Дисертації з теми "Alterations of transcription factors"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся з топ-50 дисертацій для дослідження на тему "Alterations of transcription factors".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Переглядайте дисертації для різних дисциплін та оформлюйте правильно вашу бібліографію.
Morey, Ramonell Lluís. "Chromatin alterations imposed by the oncogenic transcription factor PML-RAR." Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7138.
Повний текст джерелаIn mammals, as in plants, mutations in SNF2-like DNA helicases/ATPases were shown to affect not only chromatin structure but also global methylation patterns, suggesting a potential functional link between chromatin structure and epigentic marks. The SNF2-like containing NuRD complex is involved in gene transcriptional repression and chromatin remodeling. We have previously shown that the leukemogenic protein PMLRARα represses target genes through recruitment of DNMTs and Polycomb complex. In this thesis, we demonstrate a direct role of the NuRD complex in aberrant gene repression and transmission of epigenetic repressive marks in acute promyelocytic leucemia (APL). We show that PML-RARα binds and recruits NuRD to target genes, including to the tumor-suppressor gene RAR2. In turn, the NuRD complex facilitates Polycomb binding and histone methylation at lysine 27. Retinoic acid treatment reduced the promoter occupancy of the NuRD complex. Knock-down of the NuRD complex in leukemic cells not only prevented histone deacetylation and chromatin compaction, but also impaired DNA and histone methylation as well as stable silencing, thus favoring cellular differentiation. These results unveil an important role for NuRD in the establishment of altered epigenetic marks in APL, demonstrating an essential link between chromatin structure and epigenetics in leukemogenesis that could be exploited for therapeutic intervention.
Ruiz, Emmanuelle. "Coopération entre les inducteurs de l’EMT (EMT-TF/miRNA) et les altérations oncogéniques dans la tumorigenèse mammaire." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10069.
Повний текст джерелаCancer cells are able to reactivate the Epithelio-Mesenchymal Transition (EMT), an embryonic mechanism, to acquire mobility and dedifferentiation capacities. EMT leads to a genetic reprogramming with the reactivation of EMT inductors, mainly transcription factors (EMT-TF) and the inhibition of miRNA. Otherwise, oncogenic stresses are essentials to tumor progression. The aim of my thesis project was to have a better understanding about the cooperation between events of genetic reprogramming occurring during EMT and oncogenic stresses during mammary tumor transformation. First, a screening based on oncogenic cooperation in soft agar assay, between EMT-TFs and oncogenic stresses was performed. Following a bioinformatics analysis, different EMT-TFs signatures associated with an oncogenic stress were identified. Thus, for example, the expression of EMT-TF ZEB1 and GSC were associated with the deletion of tumor suppressor gene PTEN to transform immortalized mammary epithelial cells. An immunohistochemistry analysis on a set of 558 triple negative breast cancers validated in vivo the presence of a correlation between the expressions of GSC and PTEN. However, this association seems to be more complex. Indeed, the expression of GSC is negatively associated with the nuclear expression of PTEN while it’s positively associated with the cytoplasmic expression of PTEN. Finally, an analysis of public metadata on cancer samples as TCGA or METABRIC is ongoing to validate these in vitro signatures and wider to determine how EMT or EMT-TFs associated signatures correlate with classical oncogenic pathways.Secondly, an in silico analysis, from predictive algorithms of miRNA targets, was performed to select miRNA able to inhibit the expression of several EMT-TFs. Two miRNA (miR-495 and miR-590-3p) were identified targeting several members of four principal’s families of EMT-TFs (FOXC, Snail, bHLH and ZEB). In vitro tests were realized to validate these regulations identifying Slug as a target of miR-590-3p. Moreover, these miRNAs expression in mammary cell lines is negatively correlated with EMT-TFs expression and EMT markers. A treatment with TGF-, a major EMT inductor, decreases their expression, potentially meaning that these miRNA can negatively regulate EMT. In parallel, several EMT-TFs are able to repress the expression of miR-590-3p, acting directly on its promotor, thus creating feedback loops. Functional studies using stable expression vector of miR-590-3p suggest a secondary role of this miRNA in the regulation of EMT because miR-590-3p deregulates EMT secondary markers as N-Cadherin. Functions restauration studies are planned to determine how important these feedback loops in mammary tumor progression are. To open the project, expression of these identified miRNA will be correlated with EMT-TF associated signatures and with classical oncogenic pathways to determine the link between these three components in mammary tumorigenesis. My thesis works are shown that there is an interactome between EMT inductors, oncogenic stresses and miRNA during human mammary transformation
McElwee, Joshua J. "A comparative analysis of transcriptional alterations in long-lived insulin/IGF-1-like signaling mutants in Caenorhabditis elegans and Drosophila melanogaster /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/4982.
