene expression during sporulation in Bacillus subtilis." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276812.
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Moran, Mary Teresa. "Gaucher's disease : differential gene expression in the understanding of its pathogenesis." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621720.
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Ndimande, Gordon Sandile. "Comparative analysis of differential gene expression in the culms of sorghum." Thesis, Stellenbosch : University of Stellenbosch, 2007. http://hdl.handle.net/10019.1/2903.
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Thesis (MSc (Genetics. Plant Biotechnology))--University of Stellenbosch, 2007.Despite numerous attempts involving a variety of target genes, the identity of the key regulatory genes of sucrose metabolism in sugarcane is still illusive. To date, genomic research into sucrose accumulation in sugarcane has focused on genes that are expressed in association with stalk development/maturation, with the aim of identifying key regulatory steps in sucrose metabolism. The identification of possible controlling points, however, is complicated by the polyploid nature of sugarcane. Although these studies have yielded extensive annotated gene lists and correlative data, the identity of key regulatory genes remains elusive. A close relative of sugarcane, Sorghum bicolor, is diploid, has a small genome size and accumulates sucrose in the stalk parenchyma. The main aim of the work presented in this thesis was to use S. bicolor as a model to identify genes that are differentially expressed during sucrose accumulation in the stalk of low and high sucrose genotypes. In the first part of the study, a macroarray protocol for identification of differentially expressed genes during sorghum development was established. Firstly, the macroarray sensitivity of probe-target hybridisation was optimised with increasing amounts of target DNA i.e. 0.005-0.075 pmol. The hybridisation signal intensity increased as expected with increasing amounts of probe until the hybridisation signals reached maximum levels at 0.05 pmol. As a result, to ensure quantitative cDNA detection, probes were arrayed at 0.05 pmol when 1 μg target cDNA was used. Secondly, intra-array and inter-array membrane reproducibility was found to be high. In addition, the protocol was able to detect species of mRNA at the lowest detection limit tested (0.06%) and permits the detection of an eight-fold variation in transcript levels. The conclusion was therefore that the protocol was reproducible, robust and can reliably detect changes in mRNA levels. In the second part of the study, sugar accumulation levels in the immature and maturing internodal tissues of sorghum GH1 and SH2 genotypes were compared during the boot and softdough stages. Sugars (i.e. fructose, glucose and sucrose) accumulated differently in the immature and maturing internodes in both sorghum genotypes during the boot and softdough stages, with sucrose being the dominant sugar in both stages. Based on these differences in sugar accumulation patterns, immature and maturing internodal tissues of sorghum genotypes were compared for differentially expressed genes. A number of genes were found to be significantly differentially expressed during both stages. In order to validate the reliability of the macroarray analysis, fourteen genes were arbitrarily selected for semi-quantitative RT-PCR. Seven genes (50%) revealed a similar pattern of transcript expression, confirming the macroarray results. The other seven genes, however, showed a different expression trend compared with the macroarrays. In this study, ESTs from rice and sugarcane were used for probing sorghum. The probability of cross-hybridisation between the probes and various isoforms of the homologous sorghum sequences is thus high, potentially leading to the identification of false positives. In addition, variation in expression patterns could have been introduced by technical and biological variation. Lastly, to verify that changes in the levels of a transcript are also reflected in changes in enzyme activity, seven candidates were tested for enzyme activity. Only three i.e. soluble acid invertase (SAI), sucrose synthase (SuSy) and alcohol dehydrogenase (ADH), out of these seven genes showed enzyme activity levels reflective of the relative transcript expression. We concluded that changes in transcript levels may or may not immediately lead to similar changes in enzyme activity. In addition, enzyme activity may be controlled at transcriptional and at posttranscriptional levels. In conclusion, sugar accumulation in low (GH1) and high (SH2) sucrose sorghum genotypes is influenced by differences in gene expression. In addition, the power of macroarrays and confirmation with semi-quantitative RT-PCR for identification of differentially expressed genes in sorghum genotypes was demonstrated. Moreover, the transcript and enzyme activity patterns of SAI, SuSy and ADH genes showed expression patterns similar to those of sugarcane during sucrose accumulation. Therefore, using sorghum as a model promises to enhance and refine our understanding of sucrose accumulation in sugarcane.
