Rozprawy doktorskie na temat „CTCF protein”
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Fischer, Sabine. "Inducible systems for the characterization of insulating and repressing motifs". kostenfrei, 2009. http://d-nb.info/999863568/34.
Pełny tekst źródłaNobelen, Suzanne van de. "Touched by CTCF analysis of a multi-functional zinc finger protein /". [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/12282.
Pełny tekst źródłaPanzer, Imke [Verfasser]. "Identifizierung und Analyse von Protein-Interaktionspartnern des Isolationsfaktors CTCF / Imke Panzer". Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1063954177/34.
Pełny tekst źródłaZielke, Katrin [Verfasser], i Andreas [Akademischer Betreuer] Burkovski. "The insulator protein CTCF and cohesins are critical for Herpesvirus saimiri genome maintenance = Das Insulatorprotein CTCF und Kohäsine sind kritisch für die Erhaltung der Genome von Herpesvirus saimiri / Katrin Zielke. Betreuer: Andreas Burkovski". Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2012. http://d-nb.info/1021259632/34.
Pełny tekst źródłaSegueni, Julie. "DNA methylation changes CTCF binding and reorganizes 3D genome structure in breast cancer cells". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL020.
Pełny tekst źródłaMammalian genomes adopt a functional 3D organization where enhancer-promoter interactions are constrained within Topologically Associating Domains (TADs). The CTCF insulator protein has a dual role in this process, with binding at promoters resulting in the formation of enhancer-promoter loops (intra-TAD structure) and binding at TAD boundaries preventing the formation of inappropriate loops between neighboring domains. Importantly, perturbations of CTCF binding at specific sites in cancer cells can be caused by both changes to the DNA sequence (mutations) or DNA methylation changes (epi-mutations). We first performed precisely-calibrated CTCF ChIP-seq experiments and found that a large number of sites are differentially bound, with a substantial fraction of differential CTCF binding peaks shared among cancer cell lines. Differential CTCF peaks can both be gained and lost and are often localized close to genes associated with breast cancer transformation. We found a striking correlation between CTCF binding changes and H3K27ac changes indicating a link between CTCF binding and the activity of cis-regulatory elements (CREs). Using high-resolution Hi-C, we assessed the impact of differential CTCF binding on chromatin structure, characterizing considerable 3D genome reorganization at gene loci with perturbed CTCF peaks. Unexpectedly, we find the most drastic examples of reorganization within TADs, at the level of enhancer-promoter loops. Then, we identified DNA methylation changes as the upstream cause of CTCF binding deregulation in our breast cancer model. Using genome-wide hypomethylating agent, we were able to partially reverse observed CTCF binding changes and the gene expression changes they induced. Our work thus identifies a pervasive DNA-methylation-guided reorganization of CTCF binding and intra-TAD structure. Such recurrent patterns of epi-mutations can provide a mechanistic explanation for shared gene deregulation in cancers
Malashchuk, Ogor. "Epigenetic regulation of skin development and postnatal homeostasis : the role of chromatin architectural protein Ctcf in the control of keratinocyte differentiation and epidermal barrier formation". Thesis, University of Bradford, 2016. http://hdl.handle.net/10454/14791.
Pełny tekst źródłaMalashchuk, Igor. "Epigenetic Regulation of Skin Development and Postnatal Homeostasis The role of chromatin architectural protein Ctcf in the control of Keratinocyte Differentiation and Epidermal Barrier Formation". Thesis, University of Bradford, 2016. http://hdl.handle.net/10454/14791.
Pełny tekst źródłaShamsuddin, S. "Biochemical characterization of the interactions between a transcription factor, CTCF and its partners Y-Box binding protein-1, and the large subunit of RNA polymerase II". Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269484.
Pełny tekst źródłaAlharbi, Adel Braik M. "Characterising the Roles of Zinc Finger Proteins CTCF and ZRANB2 in Modulating Alternative Splicing". Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/27996.
Pełny tekst źródłaBall, DeAnna K. "Establishment of a recombinant CTGF expression system in vitro that models CTGF processing in vivo : structural and functional characterization of multiple mass CTGF proteins /". The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486397841221133.
Pełny tekst źródłaPi, Liya. "The role of connective tissue growth factor (ctgf) in oval cell aided liver regeneration in the 2-aaf/phx model". [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010022.
Pełny tekst źródłaTypescript. Title from title page of source document. Document formatted into pages; contains 162 pages. Includes Vita. Includes bibliographical references.
