Дисертації з теми "Genome wide screening"
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Appari, Mahesh [Verfasser]. "Genome-wide screening of biomarkers in androgen insensitivity syndrome (AIS) / Mahesh Appari." Kiel : Universitätsbibliothek Kiel, 2009. http://d-nb.info/1019866764/34.
Повний текст джерелаChrist, Ryan. "Ancestral trees as weighted networks : scalable screening for genome wide association studies." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:8f382d56-2d5d-4a4f-9b39-41700897e02e.
Повний текст джерелаLöllgen, Ruth Mari Caroline. "Genome wide screening of loss of heterozygosity in human midgut carcinoid tumors with fluorescent technique." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972556702.
Повний текст джерелаKaemena, Daniel Fraser. "CRISPR/Cas9 genome-wide loss of function screening identifies novel regulators of reprogramming to pluripotency." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31184.
Повний текст джерелаLöllgen, Ruth Mari Caroline. "Genome-wide screening of loss of heterozygosity in human midgut carcinoid tumors with fluorescent technique." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2004. http://dx.doi.org/10.18452/15047.
Повний текст джерелаBackground: Midgut carcinoid tumors are rare malignant tumors with origin in the neuroendocrine cells of the small intestine. Due to secretion of a variety of peptide hormones and biogenic amines they cause the carcinoid syndrome. Metastases are often present at first diagnosis. Despite this, patients have a realistic chance to survive for a prolonged period (30% (unresectable/metastatic disease) -79% (non-metastatic disease) 5-year survival rate) if treated by a combination of surgery and medication. Unlike their foregut counterparts, midgut carcinoid tumors are not or rarely associated with the multiple endocrine neoplasia type 1 (MEN1) syndrome. The genetic back-ground to tumorigenesis of these neoplasms is unknown. In contrast, the events involved in tumorigenesis of gastroenteropancreatic adenocarcinomas are better characterized with frequent mutations e.g. of the Smad4/DPC4, Smad2/MADR2/JV18-1 and DCC genes on chromosome 18. Methods: Eight metastatic midgut carcinoids were analysed by a genome-wide screening for loss of heterozygosity using 131 PCR-amplified fluorescent-labelled microsatellite markers. DNA sequence analysis using oligonucleotide primers flanking exons 8-11 of the Smad4/DPC4 gene and immunohistochemical staining with Smad4/DPC4 antibodies was performed. Results: Chromosome 18 was deleted in seven out of eight tumors (88%). All but one of these tumors had lost both 18p and 18q, the remaining tumor had lost the long arm but retained the short arm. Several other chromosomal alleles were lost in a subset of the tumors. Loss of heterozygosity (LOH) on chromosome 11q13, the MEN 1 locus, was not found. Smad4/DPC4 wild-type sequence and normal immunohistochemical staining for Smad4/DPC4 protein was found for all analysed tumors. Conclusions: Our finding of a high frequency of chromosome 18 deletions in 88% of the tumors strongly suggests that midgut carcinoid tumorigenesis might involve inactivation of a candidate tumor suppressor gene located in that region while Smad4/DPC4 is unlikely to be involved in that process. A more detailed analysis of the genetic events in midgut carcinoid tumors is warranted to clarify their neogenetic origin.
Riehmer, Vera [Verfasser]. "Genome-wide screening methods in tumors of the central nervous system and cancer predisposition / Vera Riehmer." Bonn : Universitäts- und Landesbibliothek Bonn, 2014. http://d-nb.info/1054691770/34.
Повний текст джерелаRudge, Felicity. "Genome-wide cDNA and RNAi screening to identify modulators of responses to a novel Wnt signalling inhibitor." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58589/.
Повний текст джерелаStravalaci, Matteo. "Identification and characterization of mediators of toxicity of Aβ oligomers by genome wide screening in Caenorhabditis elegans". Thesis, Open University, 2017. http://oro.open.ac.uk/50285/.