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Choi, Hye Won. "Differential regulation of PTH-induced primary response gene expression in osteoblasts." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1905636821&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Webb, Steven Anthony Rochford. "Evaluation of differential gene expression in Neisseria meningitidis using a Green Fluorescent Protein reporter sytem." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246674.
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Glaus, Peter. "Bayesian methods for gene expression analysis from high-throughput sequencing data." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/bayesian-methods-for-gene-expression-analysis-from-highthroughput-sequencing-data(cf9680e0-a3f2-4090-8535-a39f3ef50cc4).html.
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We study the tasks of transcript expression quantification and differential expression analysis based on data from high-throughput sequencing of the transcriptome (RNA-seq). In an RNA-seq experiment subsequences of nucleotides are sampled from a transcriptome specimen, producing millions of short reads. The reads can be mapped to a reference to determine the set of transcripts from which they were sequenced. We can measure the expression of transcripts in the specimen by determining the amount of reads that were sequenced from individual transcripts. In this thesis we propose a new probabilistic method for inferring the expression of transcripts from RNA-seq data. We use a generative model of the data that can account for read errors, fragment length distribution and non-uniform distribution of reads along transcripts. We apply the Bayesian inference approach, using the Gibbs sampling algorithm to sample from the posterior distribution of transcript expression. Producing the full distribution enables assessment of the uncertainty of the estimated expression levels. We also investigate the use of alternative inference techniques for the transcript expression quantification. We apply a collapsed Variational Bayes algorithm which can provide accurate estimates of mean expression faster than the Gibbs sampling algorithm. Building on the results from transcript expression quantification, we present a new method for the differential expression analysis. Our approach utilizes the full posterior distribution of expression from multiple replicates in order to detect significant changes in abundance between different conditions. The method can be applied to differential expression analysis of both genes and transcripts. We use the newly proposed methods to analyse real RNA-seq data and provide evaluation of their accuracy using synthetic datasets. We demonstrate the advantages of our approach in comparisons with existing alternative approaches for expression quantification and differential expression analysis. The methods are implemented in the BitSeq package, which is freely distributed under an open-source license. Our methods can be accessed and used by other researchers for RNA-seq data analysis.
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Cheng, Hai-Ying Mary. "Differential gene expression in presentation versus drug-resistant relapse AML, in search of drug resistance genes by the differential display approach." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/MQ45860.pdf.
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Gower, Adam C. "Discovering biological connections between experimental conditions based on common patterns of differential gene expression." Thesis, Boston University, 2012. https://hdl.handle.net/2144/32019.
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Thesis (Ph.D.)--Boston UniversityPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Similarities between patterns of differential gene expression can be used to establish connections between the experimental and biological conditions that give rise to them. The growing volume of gene expression data in repositories such as NCBI's Gene Expression Omnibus (GEO) presents an opportunity to identify such similarities on a large scale across a diverse collection of datasets. In this work, I have developed a pattern-based approach, named openSESAME, to identify datasets enriched in samples displaying coordinate differential expression of a query signature. Importantly, openSESAME performs this search without knowledge of the experimental groups in the datasets being searched, which allows it to identify perturbations of gene expression due to attributes that may not have been recorded. First, I demonstrated the utility of openSESAME using two gene expression signatures to query a set of more than 75,000 human expression profiles obtained from GEO. A query using a signature of estradiol treatment identified experiments in which estrogen signaling was perturbed and also discriminated between estrogen receptor-positive and -negative breast cancers. A second query using a signature of silencing of the transcription factor p63 (a key regulator of epidermal differentiation) identified datasets related to stratified squamous epithelia or epidermal diseases such as melanoma. Next, to improve the utility of openSESAME, I expanded the collection of profiles to include samples from mouse and rat, and automatically translated expression signatures for cross-species queries. Furthermore, I processed the sample annotation associated with these samples in GEO, extracting informative words and phrases and continuous (e.g., age) and categorical (e.g., disease state) variables. I have also recorded sample-specific dates and quality metrics to assess whether batch effects or outliers are affecting individual query results. Finally, I used openSESAME to query this repository with over 800 gene expression signatures from the Broad Institute's Molecular Signatures Database (MSigDB). I then used the scores of the association of each signature with each sample in the repository to build a network of the relatedness of these signatures to each other. This "constellation" of signatures can be used to determine the relationship of a query signature to other biological and experimental perturbations.