Koga, Kenichi. "MicroRNA-26a inhibits TGF-β-induced extracellular matrix protein expression in podocytes by targeting CTGF and is downregulated in diabetic nephropathy". Kyoto University, 2016. http://hdl.handle.net/2433/204573.
Pełny tekst źródłaPanek, Anna [Verfasser]. "Rolle des Connective Tissue Growth Factors (CTGF) und des PKC-enhanced Protein-Phosphatase 1 Inhibitors (KEPI) für die Funktion des adulten Herzen : Studien an transgenen Tiermodellen / Anna Naila Panek". Berlin : Freie Universität Berlin, 2008. http://d-nb.info/1023375095/34.
Pełny tekst źródłaBreuninger, Stephanie [Verfasser], Gabriele [Akademischer Betreuer] Multhoff, Gabriele [Gutachter] Multhoff i Thomas E. [Gutachter] Schmid. "Utilizing Heat Shock Protein 70 (Hsp70) as a Tumor-Specific Blood Biomarker and for the Isolation of Circulating Tumor Cells (CTCs) / Stephanie Breuninger ; Gutachter: Gabriele Multhoff, Thomas E. Schmid ; Betreuer: Gabriele Multhoff". München : Universitätsbibliothek der TU München, 2018. http://d-nb.info/1187917079/34.
Pełny tekst źródłaLaurent, Anouchka. "Caracterisation et modélisation des pathologies lymphoides présentant des gains du chromosome 21". Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7061.
Pełny tekst źródłaSomatic gains of chromosome 21 (+21) are hallmark of hematological malignancies, and children with Down Syndrome (DS, constitutive trisomy 21) are predisposed to develop leukemia. These observations strongly suggest that gains of chromosome 21 promote leukemia development; however, alone, it is not sufficient. The aim of my PhD work was to identify and functionally characterize the genetic alterations cooperating with +21. My first aim was focused on studying the impact of the JAK3A572V activating mutation in the development of cutaneous T cell lymphoma (CTCL), using a new knock-in model carrying this alteration at the endogenous locus. In this study, I showed that partial trisomy 21 (Ts1Rhr) cooperates with the JAK3A572V mutation to reduce the latency of this pathology, thus highlighting a mechanism of oncogenic cooperation. In a second aim, I identified a high incidence of genetic alterations leading to RAS/MAPK pathway activation in B cell leukemia samples carrying +21 (B-ALL+21). I have demonstrated that the KRASG12D mutation functionally cooperates with trisomy 21 in transformation process of both murine and human cellular models. In order to test new molecules to improve the treatment of LAL-B+21, I have also developed 20 xenograft models. Treatment of these models with trametinib, a RAS/MAPK pathway inhibitor, alone or in combination with conventional chemotherapies (vincristine), improve their survival. Together, these data indicate that characterizing and targeting cooperation events allow to propose novel therapeutic strategies in pediatric leukaemia with +21
Tulukcuoglu, Güneri Ezgi. "Development of microfluidic device for high content analysis of circulating tumor cells". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066583/document.
Pełny tekst źródłaMetastasis is the advanced stage of cancer progression and is the cause of 90% of deaths in cancer disease. During metastatic cascade, it is suggested that the successful metastatic initiation depends on the survival of circulating tumor cells (CTCs). CTCs are the cells that shed from the primary or secondary tumor sites into the blood circulation. it is now widely recognized as potential biomarker for companion diagnostics in which high number of CTCs in blood can indicate association with poor survival or high risk of disease progression. Besides, following the number of CTCs during the course of treatment can help to adapt the selected therapy and predict the treatment efficacy. On the other hand molecular characterization can provide patient stratification and identifying the therapeutic targets. However they are extremely rare in the bloodstream, estimated between 1-10 CTC among 6×106 leukocytes, 2×108 platelets and 4×109 erythrocytes per one mL of blood which makes their isolation very challenging. A very attractive way of isolation of CTCs is to integrate microfluidics. Microfluidics offers great advantages such as low volume of reagent consumption and short analysis times with automation as well as isolation and detection analysis can be integrated resulting in highly efficient biomedical devices for diagnostics. As parallel to state of the art, a powerful microfluidic device for circulating tumor cells capture and analysis had already been developed previously in our laboratory. The principle of capture is based on self-assembly of antibody-coated (EpCAM) magnetic beads in which the cells are enriched by EpCAM surface antigen which is found commonly in epithelial origin cancer cells. This system was already validated with cell lines and patients samples. However, the system did not allow isolation/detection of subpopulations of CTCs or performing high content molecular characterization. Therefore, my PhD project aimed at further improving the capabilities of the system on the main two aspects: targeting subpopulations of CTC and studying of protein interactions of CTCs in Ephesia System
LOCATELLI, LUIGI. "Expression of aVB6 integrin by Pkhd1-defective cholangiocytes links enhanced ductal secretion of Macrophage chemokines to progressive portal fibrosis in Congenital Hepatic Fibrosis". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41733.
