Relevant bibliographies by topics / Wnt and Notch signaling

Academic literature on the topic 'Wnt and Notch signaling'

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Published: 19 August 2021
Last updated: 1 February 2022

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Journal articles on the topic "Wnt and Notch signaling":

1

Lachej, Nadežda, Violeta Jonušienė, Augustina Mažeikė, Aušra Sasnauskienė, Daiva Dabkevičienė, Julija Šimienė, Kęstutis Sužiedėlis, and Janina Didžiapetrienė. "Changes in the expression of Notch and Wnt signalling molecules in human endometrial cancer." Acta medica Lituanica 26, no. 3 (January 11, 2020): 181–90. http://dx.doi.org/10.6001/actamedica.v26i3.4148.

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Background. Endometrial cancer is the sixth most frequent type of cancer among women worldwide. Type I adenocarcinomas account for 80–85% of endometrial cancer cases and sometimes require more aggressive treatment than the remaining part of this group. Therefore, molecular markers to stratify adenocarcinomas are needed. Materials and methods. In this study, we analysed Notch and Wnt signalling in human endometrial cancer cases to evaluate these pathway elements as potential biomarkers for type I endometrial cancer. Endometrial samples were obtained from 47 women undergoing surgery for stage I–IV endometrial cancer in the National Cancer Institute (Vilnius, Lithuania) in 2015–2016. The expression at the mRNA level of signalling molecules genes (NOTCH1, NOTCH2, NOTCH3, NOTCH4, JAG1, JAG2, DLL1, HES1, AXIN2 and CTNNB1) was analysed by the quantitative real-time polymerase chain reaction. Relative expression of NOTCH1, NOTCH4, HES1 and β-catenin proteins in endometrioid adenocarcinoma was evaluated by the Western blot method. Results. The expression level of Notch receptors, ligands, and the target gene, as well as CTNNB1 and AXIN2, was reduced in stage I endometrioid adenocarcinoma if compared to the adjacent non-tumour tissue. The expression of all receptors, ligands, and target molecules was reduced in adenocarcinomas of later stages. The statistically significant correlations between transcript amounts of Notch receptors and ligands were found. There was a statistically significant difference in the gene expression of Notch signalling pathway components between different tumour differentiation grade samples. A positive correlation between mRNA and protein the expression level of NOTCH1, NOTCH4, HES1 was determined in stage I samples. Conclusions. Analysis of 47 human endometrial cancer samples revealed a reduction in the transcript levels of Notch and Wnt signalling molecule compared to the adjacent non-tumour tissue. These results suggest tumour suppressor function of Notch and Wnt signalling in human endometrial cancer. More detailed research on these signalling pathways should reveal their importance as potential biomarkers.
2

Pinto, Inês, Mafalda Duque, Joana Gonçalves, Padma Akkapeddi, Mariana L. Oliveira, Rita Cabrita, J. Andrés Yunes, Scott K. Durum, João T. Barata, and Rita Fragoso. "NRARP displays either pro- or anti-tumoral roles in T-cell acute lymphoblastic leukemia depending on Notch and Wnt signaling." Oncogene 39, no. 5 (October 4, 2019): 975–86. http://dx.doi.org/10.1038/s41388-019-1042-9.

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Abstract T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a dismal prognosis in patients with resistant or relapsed disease. Although NOTCH is a known driver in T-ALL, its clinical inhibition has significant limitations. Our previous studies suggested that NRARP, a negative regulator of Notch signaling, could have a suppressive role in T-ALL. Here, we report that NRARP levels are significantly increased in primary T-ALL cells suggesting that NRARP is not sufficient to block NOTCH oncogenic signals. Interestingly, although NRARP overexpression blocks NOTCH1 signaling and delays the proliferation of T-ALL cells that display high levels of Notch1 signaling, it promotes the expansion of T-ALL cells with lower levels of Notch1 activity. We found that NRARP interacts with lymphoid enhancer-binding factor 1 (LEF1) and potentiates Wnt signaling in T-ALL cells with low levels of Notch. Together these results indicate that NRARP plays a dual role in T-ALL pathogenesis, regulating both Notch and Wnt pathways, with opposite functional effects depending on Notch activity. Consistent with this hypothesis, mice transplanted with T-cells co-expressing NOTCH1 and NRARP develop leukemia later than mice transplanted with T-NOTCH1 cells. Importantly, mice transplanted with T-cells overexpressing NRARP alone developed leukemia with similar kinetics to those transplanted with T-NOTCH1 cells. Our findings uncover a role for NRARP in T-ALL pathogenesis and indicate that Notch inhibition may be detrimental for patients with low levels of Notch signaling, which would likely benefit from the use of Wnt signaling inhibitors. Importantly, our findings may extend to other cancers where Notch and Wnt play a role.
3