Повний текст джерелаSooda, Anuradha. "Discovery of novel HLA-B*57:01 restricted T-cell antigens through genome-wide screening of Epstein-Barr virus." Thesis, Sooda, Anuradha (2020) Discovery of novel HLA-B*57:01 restricted T-cell antigens through genome-wide screening of Epstein-Barr virus. PhD thesis, Murdoch University, 2020. https://researchrepository.murdoch.edu.au/id/eprint/54110/.
Повний текст джерелаLawson, Jonathan Luke Done. "Genome-wide microscopy screening identifies links across processes including a conserved connection between DNA damage control and the microtubule cytoskeleton." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/253007.
Повний текст джерелаGerzenstein, Sabrina Melisa. "Pharmacogenomics of the Intraocular Pressure Response to Glucocorticoids." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_theses/285.
Повний текст джерелаVan, Anh Dao [Verfasser], and Siegfried [Akademischer Betreuer] Roth. "Genome-wide RNAi screening and the analysis of candidate genes for dorsoventral patterning in Tribolium castaneum / Dao Van Anh. Gutachter: Siegfried Roth." Köln : Universitäts- und Stadtbibliothek Köln, 2014. http://d-nb.info/1054420459/34.
Повний текст джерелаBicchieri, M. E. "A WHOLE-GENOME APPROACH TO IDENTIFY MICRORNA 'MODIFIERS' OF BREAST CANCER STEM CELL SELF-RENEWAL." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/265272.
Повний текст джерелаGhosh, Aniket [Verfasser], Mikael [Akademischer Betreuer] Simons, Herbert [Akademischer Betreuer] Jäckle, and Stefan [Akademischer Betreuer] Eimer. "Genome-wide RNAi screening reveals glial phosphoethanolamine ceramide is critical for axonal ensheathment / Aniket Ghosh. Gutachter: Mikael Simons ; Herbert Jäckle ; Stefan Eimer. Betreuer: Mikael Simons." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2012. http://d-nb.info/1044305770/34.
Повний текст джерелаGhosh, Aniket Verfasser], Mikael [Akademischer Betreuer] [Simons, Herbert [Akademischer Betreuer] Jäckle, and Stefan [Akademischer Betreuer] Eimer. "Genome-wide RNAi screening reveals glial phosphoethanolamine ceramide is critical for axonal ensheathment / Aniket Ghosh. Gutachter: Mikael Simons ; Herbert Jäckle ; Stefan Eimer. Betreuer: Mikael Simons." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2012. http://nbn-resolving.de/urn:nbn:de:gbv:7-webdoc-3784-4.
Повний текст джерелаLöllgen, Ruth Mari Caroline [Verfasser], x. [Gutachter] Arnold, x. [Gutachter] Wiedenmann, and x. [Gutachter] Zeitz. "Genome-wide screening of loss of heterozygosity in human midgut carcinoid tumors with fluorescent technique / Ruth Mari Caroline Löllgen ; Gutachter: x. Arnold, x. Wiedenmann, x. Zeitz." Berlin : Humboldt-Universität zu Berlin, 2004. http://d-nb.info/1206197919/34.
Повний текст джерелаCerrato, Giulia. "Oleate : An Atypical Cellular Stress Inducer That Stalls Protein Secretion Oleate-Induced Aggregation of LC3 at the Trans-Golgi Network Is Linked to a Protein Trafficking Blockade A Genome-Wide RNA Interference Screen Disentangles the Golgi Tropism of LC3 Live Cell Imaging of LC3 Dynamics." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL023.
