Relevant bibliographies by topics / Wnt

Academic literature on the topic 'Wnt'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Wnt"

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Suurland, Lianne, and André van Vliet. "Vermelding bezoldiging in de jaarrekening van semipublieke instellingen." Maandblad Voor Accountancy en Bedrijfseconomie 88, no. 12 (December 8, 2014): 556–73. http://dx.doi.org/10.5117/mab.88.31214.

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In dit artikel worden de resultaten van een empirisch onderzoek gepresenteerd naar de naleving van de voorschriften omtrent de toelichting in de jaarrekening op grond van de Wet normering bezoldiging topfunctionarissen publieke en semipublieke sector (WNT). We concluderen dat niet alle instellingen die onder de WNT vallen WNT-informatie in de jaarrekening hebben opgenomen. Daarnaast verschilt de kwaliteit van de verstrekte informatie, vooral voor wat betreft de tekstuele toelichtingen. Met betrekking tot commissarissen zijn vaak niet alle verplichte informatie-elementen uit de WNT vermeld. Tot slot constateren we dat het bezoldigingsbedrag volgens art. 2:383(c) BW veelal een ander bedrag is dan de bezoldiging op grond van de WNT hetgeen tot verwarring bij gebruikers van de jaarrekening kan leiden.
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He, Xi. "Wnt Signaling Went derailed Again." Cell 118, no. 6 (September 2004): 668–70. http://dx.doi.org/10.1016/j.cell.2004.09.009.

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He, Xi. "A Wnt-Wnt Situation." Developmental Cell 4, no. 6 (June 2003): 791–97. http://dx.doi.org/10.1016/s1534-5807(03)00165-5.

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Staal, Frank J. T., and Hans C. Clevers. "WNT signalling and haematopoiesis: a WNT–WNT situation." Nature Reviews Immunology 5, no. 1 (January 2005): 21–30. http://dx.doi.org/10.1038/nri1529.

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Gamit, Naisarg, Arun Dharmarajan, Gautam Sethi, and Sudha Warrier. "Want of Wnt in Parkinson’s disease: Could sFRP disrupt interplay between Nurr1 and Wnt signaling?" Biochemical Pharmacology 212 (June 2023): 115566. http://dx.doi.org/10.1016/j.bcp.2023.115566.

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Watanabe, K., and X. Dai. "Winning WNT: Race to Wnt signaling inhibitors." Proceedings of the National Academy of Sciences 108, no. 15 (March 30, 2011): 5929–30. http://dx.doi.org/10.1073/pnas.1103102108.

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Leucht, Philipp, and Jill A. Helms. "Wnt Signaling." Journal of the American Academy of Orthopaedic Surgeons 23, no. 1 (January 2015): 67–68. http://dx.doi.org/10.5435/jaaos-23-01-67.

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Willert, K., and R. Nusse. "Wnt Proteins." Cold Spring Harbor Perspectives in Biology 4, no. 9 (September 1, 2012): a007864. http://dx.doi.org/10.1101/cshperspect.a007864.

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Nusse, R. "Wnt Signaling." Cold Spring Harbor Perspectives in Biology 4, no. 5 (May 1, 2012): a011163. http://dx.doi.org/10.1101/cshperspect.a011163.

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Bussell, Katrin. "Wnt wonderland." Nature Reviews Molecular Cell Biology 2, no. 7 (July 2001): 490. http://dx.doi.org/10.1038/35080065.

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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.

