Dissertations / Theses on the topic 'Wnt'
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Lundeen, Berent. "Wnt Signaling in Human Cancers : Role of the Wnt receptor FZD9 in Myelopoiesis." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC319.
Full textMy goal was to study the importance of the expression of the FZD9, a Wnt receptor, in both normal and malignant hematopoiesis. Frizzled 9 (FZD9) is a key component of the Wnt signaling pathway, a pathway which has been shown to play a role in both normal and malignant hematopoiesis. Methylation of the CpG proximal to the transcription start site of the FZD9 gene is recognized as a prognostic factor in AML and its demethylation is a predictive factor for response to epigenetic therapy. Its function in hematopoiesis is however not known. The results show that the FZD9 promoter is in a non-permissive state in leukemic cells. Induction of myeloid differentiation in human myeloid leukemic cell fines restores FZD9 promoter permissiveness with recruitment of E2F and acetylated histone H3 and upregulation of FZD9 mRNA expression. FZD9 expression was progressively increased through the stages of myeloid differentiation in an IPS cell line. In differentiated monocytic THP1 cells, FZD9 was found in the LRPS/6 Wnt receptor complex. Incubation of differentiated cells with Wnt5a, a ligand of FZD9, triggered the decreased expression of - catenin and its nuclear localisation and the canonical Wnt-target genes (c-myc, Cyclin D1 and CD44). We detected no increase in calcium intracellular levels and thus activation of classical non-canonical pathway was not noted upon WntSa incubation. The results of my PhD suggest that the reported methylation of FZD9 promoter in AML and HR-MDS patients may participate in leukemogenesis by the maintenance of an activated Wnt canonical pathway
Nambiar, Roopa. "Zebrafish hdac1 reciprocally regulates the canonical and non-canonical Wnt pathways." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1150313622.
Full textChild, Nicholas Mark. "Wnt signalling and cardiac development." Thesis, University of Newcastle upon Tyne, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548030.
Full textSchans, Veerle Anna Maria van de. "Wnt signaling and cardiac hypertrophy." [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2009. http://arno.unimaas.nl/show.cgi?fid=14684.
Full textRichards, Alexander S. K. "Wnt Signalling in Malignant Mesothelioma." Thesis, Curtin University, 2016. http://hdl.handle.net/20.500.11937/56433.
Full textEubelen, Marie. "Mécanisme moléculaire de la voie Wnt/β-caténine Gpr124/Reck-dépendante." Doctoral thesis, Universite Libre de Bruxelles, 2019. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/280768.
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Asbrand, Christian. "Neue Mechanismen der Regulation von Conductin im Wnt-ss-Catenin-Signalweg [Wnt-beta-Catenin-Signalweg]." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/130/index.html.
Full textNg, Chun-laam, and 吳圳嵐. "Wnt inhibitory factor 1 (Wif-1) coordinates Shh and Wnt signaling activities in urorectal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48329629.
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Chow, Hei-man, and 周熙文. "Hormonal, chemical, and transcriptional regulations of Wnt/{221}-catenin signaling in mammary carcinogensis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4589100X.
Full textRailo, A. (Antti). "Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514261534.
Full textKomekado, Hideyuki. "Glycosylation and palmitoylation of Wnt-3a are coupled to produce an active form of Wnt-3a." Kyoto University, 2007. http://hdl.handle.net/2433/135740.
Full textSchwarcz, Leslie Esther. "Linking steroid hormone and Wnt signaling /." view abstract or download file of text, 2006. http://wwwlib.umi.com/cr/uoregon/fullcit?p3211226.
Full textTypescript. Includes vita and abstract. Includes bibliographical references (leaves 71-82). Also available for download via the World Wide Web; free to University of Oregon users.
Agholme, Fredrik. "Wnt signaling and metaphyseal bone healing." Doctoral thesis, Linköpings universitet, Ortopedi och idrottsmedicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-71287.