Повний текст джерелаJamrog, Laura. "Impact des altérations génétiques de PAX5 sur le développement de la lignée lymphoïde B et dans la leucémogenèse des LAL-B." Electronic Thesis or Diss., Toulouse 3, 2021. http://www.theses.fr/2021TOU30306.
Повний текст джерелаThe PAX5 (Paired boX 5) gene encodes a key transcription factor crucial for B-cell differentiation. We showed that the two PAX5 isoforms are differentially regulated but have equivalent function during early B-cell differentiation. Indeed, PAX5A and PAX5B isoforms can both induce B-cell program but may have functional differences after B-cell activation. The tight control of their expression may thus reflect a way to finely tune PAX5 dosage during B-cell differentiation process. PAX5 is a well-known haploinsufficient tumor suppressor gene in human B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and is the main target of a wide diversity of somatic alterations in childhood and adult BCP-ALL, occurring in one third of sporadic cases. However, the role of PAX5 fusion proteins in BCP-ALL initiation and transformation is ill-known. We previously reported a new recurrent t(7;9)(q11;p13) chromosomal translocation in human BCP-ALL that juxtaposed PAX5 to the coding sequence of elastin (ELN). To study the function of the resulting PAX5-ELN fusion protein in BCP-ALL development, we generated a mouse model in which the PAX5-ELN transgene is expressed specifically in B cells. PAX5-ELN-expressing mice efficiently developed BCP-ALL phenotype with a penetrance of 80%. Leukemic transformation was associated with clonal Immunoglobulin gene rearrangement and recurrent secondary mutations in Ptpn11, Kras, Pax5, and Jak3 genes affecting key signaling pathways required for cell proliferation. Our functional studies demonstrated that PAX5-ELN impairs B-cell development in vitro and in vivo and induces an aberrant expansion of the pro-B cell compartment at the preleukemic stage. Our molecular and computational approaches identified PAX5-ELN-regulated candidate genes that establish the molecular bases of the preleukemic state to drive BCP-ALL initiation. In conclusion, our study provides a new in vivo model recapitulating the multistep leukemogenesis process of human BCP-ALL and strongly implicates PAX5 fusion proteins as potent oncoproteins in leukemia development. Furthermore, there is increasing evidence for an inherited genetic basis of susceptibility to childhood BCP-ALL. In this context, four unrelated families with childhood BCP-ALL expressing heterozygous PAX5 germline point mutations were recently reported: the recurrent mutation PAX5 G183S affecting the octapeptide domain of PAX5 has been described in three families while PAX5 R38H affecting its DNA-binding paired domain has been identified in another one. We strengthen the hypothesis of inherited character of familial BCP-ALL with the description of three novel familial BCP-ALL cases in related patients that express the germline PAX5 R38H mutation. To uncover the intrinsic effect of PAX5 R38H mutant in B-cell development, we performed in vitro, and in vivo functional assays combined with a gene expression analysis, based on a retroviral complementation approach. Our results indicated that PAX5 R38H mutant acts as a strong hypomorphic variant that fails to drive B-cell differentiation and does not exert a dominant-negative effect on wild-type PAX5. Syngeneic transplantation of PAX5 R38H-expressing cells demonstrated maintenance of engraftment capacity and led to development of BCP-ALL phenotype in mice. Our transcriptomic analysis of these PAX5 R38H-expressing cells showed that PAX5 R38H drastically alters the pattern of expression of PAX5 target genes but also revealed a distinct molecular signature specific to PAX5 R38H. Together with previous unrelated family study, our observations allow to establish the recurrence of the germline PAX5 R38H mutation associated with BCP-ALL. Our data also highlight the importance of transcriptional dysregulation in leukemogenesis of familial BCP-ALL, particularly of genes involved in B-cell differentiation
Redondo, Monte Enric [Verfasser], and Philipp [Akademischer Betreuer] Greif. "Investigation of transcription factor alterations in core binding factor leukemia : implications in clonal expansion, cell metabolism and lineage fate decisions / Enric Redondo Monte ; Betreuer: Philipp Greif." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/122568269X/34.