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Mon travail a été d'étudier le rôle de l'expression de FZD9, un récepteur Wnt, dans l'hématopoïèse normale et maligne. Frizzled 9 (FZD9) est un composant clé de la voie de signalisation Wnt, une voie connue pour jouer un rôle important dans l'hématopoïèse normale et maligne. La méthylation d'un site CpG proximal de site d'initiation de la transcription du gène FZD9 est un facteur de mauvais pronostic dans les LAMs et sa déméthylation est un facteur prédictif de réponse aux thérapies épigénétiques. Sa fonction dans l'hématopoïèse n'est cependant pas connue. Au cours de ma thèse, j'ai démontré que le promoteur du gène FZD9 est dans un état non-permissif dans les cellules leucémiques. L'induction de la différenciation des cellules leucémiques restaure l'état permissif du promoteur, le recrutement du facteur E2F et de l'histone H3 acétyle permettant l'expression de FZD9. L'expression de FZD9 expression est également retrouvée au cours de la différenciation myéloïde d'une lignée IPS Dans les cellules de la lignée THP1 différenciées en monocytes, FZD9 est retrouvé dans un complexe comprenant LRP5/6 et Wnt5a. L'incubation des cellules différenciées par Wnt5a, un ligand de FZD9, déclenche la diminution de l'expression de -caténine et sa localisation nucléaire ainsi que l'expression des gènes cibles de la voie Wnt canonique (c-myc, Cyclin Dl and CD44). Nous n'avons détecté aucune augmentation des taux intracellulaires de calcium. Ces travaux suggèrent que la méthylation du promoteur de FZD9 dans les LAMs pourrait participer à la leucémogénèse en maintenant la voie b-caténine active
My 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
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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.

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Child, 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.

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Schans, 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.

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Richards, Alexander S. K. "Wnt Signalling in Malignant Mesothelioma." Thesis, Curtin University, 2016. http://hdl.handle.net/20.500.11937/56433.

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The aims of this thesis were to characterise the Wnt signalling system and its pharmacological modulation in mesothelioma derived cell lines using monolayer and three dimensional culture models. Investigations into the effects upon expression of Wnt signal components were performed by inhibiting tankyrase enzymes with the compound XAV939 and histone deacetylase enzymes with suberoylanilide hydroxamic acid. Measurement of effects was carried out using functional assays and RNA sequencing for differential gene expression.
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Eubelen, 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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La voie Wnt est une voie de signalisation importante pour l’embryogenèse, la morphogenèse et l’homéostasie des tissus au stade adulte. Des mutations dans cette voie de signalisation sont souvent associées à une létalité embryonnaire ou à des pathologies sévères.Une caractéristique singulière de la signalisation Wnt est sa grande complexité génétique. Chez les vertébrés, ce sont 19 ligands Wnt différents qui peuvent potentiellement lier les 10 membres de la famille des récepteurs Frizzled (Fz). De plus, la liaison d’un ligand Wnt à un récepteur Fz peut conduire à l’activation d’au moins trois voies de transduction distinctes. Pourtant, l’interaction Wnt/Fz est incompatible avec une reconnaissance monospécifique étant donné que Wnt et Fz interagissent via des résidus conservés dans les deux familles. Les patrons d’expression des différents Wnt et des différents Fz sont complexes et souvent chevauchant. Malgré cela, la délétion sélective d’un Wnt peut conduire à des phénotypes spécifiques non-observés lors de la délétion d’un autre ligand Wnt co-exprimé. C’est notamment le cas des ligands Wnt7a et Wnt7b. Seules leurs expressions par les progéniteurs neuronaux permettent d’activer la voie de signalisation Wnt/β-caténine dans les cellules endothéliales malgré l’expression simultanée d’autres ligands Wnt. Dès lors, comment les cellules des vertébrés sont-elles capables de discriminer les différents ligands Wnt ?L’étude de l’activation des signalisations induites par les ligands Wnt7a et Wnt7b permet d’illustrer par quel mécanisme moléculaire des co-récepteurs, tels que Gpr124 et Reck, médient la reconnaissance spécifique d’un ligand Wnt et permettent la formation d’un signalosome spécifique. Reck est un récepteur spécifique des ligands Wnt7a et Wnt7b qui permet de les discriminer de tous les autres ligands Wnt. Il interagit avec ceux-ci via une région intrinsèquement désordonnée et divergente dans la famille Wnt appelée « le peptide linker ». Etant donné que cette région est exposée au solvant et qu’elle ne comprend pas les sites d’interaction avec le récepteur Fz, elle pourrait jouer un rôle critique dans la discrimination des différents ligands Wnt. Gpr124, quant à lui, interagit avec Reck via son domaine extracellulaire et permet la co-localisation de ce dernier et des récepteurs Fz dans le même signalosome. Pour ce faire, Gpr124 interagit avec la protéine adaptatrice Dvl via son domaine intracellulaire. Le recrutement membranaire et la polymérisation de Dvl permettent la formation d’une plateforme d’ancrage facilitant la formation du complexe Reck/Gpr124/Fz/Lrp5/6 qui active alors sélectivement la voie la signalisation Wnt/β-caténine en réponse aux ligands Wnt7a et Wnt7b. L’identification d’un tel mécanisme de décodage laisse supposer qu’il pourrait exister plusieurs modules de reconnaissance spécifique adaptés à d’autres ligands Wnt assurant ainsi un réglage précis de la signalisation Wnt en fonction du contexte moléculaire de la membrane plasmique.
Doctorat en Sciences
info:eu-repo/semantics/nonPublished
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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.