Aoyama, Keisuke, Barbara Varnum-Finney, Randall T. Moon, and Irwin D. Bernstein. "The Interaction of the Wnt and Notch Pathways Modulates NK vs. T Cell Commitment." Blood 106, no. 11 (November 16, 2005): 765. http://dx.doi.org/10.1182/blood.v106.11.765.765.

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Abstract The Wnt and Notch signaling pathways have critical roles in cell fate decisions. However, the interaction of these pathways is poorly understood. Using highly purified Wnt3a and immobilized Notch ligand, Delta1ext-IgG, we investigated the mechanisms involved in Wnt and Notch signaling interactions during hematopoietic stem cell differentiation. When CD34+CD38- cord blood stem cells were cultured for 2 to 3 weeks with five growth factors (SCF 300ng/ml, Flt-3L 300ng/ml, TPO 100ng/ml, IL-6 100ng/ml, and IL-3 10ng/ml), most precursor cells lost CD34 expression and differentiated into mature cells, most of which were monocytes. However, as we previously reported, when cells were cultured with Delta1ext-IgG, we found an increased percentage of lymphoid progenitors (CD34+CD7+) and more mature lymphoid precursors (CD34-CD7+) in the cell population. The addition of purified Wnt3a (100ng/ml) alone without Delta1ext-IgG did not significantly change the percentage of CD7+ cells (1% vs. 3%). However, when both Wnt3a and Delta1ext-IgG were added, we saw an increased percentage of CD7+ cells (11% with Delta1ext-IgG alone to 27% with both) (Fig. 1A). Wnt3a also enhanced gene expression of CD3ε and preTα induced by Delta1ext-IgG. These results suggest that Wnt3a enhances the effect of Notch signaling on T-cell lineage development. To test the role of endogenous Wnt signaling, we added Dickkopf1, an inhibitor of Wnt signaling. When CD34+CD38- cells were cultured with Dickkopf1 (300ng/ml) alone for a 2 week, the percentage and number of CD56+ NK cells was unaffected. However, when cultured with Dickkopf1 and Delta1ext-IgG, the percentage and number of CD56+ NK precursor cells were increased (2% with Delta1ext-IgG alone vs. 17% with Dickkopf1 and Delta1ext-IgG; 0.2 ×105 vs. 1.5×105, p<0.01) (Fig. 1B). This result shows that decreased endogenous Wnt signaling enhances the generation of NK cells in the presence of Notch signaling. To address whether Wnt signaling affects Notch signaling by modulating protein levels, we assessed the amount of activated Notch1 intracellular domain with or without Wnt 3a by Western blot (Fig. 2A). After stimulation for 24 h, Wnt3a increased the amount of activated Notch1 intracellular domain induced by Delta1ext-IgG. Wnt3a also enhanced the expression of a primary target gene of Notch signaling, Hes1, determined by quantitative RT-PCR (Fig. 2B). In contrast, Dickkopf1 reduced Delta1ext-IgG-induced Hes1 expression. These results suggest that Wnt signaling directly modulates Notch signaling. Thus, these studies suggest that Wnt signaling is a key factor in cell fate determination at the point of NK/T cell commitment that is mediated via an interaction with Notch signaling. These studies also suggest that Wnt directly regulates Notch signaling by modulating protein turnover. Fig. 1, Fig. 2 Fig. 1, Fig. 2.
4

Batista, Mariana R., Patrícia Diniz, Daniel Murta, Ana Torres, Luís Lopes-da-Costa, and Elisabete Silva. "Balanced Notch-Wnt signaling interplay is required for mouse embryo and fetal development." Reproduction 161, no. 4 (April 2021): 385–98. http://dx.doi.org/10.1530/rep-20-0435.