Full textGardner, Samantha. "Gonadotropin-releasing hormone targets Wnt signalling." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29112.
Full textHuguet, Emmanuel L. "Wnt genes in human breast biology." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297228.
Full textChen, Demeng. "WNT SIGNALING AND HAIR FOLLICLE INITIATION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1355448596.
Full textTorres, Monica Alexandra. "WNT signaling pathways in Xenopus laevis /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6293.
Full textBaumann, Fabrizio. "Cell signalling through the Wnt pathway /." [S.l.] : [s.n.], 2004. http://www.zb.unibe.ch/download/eldiss/04baumann_f.pdf.
Full textMellin, Ronan Peter. "Investigating the function of VANGL2 in intestinal homeostasis & disease." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31186.
Full textMailavaram, Sravanthi. "Database for the Study of Biological Pathways, with Wnt Signaling Pathway Use Case." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1227118211.
Full textWitzel, Sabine. "Local Wnt11 Signalling and its role in coordinating cell behaviour in zebrafish embryos." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1162424627109-87779.
Full textGessert, Susanne. "Untersuchung potentieller Zielgene des nicht-kanonischen Wnt-Signalwegs." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-60607.
Full textHo, Sze-hang, and 何思恆. "Differential expression of Wnt inhibitors Dickkopf-1 (Dkk-1) and Wnt inhibitory factor-1 (Wif1) in the regulation of urorectal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207999.
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Master of Philosophy
Vinyoles, i. Vergés Meritxell. "Nous reguladors en la via de Wnt." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/284139.
Full textCanonical Wnt signalling is essential for embryonic development and cell proliferation. Deregulation of this pathway leads to some diseases, such as cancer. Binding of extracellular Wnt ligands to specific receptors induces the phosphorylation of Dvl-2 protein by CK1ε- associated-p120-catenin kinase, and a cascade of events that inhibit the activity of GSK3 kinase on β-catenin. As a result, β-catenin is stabilized and translocated to the nucleus where it activates the expression of target genes. Our results explain how CK1ε is quickly activated in Wnt signalling, allowing the cascade of events that accumulate β-catenin. It was previously described that CK1ε presents an autoregulation domain which strongly inhibits CK1ε kinase activity when it is phosphorylated, suggesting that a phosphatase is required to activate Wnt signalling. However, which phosphatase dephosphorylates CK1ε in Wnt and how this phosphatase regulates the pathway were not clear. In this study, we have described that PP2A permits the dephosphorylation of CK1ε upon Wnt, and we have also identified PR61ε as the regulatory subunit of PP2A that controls this CK1ε activation. PR61ε directly interacts with Fz receptor, and associates with LRP5/6-p120-catenin-CK1ε complex upon Wnt activation. Taken together, these results suggest that PR61ε specifically regulates PP2A-mediated CK1ε dephosphorylation and plays an essential role in Wnt signaling. Another key step in the pathway is the local inhibition of GSK3 activity on β-catenin, although the mechanism of this inactivation remains unclear. Two models have been proposed, one dependent on the recruitment and subsequent block of GSK3 by phosphorylated LRP5/6 coreceptor that creates an inhibitory site, and another one based on its sequestration into multivesicular bodies (MVBs). Since our group has uncovered a physical link between cadherins and p120-catenin (two proteins involved in adherens junctions) with the Wnt coreceptor LRP5/6, we wonder whether cadherins may be involved in the endocytosis of GSK3 triggered by Wnt factors. Our results demonstrate that Wnt receptor complexes containing GSK3 are internalized into multivesicular bodies and this endocytosis depends on the previous dissociation of p120-catenin and cadherin from LRP5/6 coreceptor. Thus, disruption of cadherin-LRP5/6 interaction is regulated by cadherin phosphorylation and requires the previous release of p120-catenin. Accordingly, p120-catenin and cadherin mutants unable to dissociate from the complex block GSK3 sequestration into MVBs. These mutants substantially inhibit, but do not completely prevent, the β-catenin accumulation caused by Wnt. These results elucidate how GSK3 is sequestered into MVBs and suggest that this mechanism of internalization together with the inhibition of GSK3 by direct interaction with phosphorylated LRP5/6, are both required for complete β-catenin stabilization upon Wnt stimulation.