Повний текст джерелаBorralleras, Fumaña Cristina 1988. "Correlation between cognitive phenotype, neural morphology and molecular alterations in mouse models of Williams-Beuren syndrome : new therapeutic approaches." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/388032.
Повний текст джерелаLa síndrome de Williams-Beuren (SWB) és una malaltia rara del neurodesenvolupament causada per una deleció heterozigota d’entre 26 i 28 gens contigus a la regió 7q11.23. Fins ara, una gran part de l’atenció s’ha centrat en el seu característic perfil neurocognitiu. Tot i que s’han fet progressos molt importants pel que fa a la caracterització clínica o a les correlacions genotip-fenotip, seria de gran interès aprofundir en les característiques neuropatològiques de la SWB. En aquesta tesi, hem utilitzat un model de ratolí del SWB amb una deleció heterozigota que mimetitza la deleció més comuna d’aquests pacients. Hem caracteritzat el fenotip cognitiu i comportamental d’aquests ratolins i hem identificat alteracions moleculars i neuroanatòmiques rellevants per a la malaltia. Per altra banda, hem dut a terme dues estratègies terapèutiques: una teràpia gènica i un tractament farmacològic. Els resultats obtinguts remarquen la utilitat d’aquest model animal per a l’estudi dels mecanismes subjacents a la malaltia així com també per a avaluar noves aproximacions terapèutiques.
Chanapai, Seni. "Photocontrol of artificial transcription factors." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58014/.
Повний текст джерелаPinacho, Garcia Raquel. "SP Transcription factors in psychotic disorders." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/327025.
Повний текст джерелаMüller, Susanne. "Transcription factors regulating the Btk promoter /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2717-0.
Повний текст джерелаPaik, Elizabeth Jae-Eun. "Caudal Transcription Factors in Hematopoietic Development." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10254.
Повний текст джерелаCostanzo, Federico. "Role of NER factors in transcription." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ099.
Повний текст джерелаMutations in genes coding for NER factors give rise to autosomal recessive diseases such as Xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). The phenotypes associated with these genetic syndromes spans from extreme sensitivity to UV light, with increased predisposition to cancer (for XP and combined XP/CS, mostly), mental retardation and progeria (for CS and combined XP/CS). Whether the correlation between defective DNA repair reactions and UV-sensitivity/cancer may be more intuitive, a link with neurological/progeroid symptoms is still a matter of debate. As a possible explanation, it has been proposed a connection between NER and transcription regulation. We propose additional insights on XPG and XPC roles in transcription regulation in absence of exogenous stress and how CSA and CSB orchestrate transcription arrest due to genotoxic attack. XPC was able to stably interact with NSD3 methyltransferase. Mutations in XPC also disturbed the transcriptome and the H3K36me3 distribution. Mutations in XPG deregulate gene expression and XPG is able to be recruited genome wide together with TFIIH. CSA and CSB can, as part of the ubiquitin/proteasome machinery, regulate the recruitment timing of DNA binding factors and control transcriptional program after UV irradiation. Hence, our data shed more light in NER factors role in transcription and their defective action as a cause of XP and XP/CS disorders. Additionally, our data provide explanations on the mechanism of transcription arrest following genotoxic stress and pose questions about the origins of CS phenotype
Grossman, Sharon R. (Sharon Rachel). "Combinatorial gene regulation by transcription factors." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/128406.