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This study investigated the role of Notch and Wnt cell signaling interplay in the mouse early embryo, and its effects on fetal development. Developmental kinetics was evaluated in embryos in vitro cultured from the 8-16-cell to the hatched blastocyst stage in the presence of signaling inhibitors of Notch (DAPT) and/or Wnt (DKK1). An embryo subset was evaluated for differential cell count and gene transcription of Notch (receptors Notch1-4, ligands Dll1, Dll4, Jagged1-2, effectors Hes1-2) and Wnt (Wnt3a, Lrp6, Gsk3β, C-myc, Tcf4, β-catenin) components, E-cadherin and pluripotency and differentiation markers (Sox2, Oct4, Klf4, Cdx2), whereas a second subset was evaluated for implantation ability and development to term following transfer into recipients. Notch and Wnt blockades had significant opposing effects on developmental kinetics – Notch blockade retarded while Wnt blockade fastened development. This evidences that Notch and Wnt regulate the pace of embryo kinetics by respectively speeding and braking development. Blockades significantly changed the transcription profile of Sox2, Oct4, Klf4 and Cdx2, and Notch and double blockades significantly changed embryonic cell numbers and cell ratio. The double blockade induced more severe phenotypes than those expected from the cumulative effects of single blockades. Implantation ability was unaffected, but Notch and double blockades significantly decreased fetal development to term. Compared to control embryos, Notch blockade and Wnt blockade embryos originated, respectively, significantly lighter and heavier fetuses. In conclusion, Notch and Wnt signaling interplay in the regulation of the pace of early embryo kinetics, and their actions at this stage have significant carry-over effects on later fetal development to term.
5

Zanotti, Stefano, Anna Smerdel-Ramoya, Lisa Stadmeyer, Deena Durant, Freddy Radtke, and Ernesto Canalis. "Notch Inhibits Osteoblast Differentiation and Causes Osteopenia." Endocrinology 149, no. 8 (April 17, 2008): 3890–99. http://dx.doi.org/10.1210/en.2008-0140.

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Notch receptors are determinants of cell fate decisions. To define the role of Notch in the adult skeleton, we created transgenic mice overexpressing the Notch intracellular domain (NICD) under the control of the type I collagen promoter. First-generation transgenics were small and osteopenic. Bone histomorphometry revealed that NICD caused a decrease in bone volume, secondary to a reduction in trabecular number; osteoblast and osteoclast number were decreased. Low fertility of founder mice and lethality of young pups did not allow the complete establishment of transgenic lines. To characterize the effect of Notch overexpression in vitro, NICD was induced in osteoblasts and stromal cells from Rosanotch mice, in which a STOP cassette flanked by loxP sites is upstream of NICD, by transduction with an adenoviral vector expressing Cre recombinase (Cre) under the control of the cytomegalovirus (CMV) promoter (Ad-CMV-Cre). NICD impaired osteoblastogenesis and inhibited Wnt/β-catenin signaling. To determine the effects of notch1 deletion in vivo, mice in which notch1 was flanked by loxP sequences (notch1loxP/loxP) were mated with mice expressing Cre recombinase under the control of the osteocalcin promoter. Conditional null notch1 mice had no obvious skeletal phenotype, possibly because of rescue by notch2; however, 1-month-old females exhibited a modest increase in osteoclast surface and eroded surface. Osteoblasts from notch1loxP/loxP mice, transduced with Ad-CMV-Cre and transfected with Notch2 small interfering RNA, displayed increased alkaline phosphatase activity. In conclusion, Notch signaling in osteoblasts causes osteopenia and impairs osteo-blastogenesis by inhibiting the Wnt/β-catenin pathway.
6

De Strooper, Bart, and Wim Annaert. "Where Notch and WNT Signaling Meet." Journal of Cell Biology 152, no. 4 (February 19, 2001): F17—F20. http://dx.doi.org/10.1083/jcb.152.4.f17.