Curto, Navarro Josué. "Initial events in non-canonical Wnt signaling." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/461992.
Full textCanonical and non-canonical Wnt pathway have shown to activate signaling pathways that trigger different cellular outputs. However, the initial signaling events upon ligand stimulation show some common elements. The two pathways requires the receptor Frizzled (Fz) to promote Dishevelled phosphorylation and recruitment to the signaling complex. In canonical Wnt pathway, p120-catenin associated CK1ε must be activated to allow Dvl phosphorylation and recruitment to Fz. Here we demonstrate that this two proteins are also required to promote this step upon Wnt5a stimulation. Moreover, Fz associated PR61/PP2A is also necessary to activate CK1 and induce receptor clustering. However, the dependence on these two factors is different, in non-canonical Wnt pathway p120 is not required for CK1ε association to the coreceptor since both proteins independently interact with Ror2. Moreover, p120-catenin associates to Ror2 in a tyrosine phosphorylation-dependent manner. P120-catenin stabilizes Ror2 at the membrane and avoids clathrin-mediated Ror2 internalization. On the other hand, CK1ε binding to the C-terminal part controls Ror2 total levels and prevents its lysosomal degradation. This central role of p120-catenin and CK1ε in the initial signaling events are required for later responses such as Siah2-dependent -catenin downregulation, cell invasion and cortical actin polimerization. Therefore, our results demonstrate the requirement of these two key proteins in the non-canonical Wnt pathway and describe how this pathway is activated.
Nimmrich, Inko. "Tumorspezifisch exprimierte und Wnt-1-induzierte Gene." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=959806369.
Full textSchwarz-Romond, Thomas. "Diversin, eine neue Komponente des Wnt-Signalweges." [S.l. : s.n.], 2002. http://www.diss.fu-berlin.de/2003/19/index.html.
Full textBjörklund, Peyman. "Wnt/β-Catenin Signalling in Parathyroid Tumours." Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8317.
Full textPrimary hyperparathyroidism (pHPT) due to parathyroid tumours with hypersecretion of parathyroid hormone and hypercalcaemia is a common disease with incompletely understood etiology affecting more than 1 % of the population, primarily postmenopausal women. In secondary hyperparathyroidism (sHPT), parathyroid tumours develop in response to calcium and vitamin D deficiency generally in patients with uraemia. HPT is usually treated by surgical removal of enlarged parathyroid glands.
The aim of this thesis was to examine the Wnt/β-catenin signalling pathway in parathyroid tumours.
Aberrantly accumulated β-catenin was found in all analysed pHPT and sHPT tumours, with a stabilising homozygous mutation (Ser37Ala) in 7.3% of the pHPT tumours. Truncation of the APC protein was not found. MYC, a β-catenin target gene was overexpressed in a substantial fraction of pHPT and sHPT parathyroid tumours.
A parathyroid tumour cell line (sHPT-1) was established from a hyperplastic gland removed at operation of a patient with sHPT. The cells produced parathyroid hormone and grew with a doubling time of approximately 72 hours. Stabilised nonphosphorylated transcriptionally active β-catenin was expressed. Efficient transfection of siRNA against β-catenin decreased expression of cyclin D1 and MYC, and inhibited cell growth with ensuring cell death.
The Wnt coreceptor LRP5 was found expressed with an internal deletion of 142 amino acids (LRP5Δ) in 86% and 100% of pHPT and sHPT tumours, respectively. Stabilising mutation of β-catenin and expression of LRP5Δ was mutually exclusive. Expression of LRP5Δ was required to maintain the nonphosphorylated transcriptionally active ß-catenin level, MYC expression, parathyroid cell growth in vitro, and tumour growth in transplanted SCID mice. Wnt3 ligand and LRP5Δ strongly activated transcription, and LRP5Δ was insensitive to inhibition by DKK1.