Повний текст джерелаDistinct classes of fatty acids (FAs) (saturated or cis-/trans-unsaturated carbon chains) impact on cellular and organismal physiology in a different manner. Interestingly, these diverse categories have a profound (but different) effect on autophagy, the conserved intracellular degradation mechanism that maintains energy homeostasis and protects cells against stress. Oleate, the most abundant endogenous and dietary cis-unsaturated FA, has the atypical property to induce the redistribution of the LC3 protein (peculiar sign of autophagy) in a non-canonical fashion and preferentially to the Golgi apparatus. Intrigued by these observations, which might be related to the health-improving effects of cis-unsaturated FAs (and the notorious toxicity of trans-unsaturated and saturated FAs), we decided to explore the mechanisms causing the oleate-induced relocation of LC3 to the Golgi apparatus. To achieve this goal, a robotized RNA interference genome-wide screen led to the identification of multiple genes involved in the Golgi-related protein transport, as well as in the integrated stress response. Follow-up experiments revealed that oleate affected the subcellular morphology of the Golgi apparatus, correlating with a blockade of conventional (Golgi-dependent) protein secretion that caused secretory cargo to be stalled at the level of the trans-Golgi network. The inhibition of protein secretion was observed using several experimental systems, both in vitro and in vivo. Moreover, a systematic screen searching for other chemical entities that mimic the oleate-induced cellular effects led to the identification of several compounds belonging to rather different pharmacological classes. These “oleate mimetics” also shared with oleate the capacity to block conventional protein secretion, supporting the notion that this pathway of Golgi perturbation is indeed of pharmacological relevance. In conclusion, this research work shows that oleate represents a class of molecules that act on the Golgi apparatus to cause the recruitment of LC3 and to stall protein secretion
Ndiaye, Fatou Kiné. "Étude post-GWAS des gènes de susceptibilité au diabète de type 2 : rôle phare dans la fonction de la cellule β pancréatique". Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S039/document.
Повний текст джерелаGenome-wide association studies (GWAS) have identified a plethora of single nucleotide polymorphisms (SNPs) associated with the risk of type 2 diabetes, but most often with little information about the mechanism underlying the relationship between these genetic variants associated with type 2 diabetes and the diabetic phenotype. Indeed, these SNPs are often noncoding and have a modest effect on the risk of type 2 diabetes, making difficult their functional study. At the beginning of the GWAS era, it has been suggested that susceptibility genes for type 2 diabetes are strongly involved in pancreatic β cell gene function, while no functional studies had been systematically performed. In this context, we conducted a “fishing” study to decipher this large amount of data generated by GWAS and to pinpoint potentially important genes that may be new therapeutic targets. The first objective of my thesis was to study the expression of type 2 diabetes susceptibility genes in a panel of human tissues comprising pancreatic and insulin-sensitive tissues using an unbiased technique of quantification of genes expression in order to show that these genes associated with type 2 diabetes were enriched in pancreatic β-cells. We then performed functional studies on the thirty mostly expressed genes in our cell model by insulin secretion tests, cell viability test, RNA sequencing (RNA-seq) and Western blotting in the human pancreatic β cell line (EndoC-βH1). These cells are able to secrete insulin in response to glucose and other secretagogues. Our goal was to study the role of these type 2 diabetes susceptibility genes in pancreatic β cell function, particularly in insulin secretion. Our expression study of type 2 diabetes susceptibility genes showed that their expression is significantly enriched in pancreatic β cells and the EndoC-βH1 cell line. For five genes associated with type 2 diabetes (TBC1D4, TCF19, KCNK16, CDKN2A and SLC30A8) with an already known presence and function in pancreatic β cell, we showed a significant variation in glucose-stimulated insulin secretion after gene silencing, in agreement with the literature. In addition, we identified four type 2 diabetes associated genes (PRC1, SRR, ZFAND3 and ZFAND6), with a significant decrease in insulin secretion after gene silencing without already know function in pancreatic β cell. RNA-seq has shown a significant association between the extinction of these genes and molecular networks related to the pathophysiology of type 2 diabetes (e.g. apoptosis of pancreatic cells, insulinemia, glycolysis, endoplasmic reticulum stress response...). The assessment of the expression of our four genes in the islets of obese mice (ob/ob) or treated with streptozotocin shows a positive correlation between their expression and the expression of insulin. Our study has shown that post-GWAS functional studies are important and can help to define the causal link between these genes and the disease, and therefore to make progress in the understanding of the pathophysiology of type 2 diabetes. This study allowed us to identify genes whose function in β cell was not anterior known and which are involved in pancreatic β cell function and the pathophysiology of type 2 diabetes
Merker, Sören [Verfasser], Klaus-Peter [Gutachter] Lesch, and Erhard [Gutachter] Wischmeyer. "Genome-wide screenings in attention-deficit/hyperactivity disorder (ADHD): investigation of novel candidate genes SLC2A3 and LPHN3 / Sören Merker. Gutachter: Klaus-Peter Lesch ; Erhard Wischmeyer." Würzburg : Universität Würzburg, 2014. http://d-nb.info/110974997X/34.
