Дисертації з теми "CRISPRko Screening"
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Erard, Nicolas Pascal Jean. "Optimization of molecular tools for high-throughput genetic screening." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271895.
Повний текст джерелаSheel, Ankur. "Identification of Essential Genes in Hepatocellular Carcinomas using CRISPR Screening." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1039.
Повний текст джерелаRubanova, Natalia. "MasterPATH : network analysis of functional genomics screening data." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC109/document.
Повний текст джерелаIn this work we developed a new exploratory network analysis method, that works on an integrated network (the network consists of protein-protein, transcriptional, miRNA-mRNA, metabolic interactions) and aims at uncovering potential members of molecular pathways important for a given phenotype using hit list dataset from “omics” experiments. The method extracts subnetwork built from the shortest paths of 4 different types (with only protein-protein interactions, with at least one transcription interaction, with at least one miRNA-mRNA interaction, with at least one metabolic interaction) between hit genes and so called “final implementers” – biological components that are involved in molecular events responsible for final phenotypical realization (if known) or between hit genes (if “final implementers” are not known). The method calculates centrality score for each node and each path in the subnetwork as a number of the shortest paths found in the previous step that pass through the node and the path. Then, the statistical significance of each centrality score is assessed by comparing it with centrality scores in subnetworks built from the shortest paths for randomly sampled hit lists. It is hypothesized that the nodes and the paths with statistically significant centrality score can be considered as putative members of molecular pathways leading to the studied phenotype. In case experimental scores and p-values are available for a large number of nodes in the network, the method can also calculate paths’ experiment-based scores (as an average of the experimental scores of the nodes in the path) and experiment-based p-values (by aggregating p-values of the nodes in the path using Fisher’s combined probability test and permutation approach). The method is illustrated by analyzing the results of miRNA loss-of-function screening and transcriptomic profiling of terminal muscle differentiation and of ‘druggable’ loss-of-function screening of the DNA repair process. The Java source code is available on GitHub page https://github.com/daggoo/masterPATH
Li, Meng. "Genetic dissection of the exit of pluripotency in mouse embryonic stem cells by CRISPR-based screening." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/277552.
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 джерелаPetrucci, Teresa. "Building a platform for flexible and scalable testing of genetic editors." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1143160.
Повний текст джерелаSczakiel, Henrike Lisa [Verfasser]. "Identifizierung Pathogenese-relevanter Kandidatengene im Hodgkin-Lymphom durch CRISPR/Cas9-basiertes knockout-Screening / Henrike Lisa Sczakiel." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1228859523/34.
Повний текст джерелаLam, Phuong T. "Crispr/cas9-mediated genome editing of human pluripotent stem cells to advance human retina regeneration research." Miami University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=miami1575372014701457.
Повний текст джерелаCresson, Marie. "Study of chikungunya virus entry and host response to infection." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1050.
Повний текст джерелаAlphaviruses are a group of enveloped, positive-sense RNA viruses which are distributed almost worldwide and are responsible for a considerable number of human and animal diseases. Among these viruses, the Chikungunya virus (CHIKV) has recently re-emerged and caused several outbreaks on all continents in the past decade. Despite many studies, molecular mechanisms of chikungunya virus replication and virus-host interactions remain poorly understood. The aim of my project was to better understand and characterize the CHIKV entry and the host factors involved during replication steps in mammals. Several different approaches have been used in this work. As a first step, we have demonstrated a decrease of CHIKV infection after iron treatment in form of ferric ammonium citrate and we have studied the potential role in viral entry of NRAMP2 and TFRC, two proteins involved in iron transport and known receptors for other viruses. On the other hand, we have also focused on two proteins, CD46 and TM9SF2, identified through an RNAi screen in collaboration, in order to determine if they are required as entry factors for chikungunya virus. In a last axis, we have set up and carried out a genome-wide loss of function screen with the CRISPR/Cas9 technology in order to identify host factors important for chikungunya virus entry, replication or virus-induced cell death. Although it appears that screen conditions should be optimized, we have identified potential candidates required for CHIKV infection and we are currently testing them
Mohammad, Jiyan Mageed. "Therapeutic Potential of Piperlongumine for Pancreatic Ductal Adenocarcinoma." Diss., North Dakota State University, 2019. https://hdl.handle.net/10365/31347.
Повний текст джерелаNIH
Fracassi, Giulia. "CRISPR/Cas9 screenings and in silico investigations nominate low-frequency alterations in DNA repair genes as biomarkers for castration-resistant prostate cancers." Doctoral thesis, Università degli studi di Trento, 2023. https://hdl.handle.net/11572/364383.
Повний текст джерелаLembo, Gaia. "Substrate targeting and inhibition of editing deaminases." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1144295.