Aberrant accumulation of β-catenin by stabilising mutation or expression of LRP5Δ appears as a common pathogenic pathway for hyperparathyroid disease. LRP5Δ in particular presents a potential target for therapeutic intervention.
McLaughlin, David Anthony. "Role of Wnt signalling in forebrain development." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/24959.
Full textMicallef, Rachel Antonia. "Wnt signalling in endocrine resistant breast cancer." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/41274/.
Full textCooper, Oliver Jamie. "Investigating Wnt signals in the avian somite." Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445512.
Full textLako, Majlinda. "Identifying and characterising novel human WNT genes." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242351.
Full textNalesso, Giovanna. "WNT signalling in joint repair and homeostasis." Thesis, Queen Mary, University of London, 2011. http://qmro.qmul.ac.uk/xmlui/handle/123456789/2347.
Full textLeal, Letícia Ferro. "Via Wnt/?-catenina em tumores adrenocorticais pediátricos." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/17/17144/tde-06012016-181445/.
Full textContext: CTNNB1 mutations and activation of Wnt/-catenin pathway are frequent in adult adrenocortical tumors (ACTs) but data on childhood ACTs are lacking. Objective: To investigate Wnt/-catenin pathway abnormalities and CTNNB1 mutations in childhood ACTs. Patients and Methods: Clinicopathological findings and outcome of 62 childhood ACTs patients were analyzed regarding to CTNNB1/ -catenin mutations and to the expression of Wnt-related genes (CTNNB1, a Wnt ligand: WNT4, Wnt inhibitors: SFRP1, DKK3 and AXIN1, a transcription factor: TCF7, and target genes: MYC and WISP2) by qPCR and immunohistochemistry. Results: Overall survival (OS) was higher in patients younger than 5 years (p<0.0001) and associated with less advanced tumoral stage (p<0.0001). The p.R337H P53 mutation, found in 87% of the patients, was not associated with clinicopathological findings or outcome. CTNNB1 activating mutations were found in only 4/62 ACTs (6%), all of them harboring TP53 mutation. There was association between the presence of CTNNB1 mutation and death (p=0.02). Diffuse -catenin accumulation was found in 71% of ACTs, most of them without CTNNB1 mutation. CTNNB1 mutated ACTs presented weak/moderate -catenin accumulation. Compared to normal adrenals, ACTs presented increased expression of CTNNB1 (p=0.008) and underexpression of Wnt inhibitor genes: DKK3 (p<0.0001), SFRP1 (p=0.05) and AXIN1 (p=0.04). With regards to Wnt/-catenin target genes, ACTs presented lower expression of MYC but increased expression of WISP2. Higher overall survival was associated with underexpression of SFRP1 (p=0.01), WNT4 (p=0.004) and TCF7 (p<0.01). Conclusions: In childhood ACTs, CTNNB1 mutations are rare and appear to be associated with poor prognosis. Regardless of CTNNB1 mutations, these tumors presented reduced expression of Wnt inhibitor genes (DKK3, SFRP1 and AXIN1) and increased expression of CTNNB1 and a target gene, WISP2. Thus, besides CTNNB1 mutations, additional genetic events affecting the Wnt/-catenin pathway may be involved in childhood adrenocortical tumorigenesis.
Giles, Adam Alexander. "Wnt signalling in oestrogen-induced lactotroph proliferation." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/wnt-signalling-in-oestrogeninduced-lactotroph-proliferation(35c1ba30-0755-4583-bdce-69dce1382721).html.
Full textHeiser, Patrick W. "Wnt signaling in pancreas development and disease." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3261237.
Full textArnold, Sebastian Johannes. "Wnt-, beta- Catenin Zielgene der frühen Mausentwicklung." [S.l. : s.n.], 2002. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10047791.