Повний текст джерела"Genome wide screening of genetic aberrations in nasopharyngeal carcinoma." 2002. http://library.cuhk.edu.hk/record=b6073440.
Повний текст джерела"July 2002."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2002.
Includes bibliographical references (p. 187-203).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.
Chung, Pei-Chen, and 鍾北辰. "Genome-wide screening for yeast essential genes involved in chronological aging." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/z924r9.
Повний текст джерела國立陽明大學
生命科學系暨基因體科學研究所
105
Aging is a leading factor for many diseases, which plagues people around the world. Budding yeast Saccharomyces cerevisiae (S. cerevisiae) has been used to study the mechanisms of aging for more than two decades because of its well-established genome information, and various genome-wide mutation library. Chronological lifespan (CLS), the length of time that non-dividing cell survives, is one of the important paradigms of aging studies in S. cerevisiae. There are 1,235 genes annotated to regulate CLS, while only 5 genes are essential genes. I think the result are biased since most studies use yeast deletion library to perform large-scale screening. However, the essential genes are vital for cell survive and not involved in deletion library. In this study, we took advantage of Yeast Tet-promoter Hughes Collection, in which tetracycline-regulatable promoter was used to replace each native promoter of individual essential gene, to study the role of essential genes in aging process. We first developed a microscope-based high throughput CLS assay. Results demonstrated that CLS of yTHC strains were really affected by gene mis-regulation caused by promoter replacement. Further analysis showed that the low viability group have more total and physical interaction partners and suppose that proteins involved in protein complex are more sensitive to gene mis-regulation. Functional enrichment analysis also showed that some essential genes, which involved in protein complexes, might affect CLS once they got mis-regulated. I proposed that dosage imbalance of proteins involved in protein complex might easily cause proteotoxicity stress and result in shorten CLS. The results provided insights on the roles of essential genes for CLS, gave us a hint that some essential genes were more sensitive to gene mis-reguation and worth for further studies.
Li, Wei-Hsiao, and 李偉孝. "Identification of Radioprotectors in Human Hepatocellular Carcinoma by Genome-Wide RNAi Screening." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/v458jn.
Повний текст джерела國立臺灣大學
生物化學暨分子生物學研究所
101
Hepatocellular carcinoma (HCC), the third most prevalent malignant tumor in Taiwan, has a poor prognosis due to high rates of recurrence and metastasis. Radiotherapy is one of the modalities in cancer treatments. With the recent development of stereotactic radiosurgery technology, physicians can deliver precise doses of energy to an exact location (i.e. the tumor) and thus limit collateral damage to surrounding normal tissues. Despite such an advanced technology, radiotherapy has not yet been incorporated into standard management guidelines of HCC because of the unsatisfactory clinical outcomes. In order to improve the efficacy of radiotherapy in treating HCC, we carried out a genome-wide RNA-interference (RNAi) screen in Huh7 cells (a human HCC cell line) and identified many genes as radiation protector candidates (i.e. knockdown of such genes increases the sensitivity of Huh7 cells to a predetermined dose of radiation) which might be used as potential targets for drug design to enhance radiation sensitivity of HCC. We identified twenty-one candidates from the screening results, including sixteen radioprotectors and five radiosensitizers. All of the candidates were validated by colony formation assay. Among these candidates, clusterin is the most significant radio-protector. Here we demonstrated that suppression of clusterin expression enhances the radiation-mediated cell death. Furthermore, the phenomenon caused by clusterin suppression is specific for ionizing radiation, but not for ultraviolet (UV) radiation. However, the detailed mechanisms and functions of clusterin need to be further studied and elucidated in the future.