2031-01-02
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Mapiye, Darlington S. "Normalization and statistical methods for crossplatform expression array analysis." University of the Western Cape, 2012. http://hdl.handle.net/11394/4586.
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>Magister Scientiae - MScA large volume of gene expression data exists in public repositories like the NCBI’s Gene Expression Omnibus (GEO) and the EBI’s ArrayExpress and a significant opportunity to re-use data in various combinations for novel in-silico analyses that would otherwise be too costly to perform or for which the equivalent sample numbers would be difficult to collects exists. For example, combining and re-analysing large numbers of data sets from the same cancer type would increase statistical power, while the effects of individual study-specific variability is weakened, which would result in more reliable gene expression signatures. Similarly, as the number of normal control samples associated with various cancer datasets are often limiting, datasets can be combined to establish a reliable baseline for accurate differential expression analysis. However, combining different microarray studies is hampered by the fact that different studies use different analysis techniques, microarray platforms and experimental protocols. We have developed and optimised a method which transforms gene expression measurements from continuous to discrete data points by grouping similarly expressed genes into quantiles on a per-sample basis. After cross mapping each probe on each chip to the gene it represents, thereby enabling us to integrate experiments based on genes they have in common across different platforms. We optimised the quantile discretization method on previously published prostate cancer datasets produced on two different array technologies and then applied it to a larger breast cancer dataset of 411 samples from 8 microarray platforms. Statistical analysis of the breast cancer datasets identified 1371 differentially expressed genes. Cluster, gene set enrichment and pathway analysis identified functional groups that were previously described in breast cancer and we also identified a novel module of genes encoding ribosomal proteins that have not been previously reported, but whose overall functions have been implicated in cancer development and progression. The former indicates that our integration method does not destroy the statistical signal in the original data, while the latter is strong evidence that the increased sample size increases the chances of finding novel gene expression signatures. Such signatures are also robust to inter-population variation, and show promise for translational applications like tumour grading, disease subtype classification, informing treatment selection and molecular prognostics.
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Voelker, Courtney Christine Joan. "Differential gene expression of cortical layer V pyramidal neuron subpopulations during development." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436930.
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Lewis, Marie. "Cell survival, biofilm formation and differential gene expression of two opportunistic pathogens." Thesis, University of Exeter, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410813.
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Kapushesky, Misha. "Construction and analysis of a multi-species atlas of differential gene expression." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608589.
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Tchakounte, Wakem Seguy. "A Comparison of Methods Taking into Account Asymmetry when Evaluating Differential Expression in Gene Expression Experiments." Thesis, North Dakota State University, 2018. https://hdl.handle.net/10365/28874.
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Gene expression technologies allow expression levels to be compared across treatments for thousands of genes simultaneously. Asymmetry in the empirical distribution of the test statistics from the analysis of a gene expression experiment is often observed. Statistical methods exist for identifying differentially expressed (DE) genes while controlling multiple testing error while taking into account the asymmetry of the distribution of the effect sizes. This paper compares three statistical methods (Modified Q-value, Modified SAM, and Asymmetric Local False Discovery Rate) used to identify differentially expressed (DE) genes that take into account such patterns while controlling false discovery rate (FDR). The results of the simulation studies performed suggest that the Modified Q-values outperforms the other methods most of the time and also better controls the FDR.