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7

Okuhashi, Yuki, Yusuke Takahashi, Mika Ohtaka, Erika Shiratori, Shijyun O, Mai Itoh, and Shuji Tohda. "Effects of GLI1 and CTNNB1 Knockdown on Notch Signaling and Proliferation of AML and T-ALL Cell Lines." Blood 124, no. 21 (December 6, 2014): 1042. http://dx.doi.org/10.1182/blood.v124.21.1042.1042.

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Abstract Objective: Although Hedgehog (Hh) and Wnt signaling pathways are known to play a role in cancer cell growth, their specific effects on leukemia cells are not fully understood. Previously we reported that the Hh inhibitor, cyclopamine, and the Wnt inhibitor, quercetin, suppressed the growth of leukemia cells. However, a specific inhibitory role of these chemical compounds on Hh and Wnt signaling could not be confirmed since these compounds also have off-target effects. Therefore the effects of specific inhibition of Hh and Wnt signaling pathways must be investigated in detail. In our previous study, we reported that small interfering RNA (siRNA)-mediated knockdown of NOTCH1 and NOTCH2 suppressed growth of T-ALL cell lines. In this context, the relationship between Hh, Wnt, Notch and mTOR signaling; known to regulate stemness; has not been fully elucidated. To address these questions, the effects of siRNA-mediated knockdown of GLI1 and CTNNB1 (Catenin beta 1), which respectively mediate Hh and Wnt signaling, on cell proliferation as well as Notch and mTOR signaling were studied in AML and T-ALL cell lines. Methods: Two AML cell lines (NB4 and THP-1) and 2 T-ALL cell lines (DND41 and Jurkat) were used in this study. siRNAs targeting GLI1 (siGL), CTNNB1 (siCT), NOTCH1 (siN1) or control siRNA were transfected into cells by using the pipette tip chamber-based electroporation system. The effects of siGL and siCT transfection on cell proliferation were examined using a colorimetric WST-8 assay and by observing cytospin preparations of the harvested cells. The effects on mRNA and protein expression were examined by quantitative RT-PCR and immunoblotting, respectively. Results: Transfection with siGL and siCT selectively suppressed the expression of GLI1 and CTNNB1, respectively. siRNA treatment did not lead to any significant effects on cell proliferation or morphology in all tested cell lines. In NB4 cells, GLI1 as well as CTNNB1 knockdown increased the level of NOTCH1, the cleaved NOTCH1 fragment (active form of NOTCH1), HES1, and phosphorylated mTOR protein. In the other cell lines, the expression of these proteins was not significantly altered by siGL and siCT. Discussion: siRNA-mediated knockdown experiments suggested that Hh and Wnt signaling had insignificant effect on the proliferation of the leukemia cell lines used in this study. We report a novel interaction, namely, the activation of Notch and mTOR signaling by the suppression of Hh and Wnt signaling in NB4 cells. The molecular mechanism and significance of this phenomenon as well as its translation to other cell lines needs further examination. We propose that this finding must be taken into account when Hh- and Wnt-targeted therapy against leukemia are developed. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
8

Plentz, Ruben R., Samarpita Barat, Xi Chen, Cuong Bui, Przemyslaw Bozko, and Nisar P. Malek. "Notch and wnt-beta catenin pathways as targets of γ-secretase inhibitor IX (GSI) mediated therapy in CD44+ gastric cancer (GC) cells." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 99. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.99.