Pełny tekst źródłaMacPherson, Melissa. "Biochemical Studies of the CTCF Insulator Protein: Determination of Protein Interactions with CTCF using Tandem Affinity Purification, Characterization of its Post-translational Modification by the Small Ubiquitin-like Modifier Proteins and Studies of CTCF DNA Looping Ability". Thesis, 2010. http://hdl.handle.net/1807/26205.
Pełny tekst źródłaJohanson, Michael. "An Investigation of Insulator Proteins in Mosquito Genomes". Thesis, 2013. http://hdl.handle.net/1969.1/151362.
Pełny tekst źródła"Functional characterization of CCCTC-binding factor (CTCF) in the pathogenesis of hepatocellular carcinoma". 2013. http://library.cuhk.edu.hk/record=b5884412.
Pełny tekst źródłaThesis (Ph.D.)--Chinese University of Hong Kong, 2013.
Includes bibliographical references (leaves 154-187).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Chien, Chia-Hung, i 簡嘉宏. "Functional Analysis of Zebrafish CTGF gene promoter by Transgenic Assay with Green Fluorescent Protein (GFP) Reporter Gene". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/30067652716686339852.
Pełny tekst źródła臺灣大學
口腔生物科學研究所
95
Connective tissue growth factor (CTGF), a member of CCN family, is a cysteine-rich, secreted, extracellular matrix-associated protein that regulates diverse cellular functions in different cell types. It modulates many cellular functions, including cell proliferation, migration, adhesion, and extracellular matrix production. Evidence suggests that there is a distinctive function of CTGF in the skeletal development. For instance, during Meckel''s cartilage development, CTGF acts as a down-stream molecule of TGF-β to stimulate cell-cell interactions and the expression of condensation-associated genes. Actually, TGF-β response element is located on the CTGF gene, and CTGF can exert many functions by the induction of TGF-β. The aim of this study was to analyze the zebrafish CTGF promoter. Its cognate genomic DNA fragments were amplified by polymerase chain reaction (PCR). Upstream promoter (enhancer) fragments were constructed with EGFP (enhanced green fluorescent protein) reporter gene or with HSV-tymidine kinase (TK) basal promoter and analyzed in vivo by transient transgenic assays using zebrafish embryos. Results demonstrate that the constructs of pZF-CTGF(-2893/ +105)-EGFP1 [pCTGF- EGFP1] and pZF-CTGF(-1593/-1462)-HSV-TK-EGFP1 [pCTGF-E2-TK EGFP1]can drive the specific expression of GFP in zebrafish embryo(5dpf). The expression sites include mandible, cranium, cornea, heart, somite, notochord, floor plate, fin bud, and epidermis. It is identical to in situ hybridization result. Furthermore,the proximal promoter constructs of the pZF-CTGF(-195/+22)-EGFP1 [pCTGF-P200- EGFP1], pZF-CTGF(-64/+22)-EGFP1 [pCTGF-vTATA-EGFP1] and pZF-CTGF(-195/-44)- HSV-TK-EGFP1 [pCTGF-195xTATA-TK-EGFP1] can also drive expression of GFP in zebrafish embryo(5dpf). The expression sites include notochord and somite. However, the expression area is fewer. The zebrafish transgenic stable lines were not obtained from pZF-CTGF(-2893/+105)-EGFP1 [pCTGF-EGFP1] construct yet. The results suggest that the tissue-specific regulatory elements of the zebrafish CTGF reside within the upstream conserved region (-1593/-1462) and proximal promoter region (-195/ +22), and the regulatory mechanism of CTGF may be conserved among the vertebrate species.
Singh, Simranjit. "Redox regulation of protein phosphatase-1 and ER stress regulation of connective tissue growth factor in cardiomyocytes". Doctoral thesis, 2017. http://hdl.handle.net/11858/00-1735-0000-0023-3E92-5.
Pełny tekst źródłaKittana, Naim. "Role of Secretory Processes in Cardiac Fibroblasts for Heart Failure Development and Progression". Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0023-9947-D.
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