Ghosh, Aniket. "Genome-wide RNAi screening reveals glial phosphoethanolamine ceramide is critical for axonal ensheathment." Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-000D-EF82-A.
Повний текст джерелаRamos, Pedro André Dias. "Genome-wide shRNA screening identifies genes involved in fulvestrant resistance in breast cancer." Master's thesis, 2016. http://hdl.handle.net/10362/19135.
Повний текст джерелаWu, Yi-Hsin, and 吳以新. "Establishing CRISPR interference-based genome-wide screening platform for identification of novel genes in macrophage alternative polarization." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/m99x3g.
Повний текст джерела國立臺灣大學
分子醫學研究所
107
Macrophages are crucial players in immune regulation. They have a wide spectrum of activation states depend on the diverse surrounding stimuli they receive. Classical activation (M1) and alternative activation (M2) are described as two extremes of their polarized states, which elicit pro-inflammatory responses and anti-inflammatory responses respectively to maintain tissue homeostasis. Regnase-1 is a ribonuclease essential in controlling immune responses by regulating mRNA decay of proinflammatory cytokines, and it is reported to be important in promoting macrophage M2 polarization in which ER stress, ROS and autophagy are involved. However, detailed regulatory mechanism of this pathway is remained unclear. The goal of our study is to perform a genome-scale CRISPRi-dCas9 screening to explore new regulators in Regnase-1 mediated M2 polarization. By flow cytometry detection of M2 markers expression, we can identify genes that after CRISPRi disruption and Regnase-1 overexpression lead to decreased M2 expression, as potential regulators in this pathway. We have tested and compared the M2 phenotypes of four mice macrophage cell lines and examined the M1/M2 discrimination of several M2 markers by flow cytometry analysis. Our results demonstrated the M2 discriminating ability of Egr2 and CD206, which by flow cytometry detection can together be used to distinguish M2 phenotypes in both BMDMs and immortalized BMDMs. We have also established CRISPRi-Regnase-1 and inducible Regnase-1 overexpression system for further proof-of-principle screening and the preparations of the large-scale screening. Our data also infer a potential relation between ER stress related protein and M2 polarization, which is to be further investigated in the future works.
Sanchez, Torres Viviana. "Escherichia coli Enhanced Hydrogen Production, Genome-wide Screening for Extracellular DNA, and Influence of GGDEF Proteins on Early Biofilm Formation." Thesis, 2010. http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8889.
Повний текст джерелаLöllgen, Ruth Mari Caroline [Verfasser]. "Genome wide screening of loss of heterozygosity in human midgut carcinoid tumors with fluorescent technique / von Ruth Mari Caroline Löllgen." 2004. http://d-nb.info/972556702/34.
Повний текст джерелаPeter, Josephine Jasmine. "Identification of yeast genes enabling efficient oenological fermentation under nitrogen-limited conditions." Thesis, 2018. http://hdl.handle.net/2440/113360.
Повний текст джерелаThesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Agriculture, Food and Wine, 2018.
Merker, Sören. "Genome-wide screenings in attention-deficit/hyperactivity disorder (ADHD): investigation of novel candidate genes SLC2A3 and LPHN3." Doctoral thesis, 2014. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-100129.