Повний текст джерелаCataloged from PDF of thesis. "The Table of Contents does not accurately represent the page numbering"--Disclaimer page.
Includes bibliographical references.
Combinatorial gene regulation is encoded in enhancers and promoters in the form of binding sites for transcription factors (TFs), which collaboratively recruit the transcriptional machinery and drive gene expression. Using high-throughput and quantitative technologies developed by our lab and others, we studied TF binding sites in enhancers from numerous different cell types and regulatory systems, shedding light general principles of motif composition and organization in typical cellular regulatory elements. We find extensive synergy between TF binding sites, some with organizational constraints and some with flexible positioning. We demonstrate that different TFs bind at distinct positions within regulatory elements, suggesting a new type of architectural constraint in enhancers. Importantly, our analysis of both TF organization and cooperativity revealed distinctive patterns that separates TFs into potential functional classes. Together, our results suggest a structure of the regulatory code at the level of TF function and generate new hypotheses about regiospecific binding patterns and functions of TF classes within enhancers.
by Sharon R. Grossman.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biology
Greberg, Maria Hellqvist. "Cloning and characterization of FREACs, human forkhead transcription factors." Göteborg : Dept. of Cell and Molecular Biology, Göteborg University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39751934.html.
Повний текст джерелаPatel, Vyoma. "Monocyte subset functional alterations with increased cardiovascular risk factors." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20501.
Повний текст джерелаZhang, Mei. "Molecular alterations induced by dysregulated PKA activity in bone development and homeostasis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397578707.
Повний текст джерелаKoo, Sonya Janet. "Downstream targets of motor neuron transcription factors /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3190171.
Повний текст джерелаKinyanjui, Margaret. "Targeting Th2 transcription factors in experimental asthma." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18717.
Повний текст джерелаLes cellules CD4+ T à antigènes spécifiques transfèrent par adoption l'inflammation pulmonaire constituées principalement de lymphocytes et d'éosinophiles. L'habileté de celles-ci à transférer des cellules T pour induire l'inflammation est dépendante de leur expression de cytokines Th2. De manière à mieux comprendre le mécanisme par lequel les cellules T transmises par adoption induisent l'inflammation pulmonaire, nous avons choisi de moduler l'expression de GATA-3) ou l'activité de (STAT-6) des deux régulateurs-clés de production de cytokine Th2. Afin de modifier l'expression de GATA-3 dans les cellules T destinées au transfert par adoption, nous avons utilisé un rétrovirus recombinant concentré avec une filtration par centrifugeuse. Ce procédé a dramatiquement augmenté leurs titres et ainsi leur habileté à transduire les cellules CD4+ T en culture primaire. Nous avons utilisé un rétrovirus recombinant qui encode la GATA-3 et / ou la protéine fluorescente verte (EGFP). En couplant in vitro la stimulation d'antigènes avec la transduction par vecteur viral, nous avons généré des cellules CD4+ T à antigènes spécifiques exprimant de l'EGFP seul ou bien de la GATA-3 et de l'EGFP. Lorsque transféré dans un rat qui avait subséquemment été provoqué avec des antigènes, ces cellules CD4+ T induisent une réaction aux inflammations pulmonaires avec une augmentation des lymphocytes et éosinophiles. Cette réaction inflammatoire fut accrue chez les animaux recevant les cellules T surexprimant la GATA-3. L'analyse des cellules infiltrantes a aussi révélé que bien que les cellules EGFP+ étaient présentes dans les poumons suivant la provocation par antigènes, elles étaient constituées seulement d'une petite fraction de cellules CD4+ T recrutées dans les poumons. Ainsi, la GATA-3 amplifie la réaction inflammatoire des poumons induite par antigènes en augmentant l'habileté des cellules T à antigènes spécifiques à recruter
Ali, Asif. "Transcription factors in parathyroid development and embryology." Thesis, Open University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489906.