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99 Background: GC is the second most common cause of cancer related death worldwide. New palliative therapeutic approaches to treat GC are of urgent need. Targeting cancer stem cells (CSC) could be an effective approach to treat GC. Recent studies have indicated that Notch signaling and wnt-beta-catenin pathways are crucial for CSC development. In this study, we mainly focused on inactivation of both Notch and wnt-beta-catenin pathways in CSC CD44+ GC cells using GSI. Methods: For our experiments we have used the GC cell line MKN45, as it showed expression of both targets (CD44,Hes1). For in vitro experiments proliferation, wound healing, invasion and tumorsphere assays were performed to analyze the migration, invasive and tumorigenic potential of CD44+ sorted GC initiating cells after GSI treatment. Western blot analyses of downstream signaling targets of Notch and wnt-beta catenin were tested after GSI treatment. SiRNA experiments for Notch1 and CD44 were also performed in order to confirm the Notch and wnt-beta-catenin pathway crosstalk. For in vivo analysis sorted CD44+ cells were subcutaneously injected into NMRI-nu/numice and were treated with vehicle or GSI. Results: CD44+ sorted MKN45 cells showed high expression of Hes1 as compared to the CD44- cell population. GSI treatment showed effective inhibition of cell proliferation, migration, invasion and tumor sphere formation of CD44+ cells. Interestingly, amongst all Notch receptors, Notch1 was found to be important in mediating the crosstalk between Notch and wnt-beta-catenin signaling cascades in CD44+ GC cells. Moreover, upon silencing of both CD44 and Notch1 by SiRNA showed effective inhibition of downstream targets and reconfirmed the proposed hypothesis of CD44 mediated Notch and wnt/beta-catenin crosstalk in GC cells. Conclusions: Our study highlights the crosstalk between Notch and wnt-beta-catenin in GC CD44+ cells. GSI could be an alternative drug to treat human GC as it effectively targets the CD44+ GC cells thus, completely reducing all the chances of relapse and metastasis associated with GC. Therefore, GSI therapy can open up new avenues for GC treatment with improved / better clinical outcome.
9

Ballhause, Tobias M., Shan Jiang, Anke Baranowsky, Sabine Brandt, Peter R. Mertens, Karl-Heinz Frosch, Timur Yorgan, and Johannes Keller. "Relevance of Notch Signaling for Bone Metabolism and Regeneration." International Journal of Molecular Sciences 22, no. 3 (January 29, 2021): 1325. http://dx.doi.org/10.3390/ijms22031325.

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Notch1-4 receptors and their signaling pathways are expressed in almost all organ systems and play a pivotal role in cell fate decision by coordinating cell proliferation, differentiation and apoptosis. Differential expression and activation of Notch signaling pathways has been observed in a variety of organs and tissues under physiological and pathological conditions. Bone tissue represents a dynamic system, which is constantly remodeled throughout life. In bone, Notch receptors have been shown to control remodeling and regeneration. Numerous functions have been assigned to Notch receptors and ligands, including osteoblast differentiation and matrix mineralization, osteoclast recruitment and cell fusion and osteoblast/osteoclast progenitor cell proliferation. The expression and function of Notch1-4 in the skeleton are distinct and closely depend on the temporal expression at different differentiation stages. This review addresses the current knowledge on Notch signaling in adult bone with emphasis on metabolism, bone regeneration and degenerative skeletal disorders, as well as congenital disorders associated with mutant Notch genes. Moreover, the crosstalk between Notch signaling and other important pathways involved in bone turnover, including Wnt/β-catenin, BMP and RANKL/OPG, are outlined.
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Kaemmerer, Elke, Min Kyung Jeon, Alexander Berndt, Christian Liedtke, and Nikolaus Gassler. "Targeting Wnt Signaling via Notch in Intestinal Carcinogenesis." Cancers 11, no. 4 (April 18, 2019): 555. http://dx.doi.org/10.3390/cancers11040555.