Повний текст джерелаDas Aufmerksamkeitsdefizit/Hyperaktivitätssyndrom (ADHS) ist eine hoch prävalente und bereits in der Kindheit beginnende Neuroentwicklungsstörung, die eine erhebliche Persistenz ins Jugend- und Erwachsenenalter aufweist. In den vergangenen Jahren wurde eine Vielzahl von genomweiten Studien zu ADHS durchgeführt, welche zur Identifizierung zahlreicher genetischer Varianten an unterschiedlichen chromosomalen Loci geführt und somit die genetisch komplexe polygene Natur dieser Störung zur Geltung gebracht haben. Auf diese Weise traten auch neue Kandidatengene zutage, wie zum Beispiel das Gen für die Glukosetransporter-Isoform-3 (SLC2A3) und das Gen, welches Latrophilin-3 kodiert (LPHN3). Innerhalb dieser Thesis wurden beide Gene in Form von zwei voneinander getrennten Projekten untersucht. Das erste Projekt beschäftigte sich mit humanen ADHS-assoziierten SLC2A3-Polymorphismen und ihrer potentiellen physiologischen Bedeutung. Für diesen Zweck wurden Genexpressionsanalysen in peripheren Zellmodellen sowie funktionelle EEG-Messungen im Menschen durchgeführt. Im zweiten Projekt ging es um das murine Gen Lphn3 mit dem Ziel, eine Mauslinie zu entwickeln, die ein genetisch verändertes Lphn3 mit konditionalem Knockout-Potenzial aufweist. In diesem Zusammenhang wurde ein spezifischer DNA-Vektor verwendet, der auf den Lphn3-Genlocus in murinen embryonalen Stammzellen (ES-Zellen) abzielte, was eine Voraussetzung für die Erzeugung von geeigneten chimären Mäusen darstellt. Die Ergebnisse des ersten Projektes legten nahe, dass SLC2A3-Duplikationsträger erhöhte SLC2A3-mRNA-Expression in peripheren Blutzellen aufweisen sowie signifikant veränderte ereigniskorrelierte Potentiale während eines Tests kognitiver Reaktionskontrolle sowie eines Arbeitsgedächtnis-Tests, was möglicherweise von veränderter präfrontaler Hirnaktiviät bzw. Gedächtnis-Prozessierung begleitet wird. Interessanterweise zeigten ADHS-Patienten mit T-Allel des im SLC2A3-Gen liegenden SNPs rs12842 ebenfalls deutliche Effekte während dieser EEG-Messungen, allerdings in entgegengesetzter Form zu den zuvor genannten SLC2A3-Duplikationsträgern mit ADHS, was auf einen gegensätzlichen molekularen Mechanismus hindeutet. Zudem stellte sich heraus, dass der Einfluss der zuvor genannten SLC2A3-Varianten auf verschiedene EEG-Parameter innerhalb der ADHS-Gruppe generell deutlich stärker ausgeprägt war als in der gesunden Kontrollgruppe, also einen beachtlichen Interaktionseffekt impliziert. Bezüglich des zweiten Projektes konnten bisher Zwischenergebnisse erzielt werden: das erfolgreiche Targeting des Lphn3-Gens in murinen ES-Zellen sowie die Produktion hochchimärer, phänotypisch unauffälliger und größtenteils fertiler Maus-Chimären. Obgleich die Keimbahntransmission des modifizierten Lphn3-Allels bislang noch nicht eingetreten ist, gibt es noch eine Reihe an neugeborenen chimären Mäusen, die in nächster Zeit erst noch getestet werden müssen. Zusammenfassend deuten die Ergebnisse darauf hin, dass Variationen des SLC2A3-Gens, die mit ADHS assoziiert sind, mit transkriptionellen und funktionellen Veränderungen im Menschen einhergehen. Zukünftige Forschungsarbeiten werden dabei helfen, die molekularen Netzwerke und neurobiologischen Grundlagen zu verdeutlichen, die an diesen Effekten beteiligt sind und offenbar zu dem komplexen klinischen Bild von ADHS beitragen. Angesichts der steigenden Zahl an Publikationen über Latrophiline in den letzten Jahren und der unzähligen Forschungsmöglichkeiten, die ein konditionaler Knockout von Lphn3 in Mäusen bietet, stellt die derzeit laufende Etablierung einer entsprechenden Mauslinie einen vielversprechenden Ansatz dar, dieses Gen und seine Rolle für ADHS zu untersuchen