Повний текст джерелаYoung, Neville Jonathan. "The role of transcription factors in odontogenesis." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393692.
Повний текст джерелаBidon, Baptiste. "Mediator and NER factors in transcription initiation." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ093/document.
Повний текст джерелаThe synthesis of messenger RNA is a highly regulated process. During transcription initiation, a large number of proteins are recruited to gene promoter, including the RNA polymerase II, general transcription factors, co-activators, chromatin remodellers and the Mediator complex. Some DNA repair factors from the NER pathway are also recruited. Using cells derived from patients bearing mutations in either MED12 gene or XPC gene, we studied the roles of such proteins in transcription. MED12 patients are mostly characterised by intellectual disability and developmental delay. We showed that MED12 is implicated in the transcription regulation of immediate early genes like JUN, known for its role in neurological development and neuronal plasticity. JUN expression is markedly altered by MED12 mutations. We also showed that the position of the mutation influences this alteration, bringing possible explanation for inter-patients symptom variability. Meanwhile, XPC patients are mostly characterized by photosensitivity. We showed that XPC protein, which engages one of the NER pathways, is implicated in chromatin post-translational modification. Together with E2F1, it helps the recruitment of GCN5 acetyl-transferase to promoter of a certain set of genes. On the promoter, GCN5 notably cooperates with TFIIH to modify the chromatin environment during transcription initiation. In addition to help the comprehension of the transcription mechanisms, these results bring knew insight into the aetiology of mutations associated diseases
Friedrich, Dhana. "Oscillatory transcription factors and stochastic gene expression." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/22053.
Повний текст джерелаTranscription factors (TFs) are receiver and compiler of cell signaling, transmitting incoming inputs into cellular responses that enable cells, organs and organisms to respond and adapt to a changing environment. In the past, it has been shown that many TFs exhibit oscillations of nuclear abundance over time when activated. One of these TFs is the tumor suppressor p53, a central hub in the signaling network regulating the cellular stress response, controlling cell fate decisions by changing the expression of hundreds of target genes. Aberrations in p53’s activity are related to severe human malignancies such as cancer. The dynamics of its nuclear accumulation are stimulus dependent and enable the p53 pathway to mediate distinct responses to cellular stress. However, the molecular mechanisms translating such dynamics to altered gene expression remain elusive. In this thesis, I analyzed how oscillations of p53 affect the transcriptional regulation of target genes in single-cells and at individual promoters. I chose a panel of seven targets and employed a combinatorial approach of single-molecule fluorescence in-situ hybridization and mathematical analysis. I present quantitative, time-resolved measurements of target gene mRNA expression and transcriptional bursting activity with single-cell and single-molecule resolution. The resulting data show characteristic principles how p53 nuclear accumulation increases transcriptional bursting upon stimulation and reveal gene-specific modulations. P53 target promoters are regulated by changing the fraction of active promoters, indicating burst frequency regulation. Based on this, genes can be grouped along three archetypes of promoter activity: sustained, transient and pulsatile. These archetypes cannot solely be explained by nuclear p53 levels or promoter binding of total p53. Instead, I provide evidence that the time-varying acetylation state of p53’s C-terminal lysine residues is critical for this gene-specific regulation.
Gillis, William Joseph. "The evolution of metazoan GATA transcription factors /." Connect to title online (Scholars' Bank) Connect to title online (ProQuest), 2008. http://hdl.handle.net/1794/8568.
Повний текст джерелаTypescript. Includes vita and abstract. "This dissertation includes both ... previously published and unpublished co-authored material"--P. v. Includes bibliographical references (leaves 120-135). Also available online in Scholars' Bank; and in ProQuest, free to University of Oregon users.
Gillis, William Joseph 1981. "The evolution of metazoan GATA transcription factors." Thesis, University of Oregon, 2008. http://hdl.handle.net/1794/8568.