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Proliferation and differentiation of intestinal epithelial cells is assisted by highly specialized and well-regulated signaling cascades. The Wnt pathway, which is one of the fundamental pathways in the intestine, contributes to the organization of proliferative intestinal crypts by positioning and cycling of intestinal stem cells and their derivatives. The Wnt pathway promotes differentiation of intestinal secretory cell types along the crypt-plateau and crypt-villus axis. In contrast to the Wnt pathway, the intestinal Notch cascade participates in cellular differentiation and directs progenitor cells towards an absorptive fate with diminished numbers of Paneth and goblet cells. Opposing activities of Notch and Wnt signaling in the regulation of intestinal stem cells and the enterocytic cell fate have been elucidated recently. In fact, targeting Notch was able to overcome tumorigenesis of intestinal adenomas, prevented carcinogenesis, and counteracted Paneth cell death in the absence of caspase 8. At present, pharmacological Notch inhibition is considered as an interesting tool targeting the intrinsic Wnt pathway activities in intestinal non-neoplastic disease and carcinogenesis.
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Dissertations / Theses on the topic "Wnt and Notch signaling":

1

Batista, Mariana Raposo. "Notch and Wnt signaling interplay on regulation of early embryo development." Doctoral thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2020. http://hdl.handle.net/10400.5/20972.

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Tese de Doutoramento em Ciências Veterinárias, na especialidade de Ciências Biológicas e Biomédicas
Mammalian early embryo development requires action of a complex network of cell signaling pathways that coordinates cellular proliferation and differentiation events. Notch is a major regulator in embryonic and adult scenarios, also interplaying with other signaling pathways, such as Wnt. The objective of this work was to determine Notch signaling status in early embryo development and its influence on cellular differentiation and pluripotency maintenance, and on embryo competence to implant and develop to term. Additionally, the Notch/Wnt interplay was investigated in this scenario. Firstly, we analyzed individual embryo transcription of Notch components and their relation with transcription of pluripotency and differentiation gene markers (Sox2, Oct4, Klf4, Cdx2). Secondly, a pharmacological approach was used to induce Notch signaling (recombinant JAGGED1 and 2) and to inhibit Notch and/or Wnt signaling (DAPT and/or DKK1, respectively). Finally, embryos treated with DAPT and/or DKK1 were transferred to recipient females and implantation competency (at Day5 of gestation) and development to term (Day18) were evaluated. Results showed that transcription of Notch1-2, Jagged1-2 and Hes1 was highly prevalent and dynamic along stages of development. Transcription of Notch1, Notch2, Jagged2 and Hes1 correlated with each other and with that of Sox2, Oct4, Klf4 and Cdx2. In vitro embryo culture supplementation with JAGGED1 had no effect on embryo developmental kinetics, whereas supplementation with JAGGED2 abolished Jagged1 transcription, downregulated Cdx2 transcription and inhibited blastocyst hatching. Notch and Wnt had opposing effects on developmental kinetics, as Notch blockade retarded development and hatching, while Wnt blockade fastened it. We found evidences of Notch and Wnt interplay in early embryos as double blockade produced more severe phenotypes than expected by cumulative effects of single blockades. Notch and double blockade altered trophectoderm cell numbers and inner cell mass to trophectoderm ratio and all blockades altered transcription of Sox2, Oct4, Klf4 and Cdx2 throughout development. Implantation was unaffected by treatment, but Notch and double blockades affected the rate of Day18 developed fetuses. Notch blockade produced lighter and Wnt blockade heavier fetuses. Overall, results indicate that Notch is active in early embryo development where, together with Wnt, plays a significant role in controlling the pace of differentiation and proliferation of the blastocyst, ultimately affecting development to term.
RESUMO - As vias de sinalização Notch e Wnt na regulação do desenvolvimento embrionário precoce - O desenvolvimento embrionário precoce em mamíferos requer a ação coordenada de eventos de proliferação e diferenciação celulares. A correcta coordenação destes eventos está dependente de uma complexa rede de vias de sinalização intercelular. Uma das vias de sinalização intercelular mais conservadas em metazoários é a via Notch. Esta é responsável pela organização da diferenciação celular e manutenção da pluripotência em vários tecidos, quer na embriogénese quer na vida adulta, e interage com outras vias de sinalização, tal como a via Wnt, para este fim. O objetivo deste trabalho foi a determinação da presença e atividade da via Notch no desenvolvimento embrionário precoce em embriões de murganho entre os 3.5 e os 4.5 dias post coitum (dpc). Adicionalmente procurou saber-se quais os elementos da via responsáveis pela transdução de sinal e se a sinalização Notch atua em conjunto com a via Wnt neste cenário. Finalmente procurou estabelecer-se a existência de relações entre os elementos da via Notch e marcadores de estados de pluripotência (Sox2, Oct4, Klf4) e diferenciação (Cdx2) embrionários, assim como a possível influência das vias Notch e Wnt na capacidade de implantação embrionária e no desenvolvimento fetal até termo. A transcrição dos componentes da via Notch (recetores Notch1-4; ligandos Delta-like1 e 4 e Jagged1-2; e efetores Hes1-2) e dos marcadores Sox2, Oct4, Klf4 e Cdx2 foi analisada em embriões individuais e inteiros recorrendo à técnica de PCR em tempo real. De seguida, foi usada uma abordagem farmacológica in vitro para induzir a via Notch com proteínas recombinantes JAGGED1 e JAGGED2, e para inibir as vias Notch e Wnt com DAPT (um inibidor da gama-secretase) e/ou DKK1 (um inibidor competitivo da via), respectivamente. Os embriões foram recolhidos in vivo aos 2.5 dpc e postos em cultura in vitro até aos 4.5 dpc com os respetivos tratamentos. Desta forma foram analisados a cinética de desenvolvimento embrionário dos 3.5 aos 4.5 dpc, a contagem diferencial de células da trofectoderme (TE) e do botão embrionário (ICM), e a transcrição de genes das vias Notch e Wnt e dos marcadores de pluripotência/diferenciação em embriões de 3.5 dpc. Finalmente, blastocistos e blastocistos expandidos tratados com DAPT e/ou DKK1 foram transferidos aos 4.0 dpc para fêmeas recetoras e analisaram-se as taxas de implantação aos 5 dias de gestação e a taxa de desenvolvimento fetal aos 18 dias de gestação, assim como os pesos dos fetos resultantes...
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2