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Ng, 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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In vertebrates, the urogenital sinus and the hindgut are connected at a hollow region called cloaca. A midline mesenchymal structure known as urorectal septum (urs) descends from the ventral body wall to separate the urogenital sinus from the hindgut before the formation of an anal opening. Subsequent cloaca membrane regression at the ventral midline of the genital tubercle (GT) is crucial for the formation of an anal opening. These two events are important during cloaca septation in urorectal development. Mice with defective Shh or Wnt signaling displayed similar urorectal defects such as GT agenesis, un-partitioned cloaca (persistent cloaca) and proximal urethral opening that are attributable to increased cell apoptosis. Furthermore, Shh and Wnt signal transduction coordinate with each other and regulate cell survival of the developing urorectum. However, the molecular mechanisms by which these two signaling pathways coordinate in urorectal development remain unclear. We previously identified Wnt inhibitory factor1 (Wif1) from Affymetrix array analysis for genes/pathways that is implicated in urorectal development. Wif1 is a secreted protein that binds directly to Wnt ligands preventing Wnts from binding to receptors. This leads to -catenin degradation and thereby inhibits their activities. It is known that Wif1 binds to Wnt3a and Wnt5a with high affinity and deletion of Wnt3a, Wnt5a and -catenin in mice caused GT agenesis, persistent cloaca and proximal hypospadias. Using ETU-induced anorectal malformations model, I found out that Wif1 is ectopically expressed in the un-tubularized and un-septated urorectum. Wif1 is mainly expressed at the fusing endoderm that associates with programmed cell death during cloaca septation. Exogenous addition of Wif1 protein in urorectum culture also caused cloaca membrane disintegration, and proximal urethral opening that may be due to aberrant apoptosis. Shh and Wif1 are differentially expressed at the cloaca endoderm. In normal mice, Shh is highly expressed at the cloaca endoderm except those Wif1-expressing endodermal cells. Blockage of Shh pathway by cyclopamine in urorectum culture induced ectopic expression of Wif1, concomitant with genital tubercle hypoplasia and un-septated cloaca. More importantly, deletion of Shh in mice hastened Wif1 expression at the cloaca membrane endoderm and elicited increased cell death in the Wif1 expressing endoderm. Wif1-/- embryos display urorectal defects including delayed genital outgrowth and proximal hypospadias. Therefore, disruption of spatiotemporal expression of Wif1 could lead to defective Wnt signaling and contributes to abnormal urorectal development in Shh-/- mutant. Current study revealed that Wif1 is involved in urorectal development and is implicated in urorectal defects. It may function as a pro-apoptotic factor to regulate endodermal cell death which is essential for the septation process. Its specific expression is restricted at the midline cloaca endoderm by Shh signaling to inhibit local Wnt--catenin activities during cloaca septation. I proposed novel hypothetical models to explain (1) the significance of the tempo-spatial expression of Wif1; (2) the significance of cell death; and (3) the molecular mechanism that Shh signaling regulates Wnt signaling activities through Wif1 in urorectal development.
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Surgery
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Doctor of Philosophy
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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.

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Railo, 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.