Повний текст джерелаThis thesis explores the origin and evolution of animal germ layers via evolutionary-developmental analyses of the GATA family of transcription factors. GATA factors identified via a conserved dual zinc-finger domain direct early germ layer specification across a wide variety of animals. However, most of these developmental roles are characterized in invertebrate models, whose rapidly evolved sequences make it difficult to reconstruct evolutionary relationships. This study reconstructs the stepwise evolution of metazoan GATA transcription factors, defining homologous developmental roles based upon clear orthology assignments. We identified two GATA transcription factors ( PdGATA123 and PdGATA456 ) from the marine annelid Platynereis dumerilii to aid comparison of protostome and deuterostome GATA factors. Our phylogenetic analyses defined these as protostome orthologs of GATA1/2/3 and GATA4/5/6 vertebrate subfamilies, while the mRNA localization of the Platynereis GATAs showed ectodermal versus endomesodermal germ layer restrictions, similar to their vertebrate orthologs. To define the phylogenetic relationships of more divergent genes in the invertebrate models, we identified GATA homologs from recently sequenced protostome genomes. Molecular phylogenetic analyses, comparisons of intron/exon structure, and conserved synteny confirm all protostome GATA transcription factor genes are members of either the GATA123 or GATA456 class. These data allowed us to identify multiple protostome-specific duplications of GATA456 homologs and reconstruct the origin and relationships of all arthropod GATA genes. To probe GATA transcription factor evolution in deuterostomes, including vertebrates, we identified GATA factors in basal deuterostomes, including the cephalochordate Branchiostoma floridae and the hemichordate Saccoglossus kowalevskii. Phylogenetic analyses of these data independently confirmed that the ancestral deuterostome and chordate--like the bilaterian ancestor--possessed only two GATA transcription factors. This work was facilitated by a bioinformatics platform we are developing to identify gene families from preassembled genomic sequence. We generated anti- PdGATA antibodies to further explore the role of Platynereis GATAs in germ layer formation. We identified multiple presumptive endomesodermal cells in which nuclear localization of PdGATA456 protein first occurs and utilized PdGATA456 protein localization to follow endomesodermal cell populations throughout development. These analyses represent some of the first cellular and molecular analyses of Platynereis germ layer formation. This dissertation includes both my previously published and unpublished co-authored material.
Adviser: Stephan Q. Schneider
Matthews, Chris. "Economic and social factors behind housing alterations in Windsor, Ontario." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ30967.pdf.
Повний текст джерелаRoberts, Karen. "Regulation of melanocyte-specific transcription by the transcription factors BRN-2 and microphthalmia." Thesis, Institute of Cancer Research (University Of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286144.
Повний текст джерелаLi, Yuxin. "The DEC1 transcription factor : oncogenic involvement and molecular mechanisms on transcription regulation /." View online ; access limited to URI, 2003. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3115632.
Повний текст джерелаJadlowsky, Julie Kendal. "Dual control of HIV transcription elongation virus-specific negative control by NELF-E is counterbalanced by positive transcription factor P-TEFb /." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1228234927.
Повний текст джерелаEustis, Robyn Lynn. "The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation." PDXScholar, 2015. https://pdxscholar.library.pdx.edu/open_access_etds/2522.
Повний текст джерелаBielecka, Monika. "Analysis of transcription factors under sulphur deficiency stress." Phd thesis, kostenfrei, 2007. http://opus.kobv.de/ubp/volltexte/2007/1481/.
Повний текст джерелаMontelius, Andreas. "Role of transcription factors in sensory neuron specification /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-115-9/.
Повний текст джерелаAndersson, Tove. "Transcription factors regulating the immunoglobulin heavy chain locus /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3559-9/.
Повний текст джерелаLi, Yifan. "Gene regulation by WT1 and related transcription factors." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509772.
Повний текст джерелаJahangiri, Leila. "Combinatorial gene regulation by T-domain transcription factors." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610328.