Повний текст джерелаMerenda, Alessandra. "Development of a new screening system for the identification of RNF43-related genes and characterisation of other PA-RING family members." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267982.
Повний текст джерелаSPATARO, CLARISSA. "IDENTIFICATION OF NEW MYC DEPENDENCIES AMONG RNA-BINDING PROTEINS." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/909490.
Повний текст джерелаBasso, Pauline. "Exolysine, un facteur de virulence majeur de Pseudomonas aeruginosa." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV063/document.
Повний текст джерелаPseudomonas aeruginosa is a human opportunistic pathogen responsible for nosocomial infections associated with high mortality. The type III secretion system (T3SS) and T3SS-exported toxins have been considered as key infectivity virulence factors. Our team recently characterized a group of strains lacking T3SS, but employing a new pore-forming toxin of 172 kDa, named Exolysin (ExlA) that provokes cell membrane disruption. In this work we demonstrated that the ExlA secretion requires ExlB, a predicted outer membrane protein encoded in the same operon, showing that ExlA-ExlB define a new active Two-Partner Secretion (TPS) system. In addition to the TPS secretion signals, ExlA harbors several distinct domains, which comprise hemagglutinin domains, five Arginine-Glycine-Aspartic acid (RGD) motifs and a non-conserved C-terminal region lacking any identifiable sequence motifs. Cytotoxic assays showed that the deletion of the C-terminal region abolishes host-cell cytolysis. Using liposomes and eukaryotic cells, including red blood cells, we demonstrated that ExlA forms membrane pores of 1.6 nm. Based on a transposon mutagenesis strategy and a high throughput cellular live-dead screen, we identified additional bacterial factors required for ExlA-mediated cell lysis. Among 7 400 mutants, we identified three transposons inserted in genes encoding components of the Type IV pili, which are adhesive extracellular appendices. Type IV pili probably mediate close contact between bacteria and host cells and facilitate ExlA cytotoxic activity. These findings represent the first example of cooperation between a pore-forming toxin of the TPS family and surface appendages to achieve host cell intoxication. Using mice primary bone marrow macrophages we showed that ExlA pores provoke activation of Caspase-1 via the NLRP3-inflamasomme followed by the maturation of the pro-interleukin-1ß. Mining of microbial genomic databases revealed the presence of exlA-like genes in other Pseudomonas species rarely associated with human infections P. putida, P. protegens and P. entomophila. Interestingly, we showed that these environmental bacteria are also able to provoke Caspase-1 cleavage and pro-inflammatory cell death of macrophages. Finally, genome-wide loss-of-function CRISPR/cas9 RAW library screen revealed that several components of the immune system response, indirectly linked to Caspase-1 are involved in the ExlA-mediated cell lysis. Moreover, we found at least three sgRNAs targeting miRNA, mir-741 were highly enriched in resistant macrophages challenged by ExlA. This miRNA regulates enzymes (St8sIa1 and Agpat5) in the sphingolipids and glycerophololipids biosynthesis pathways, suggesting that ExlA activity may require proper lipid environment
Weber, Julia Maria [Verfasser], Radu Roland [Akademischer Betreuer] Rad, Heinrich [Gutachter] Leonhardt, Radu Roland [Gutachter] Rad, and Angelika [Gutachter] Schnieke. "Transposon- and CRISPR-based tools for tumour suppressor gene screening in vivo / Julia Maria Weber ; Gutachter: Heinrich Leonhardt, Radu Roland Rad, Angelika Schnieke ; Betreuer: Radu Roland Rad." München : Universitätsbibliothek der TU München, 2021. http://d-nb.info/1236342879/34.
Повний текст джерелаALFRED, VICTOR IFEOLUWA. "GENETIC SCREENING TO IDENTIFY INTERACTORS OF ESCRT-II SUBUNIT, VPS25, AND PRELIMINARY CHARACTERISATION OF CANDIDATES." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/560382.
Повний текст джерелаMathews, Bobby. "A zebrafish model system for drug screening in diabetes." Thesis, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-17847.
Повний текст джерелаSingh, V. "Applying bioinformatic tools to better understand eye diseases." Thesis, 2020. https://eprints.utas.edu.au/35302/1/Singh_whole_thesis.pdf.
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.
Yang, Miao-Chia, and 楊苗佳. "Using CRISPR/Cas9-Mediated GLA-null Cell Lines as An In Vitro Drug Screening Model for Fabry Disease." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/49926843078539991979.