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Abstract Wnt genes encode secreted signalling molecules that control embryonic development including organogenesis, while dysregulated Wnt signalling is connected to many diseases such as cancer. Specifically, Wnts control a number of cellular processes such as proliferation, adhesion, differentiation and aging. Many Wnt proteins activate the canonical β-catenin signalling pathway that regulates transcription of a still poorly characterized set of target genes. Wnts also transduce their signaling in cells via β-catenin-independent “non-canonical” pathways, which are not well understood. In this study, Wnt-11 signalling mechanisms in a mammalian model cell line and roles of Wnt-11 in heart development were analyzed in detail. In addition the aim was to identify new Wnt target genes by direct chromatin immunoprecipitation and Affymetrix GeneChip assays in the model cells exposed to Wnt-3a. Our studies reveal that Wnt-11 signalling coordinates the activity of key cell signalling pathways, namely the canonical Wnt/β-catenin, the JNK/AP-1, the NF-κB and PI3K/Akt pathways in the CHO cells. Analysis of the Wnt-11-deficient embryos revealed a crucial role in heart organogenesis. Wnt-11 signalling coordinates cell interactions during assembly of the myocardial wall and Wnt-11 localizes the expression of N-cadherin and β-catenin to specific cellular domains in the embryonic ventricular cardiomyocytes. Collectively these studies reveal that the mammalian Wnt-11 behaves as a non-canonical Wnt and that it is a critical factor in the coordination of heart development. Specifically, it controls components of the cell adhesion machinery. Analysis of the Wnt target genes revealed a highly context-dependent profile in the Wnt-regulated genes. Several new putative target genes were discovered. Out of the candidate Wnt target genes, Disabled-2 was identified as a potential new direct target for Wnt signalling.
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Books on the topic "Wnt"

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Barrett, Quinn, and Lawrence Lum, eds. Wnt Signaling. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6393-5.

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Vincan, Elizabeth, ed. Wnt Signaling. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-469-2.

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Vincan, Elizabeth, ed. Wnt Signaling. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-249-6.

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Elizabeth, Vincan, ed. Wnt signaling. New York, NY: Humana Press, 2008.

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Wnt signaling in development. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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Kühl, Michael. Wnt signaling in development. Georgetown, Tex: Landes Bioscience, 2003.

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Kühl, Michael. Wnt signaling in development. Georgetown, TX: Landes Bioscience/Eurekah.com ; Kluwer Academic/Plenum Publishers, 2002.

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Schulte, Gunnar, and Pawel Kozielewicz, eds. Pharmacology of the WNT Signaling System. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85499-7.

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Goss, Kathleen H., and Michael Kahn, eds. Targeting the Wnt Pathway in Cancer. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-8023-6.

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Hoppler, Stefan, and Randall T. Moon, eds. Wnt Signaling in Development and Disease. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118444122.

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Book chapters on the topic "Wnt"

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Yadav, Anuradha, and Rajnish Kumar Chaturvedi. "WNT." In Encyclopedia of Signaling Molecules, 5998–6004. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101790.

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Yadav, Anuradha, and Rajnish Kumar Chaturvedi. "WNT." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101790-1.

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Robert, Jacques. "Wnt Pathway." In Textbook of Cell Signalling in Cancer, 93–100. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_7.

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Kypta, Robert M. "Wnt Signaling." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_6257-3.

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Kypta, Robert M. "Wnt Signaling." In Encyclopedia of Cancer, 4858–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6257.

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Ghosh, Noyel, Sharmistha Chatterjee, and Parames C. Sil. "Wnt Signaling." In Encyclopedia of Molecular Pharmacology, 1579–91. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_230.

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Ghosh, Noyel, Sharmistha Chatterjee, and Parames C. Sil. "Wnt Signaling." In Encyclopedia of Molecular Pharmacology, 1–13. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_230-1.

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Kypta, Robert M. "Wnt Signaling." In Encyclopedia of Cancer, 3953–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6257.

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Robert, Jacques. "La voie Wnt." In Signalisation cellulaire et cancer, 103–10. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_8.

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Yadav, Vikas, Njainday Jobe, Lubna Mehdawi, and Tommy Andersson. "Targeting Oncogenic WNT Signalling with WNT Signalling-Derived Peptides." In Pharmacology of the WNT Signaling System, 279–303. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_528.