Full textWehrle, Christian. "Wnt/beta-Catenin-Zielgene in der Mausentwicklung." [S.l. : s.n.], 2003. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11126466.
Full textSheldahl, Laird Charles. "Molecular components of the Wnt/calcium pathway /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6294.
Full textLouie, Sarah. "Wnt signaling regulated by Frizzled and HIPK1 /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6267.
Full textAnnavarapu, Srinivas Rao. "Characterisation of Wnt signalling pathway in rhabdomyosarcoma." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3009225/.
Full textDerry, Sarah White. "Calcium induced Naked1 activity in Wnt signaling." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/6565.
Full textZiegler, Slava. "Identifizierung und Charakterisierung neuer tumorrelevanter Gene, die unter Kontrolle des Wnt-[beta]-Catenin-Signalwegs [Wnt-beta-Catenin-Singalwegs] stehen." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971635307.
Full textKramer, Monika [Verfasser]. "The WNT/β-catenin [WNT-beta-catenin] pathway : profibrotic signaling in fibroblasts in idiopathic pulmonary fibrosis / vorgelegt von Monika Kramer." Giessen : VVB Laufersweiler, 2010. http://d-nb.info/1009523570/34.
Full textVouyovitch, Cécile. "Implication de l’hormone de croissance autocrine dans le cancer du sein humain." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10131.
Full textStudies of our group demonstrated that autocrine human growth hormone promotes proliferation, apoptotic resistance, invasion and migration of human mammary carcinoma cells. The objective of my Ph.D was to understand the role of autocrine hGH in mammary tumour progression following two aspects. On one hand, characterising its impact on tumour angiogenesis and then analysing the crosstalk between GH and Wnt signalling pathways. In the first part, we demonstrated that autocrine hGH from human mammary carcinoma cell line MCF- 7, stimulates proliferation, survival, migration and invasion of human microvascular endothelial cell line and enhances in vitro tubulogenesis. These effects are mediated through the hGHR and stimulates the expression of the proangiogenic factor VEGF-A. Antagonizing VEGF-A action with bevacizumab inhibited the proangiogenic actions of autocrine hGH in vitro. Using a xenograft nude mice model we have shown that sustained angiogenesis and lymphangiogenesis are activated by autocrine hGH production by mammary carcinoma cells. Thus, autocrine hGH participates in the expansion of the vascular network during breast cancer formation. The Wingless (Wnt) signalling pathway is an important actor during embryonic development and in the adult. Here, we showed that autocrine hGH stimulates the expression of several actors of the Wnt pathway, including WNT4. Human breast cancer biopsies overexpressed WNT4 as compared to normal breast. WNT4 production is JAK2 kinase-dependent and synergizes with autocrine hGH on mammary carcinoma cell proliferation. Forced expression of WNT4 in normal human mammary epithelial cell lines stimulates their proliferative, survival and migratory capacities and the formation of colonies in soft agar. These effects are mediated through the transcriptional and translational activation of key regulators of cell cycle and survival. Phenotypic changes are induced by forced expression of WNT4 in mammary epithelial cells and associated with increased expression of mesenchymal markers, cytoskeletal remodelling factors and cell migration activators. Human breast cancer progression is thus activated by autocrine effects of hGH on WNT4 expression and deregulated expression of WNT4 in mammary epithelial cells induces the establishment of a pre-tumorigenic phenotype
Martin, Jennifer. "Wnt regulated transcription factor networks mediate vertebrate cardiogenesis." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources. Online version available for University members only until Feb. 15, 2012, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25801.
Full textPapoutsi, Tania. "Regulation of cardiogenesis by putative WNT signalling pathways." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1325.
Full textSimeonidis, Iordanis. "The role of WNT signalling in central synaptogenesis." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497269.
Full textLucas, Fiona Ralitsa. "The role of WNT-7a in cerebellar development." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394389.
Full textAntoni, Laurent Paul. "The regulation of myogenic differentiation by WNT signalling." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414996.
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