Повний текст джерела國立陽明大學
藥理學研究所
104
Fabry disease is a hereditary, X-linked lysosomal storage disease resulting from deficient activity of the lysosomal α-galactosidase A. It leads to progressive accumulation of glycosphingolipids particularly globotriaosylceramide (GL-3) in lysosomes of the heart, kidneys, skin and various tissues. Regular administration of recombinant human alpha Gal A (rh-α-GLA), termed enzyme replacement therapy (ERT) is currently available as the only effective treatment for the Fabry patients with GL-3 accumulation. However, the rh-α-GLA driven GL-3 clearance has the limitations, i.e. rh-α-GLA is physiologically instable and quickly degraded in cells. Moreover, lacking of an appropriate in vitro disease model restricted the pharmaceutical studies for improving the ERT treatment. Therefore, it is worth to establish a cell model of Fabry disease (FD) as the platform to screen the potential candidates for prolonging its potency. By utilizing the CRISPR/Cas9 genome editing system, we generated the GLA disruption in HEK293T cells that was completely devoid of detectable GLA protein expression and enzyme activity, providing a clear background to investigate rh-α-GLA cellular pharmacokinetics. The administrated rh-α-GLA was decreased with time and had a half-life of 24 hrs in the GLA-null cells. Base on the GLA deficient cell line, we applied to discover the potential drug or small molecular to restore rh-α-GLA activity. Co-treatment of chaperone drug, N-butyldeoxygalactonojirimycin (NB-DGJ), and protease inhibitor, E64, with ERT significantly prolonged rh-α-GLA activity by over two-folds compared to ERT alone. In addition, NB-DGJ and E64 significantly decreased GL-3 accumulation in the Fabry patients-derived fibroblast. Next, we expanded the screening range of drug and identified the activity for discovering other potential drugs. We screened 64 drugs combining ERT in GLA-null cells and discovered that Calpain inhibitor II, E64C, 2-NBDG, β-D-Galactose pentapivalate, 2-Deoxy-D-galactose, Finasteride, Diazepam, Theophylline, Trazodone, Benzamidine, 3-Methyladenine, Carbamazepine, Selegiline, Sulpiride and Fluorouracil could prolong rh-α-GLA activity. By creating this model, we provide a novel in vitro tool with which to screen potential compounds to avoid short period of GLA activity in human body.
Simon, Laura. "Use of chemogenomic approaches to characterize RUNX1-mutated Acute Myeloid Leukemia and dissect sensitivity to glucocorticoids." Thesis, 2020. http://hdl.handle.net/1866/24841.
Повний текст джерелаRUNX1 is an essential transcription factor for definite hematopoiesis and plays important roles in immune function. Mutations in RUNX1 occur in 5-13% of Acute Myeloid Leukemia (AML) patients (RUNX1mut ) and are associated with adverse outcome, thus highlighting the need for better genetic characterization and for the design of efficient therapeutic strategies for this particular AML subgroup. Although most RUNX1 mutations in AML are believed to be acquired, germline RUNX1 mutations are observed in the familial platelet disorder with predisposition to hematologic malignancies (RUNX1-FPD, FPD/AML) in which about 44% of affected individuals progress to AML. By performing RNA-sequencing of the Leucegene collection, we revealed that RUNX1 allele dosage influences the association with cooperating mutations, gene expression profile, and drug sensitivity in RUNX1mut primary AML specimens. Validation of RUNX1 mutations led to the discovery that 30% of RUNX1 mutations in our AML cohort are of germline origin, indicating a greater than expected proportion of cases with familial RUNX1 mutations. Chemical screening showed that most RUNX1mut specimens are sensitive to glucocorticoids (GC) and we confirmed that GCs inhibit AML cell proliferation via interaction with the Glucocorticoid Receptor (GR). We observed that specimens harboring RUNX1 mutations expected to result in low residual RUNX1 activity were most sensitive to GCs, and that co-associating mutations, such as SRSF2mut, as well as GR levels contribute to GC-sensitivity. Accordingly, acquired GC-sensitivity was achieved by negatively regulating RUNX1 expression in human AML cells, which was accompanied by upregulation of the GR. GC-induced transcriptome analysis revealed that GC-induced differentiation of AML cells might be a mechanism at play in the antiproliferative response to these drugs. Most critically, functional genomic screening identified the transcriptional repressor PLZF (ZBTB16) as a specific modulator of the GC response in sensitive and resistant AML cells. These findings provide additional characterization of RUNX1mut AML, further stressing the importance of germline testing for patients carrying deleterious RUNX1 mutations. Our results also identified a novel role for RUNX1 in the GR signaling network and support the rationale of investigating GC repurposing for RUNX1mut AML in preclinical models. Finally, we provided insights into the mechanism of action of GCs, which positions PLZF as an important factor promoting resistance to glucocorticoids in AML.
Cloutier, Véronique. "Criblage génétique et caractérisation fonctionnelle des mutations dans le gène CHD2 associé à l’épilepsie dans un modèle de poisson zèbre." Thèse, 2018. http://hdl.handle.net/1866/21388.
Повний текст джерела