Повний текст джерелаJager, S. M. de. "Isolation and characterisation of Arabidopsis E2F transcription factors." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.605016.
Повний текст джерелаAndersen, K. G. "Immune modulation using inducible lineage-specific transcription factors." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595497.
Повний текст джерелаWest, Adam Geoffrey. "Molecular interactions of the MADS-box transcription factors." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362415.
Повний текст джерелаBrown, A. Louise. "Molecular characterisation of zebrafish ETS-domain transcription factors." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362472.
Повний текст джерелаGay, Robert Daniel. "Neuronal gene regulation by POU family transcription factors." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267026.
Повний текст джерелаWrighton, N. C. "Transcription factors regulating the human beta-globin genes." Thesis, University College London (University of London), 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382204.
Повний текст джерелаMiles, Anna Louise. "V-ATPase regulation of Hypoxia Inducible transcription Factors." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/283217.
Повний текст джерелаIazzetti, Paul Christopher. "High-throughput binding characterization of bacterial transcription factors." Thesis, Boston University, 2014. https://hdl.handle.net/2144/11020.
Повний текст джерелаTuberculosis (TB) is a global pandemic responsible for the deaths of 1.5 million people annually. A third of the world's population is thought to harbor the latent form of the disease, and a disproportionate majority of TB cases are reported in Asia and Africa where poor infrastructure impedes proper treatment. Non-adherence to drug regimens has helped foster the rise of multi drug-resistant tuberculosis, with implications for those in the developed world. Treatment of the disease is hindered by an inadequate understanding of its causative agent, the pathogen Mycobacterium tuberculosis (MTB). Decreases in thecost of gene sequencing have heralded a new era of genomic technologies such as chromatin immunoprecipitation sequencing (ChiP-Seq), which can generate comprehensive in-vivo genomic binding data for transcription factors and help elucidate the workings of bacterial regulatory networks. In this work we explore the in vitro binding behavior of MTB transcription factors important to disease pathogenesis using electrophoretic mobility shift assays (EMSAs) and High-Throughput Sequencing- Fluorescent Ligand Interaction Profiling (HiTS-FLIP). We compare this data to high-throughput in vivo binding data generated by ChiP-Seq to assessing binding patterns across in vitro and in vivo conditions, and demonstrate the use of HiTS-FLIP as a powerful complement to ChiP-Seq for accurately characterizing transcription factor binding affinity. The results of this work lay the foundation for an integrated experimental workflow combining high-throughput in vitro and in vivo transcription factor binding data to better understand transcription factor behavior in vivo.
Sangwung, Panjamaporn. "Kruppel-Like Transcription Factors: Master Regulators of VascularEndothelium." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499426148493334.
Повний текст джерелаChen, Xi. "The DNA-binding specificity of forkhead transcription factors." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/the-dnabinding-specificity-of-forkhead-transcription-factors(bc02fd29-30d0-47da-9b4f-448687504463).html.
Повний текст джерелаPomeranz, Karen M. "Regulation of FoxO transcription factors in breast cancer." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4253.
Повний текст джерелаBermudez, Vladimir Paredes. "Role of transcription factors in eukaryotic DNA replication /." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9924864.
Повний текст джерелаKetola, Ilkka. "GATA transcription factors during testicular development and disease." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/ketola/.
Повний текст джерелаHopwood, Blair. "Towards characterisation of histone H1 gene transcription factors /." Title page, contents and summary only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phh799.pdf.
Повний текст джерелаSALA, TEA. "Functional analysis of MYB transcription factors in Arabidopsis." Doctoral thesis, Università degli Studi di Milano, 2005. http://hdl.handle.net/2434/59749.
Повний текст джерелаCominelli, E. "PLANT TOLERANCE TO DROUGHT: MODULATION OF TRANSCRIPTION FACTORS." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/150909.
Повний текст джерелаBhattarai, Arati. "The orientation of the Pyrococcus furiosus transcription factor TFB2 in the transcription initiation complex." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1938.
Повний текст джерела