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Conference papers on the topic "Wnt"

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Гончарова, Анна Сергеевна, Анна Александровна Шульга, and Дмитрий Юрьевич Гвалдин. "ОЦЕНКА ЭКСПРЕССИИ ГЕНОВ WNT-СИГНАЛИНГА В КСЕНОГРАФТАХ КОЛОРЕКТАЛЬНОГО РАКА ЧЕЛОВЕКА ПРИ ВОЗДЕЙСТВИИ WNT-ИНГИБИТОРОМ XAV-939." In Научные исследования в современном мире. Теория и практика: сборник статей XXIII международной научной конференции (Санкт-Петербург, Декабрь 2023). Crossref, 2024. http://dx.doi.org/10.37539/231204.2023.77.86.005.

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Сигнальный путь Wnt играет важную роль в процессе образования опухоли и формирования её злокачественности. Целью данного исследования было изучить влияние противоопухолевого препарата XAV-939 на уровень экспрессии двух генов, вовлеченных в каскад реакций Wnt-пути - Wnt3 и CTNNB1 .
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Bhattacharya, Debanjan, Dan Zhu, Satoru Osuka, Saroja Narra Devi, and Erwin G. Van Meir. "Abstract 3477: ADGRB3 is epigenetically silenced in WNT-medulloblastoma and inhibits WNT signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3477.

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Bhattacharya, Debanjan, Dan Zhu, Satoru Osuka, Saroja Narra Devi, and Erwin G. Van Meir. "Abstract 3477: ADGRB3 is epigenetically silenced in WNT-medulloblastoma and inhibits WNT signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3477.

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Fernández-Llamazares, Ana I., Kevin C. M. Hermans, Peter Timmerman, and W. Matthijs Blankesteijn. "Mimicking the Binding Sites of Wnt Proteins: Rational Design of Wnt/Fzd-Signaling Modulators." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.212.

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Azam, M. R., A. I. Bhatti, A. Arshad, and M. Z. Babar. "Sensitivity analysis of Wnt Signaling Pathway." In 2013 10th International Bhurban Conference on Applied Sciences and Technology (IBCAST 2013). IEEE, 2013. http://dx.doi.org/10.1109/ibcast.2013.6512143.

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Xu, Xian, and Yanbin Yu. "Modeling and Verifying WNT Signaling Pathway." In Third International Conference on Natural Computation (ICNC 2007). IEEE, 2007. http://dx.doi.org/10.1109/icnc.2007.476.

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Kolosionek, Ewa, Rajneesh Malthotra, Henric Olsson, and Stephen Delaney. "Activation of WNT co-receptor LRP5 is required for WNT and TGF-ß1 induced fibroblast activation." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2581.

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Li, Yonghe, Wenyan Lu, and Taj D. King. "Abstract 4600: Regulation of Wnt/β-catenin signaling by Wnt co-receptor LRP6 in colorectal cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4600.

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Nayakanti, S. R., A. Tretyn, S. Dabral, M. Boehm, A. Wietelmann, B. Kojonazarov, W. Janssen, W. Seeger, R. T. Schermuly, and S. S. Pullamsetti. "Wnt-Signaling Pathway Drives Right Ventricular Remodeling." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6072.

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Bos, Isabella Sophie T., Hoeke A. Baarsma, Andrew J. Halayko, and Reinoud Gosens. "Functional Wnt Signaling In Airway Smooth Muscle." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2126.

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Reports on the topic "Wnt"

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Olson, Daniel J. WNT-5a and WNT-4 Regulates Cell Growth in C57MG Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada299744.

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Olson, Daniel J. Wnt-5a and Wnt-4 Regulates Cell Growth in C57MG Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada314665.

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He, Xi. WNT-1 Signaling in Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada395338.

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He, Xi. WNT-1 Signaling in Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, April 2002. http://dx.doi.org/10.21236/ada414818.

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Tharakan, Robin. Deregulated Wnt Signaling in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada511062.

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Tharakan, Robin. Deregulated Wnt Signaling in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada521354.

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He, Xi. Wnt-1 Signaling in Mammary Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, April 2000. http://dx.doi.org/10.21236/ada384378.

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Houghtaling, Scott. Deregulated Wnt Signaling in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada478739.

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Alexander, Caroline M. Wnt-Induced Progenitors: Are They Highly Mutable? Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada429614.

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Kitajewski, Jan. WNT Proteins in Mammary Epithelial Cell Transformation. Fort Belvoir, VA: Defense Technical Information Center, July 1997. http://dx.doi.org/10.21236/ada329512.

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