Hoyle, Sarah. "The interactions between the Wnt and Notch signalling pathways." Thesis, University of Manchester, 2009. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520711.

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3

Hidalgo, Sastre Ana. "Crosstalk between Notch and Wnt signalling pathways in vertebrates." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/crosstalk-between-notch-and-wnt-signalling-pathways-in-vertebrates(9b4411a3-cd03-4af3-b3b5-8c432c7a2c68).html.

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The development of complex metazoans depends on the integration of a handful of signalling pathways that eventually modulate precise patterns of gene expression. The fact that just a few pathways are involved in the generation of such complexity in different organisms, suggests that these are highly regulated and conserved processes. The accurate spatio-temporal coordination of the signalling pathways controls the assignation of different cell fates and their patterning into tissues and organs. The source of diversity relies on the different possible interactions between signalling pathways, such as, the combination of signals and the order in which they are received by the cell or crosstalk. Due to their importance in development, abnormal signalling through these pathways has been strongly associated with developmental disorders, cancers and other diseases. The Notch and Wnt signalling pathways are key components of the intricate network that controls gene expression during development, and genetic analysis in Drosophila has highlighted that interactions between these two signalling pathways are important during this process.This thesis investigates the cross-regulatory interactions between Notch and Wnt signalling pathways in mammals. Using transcriptional reporter assays and biochemical analysis, I have found two molecular mechanisms underlying the inhibitory crosstalk between Notch and β-catenin, the effector of Wnt signalling pathway, in mammalian cells. At the membrane Notch inhibits β-catenin transcriptional activity through Deltex mediated endocytosis of Notch and a component required for β-catenin activation. This is similar to results observed in Drosophila. In the nucleus, I have identified a novel mechanism by which NICD-dependent transcription of Hes/Hey family of transcription factors prevents the activation of Wnt signalling pathway. This mechanism involves the formation of a physical complex between Hey1 and β-catenin/TCF, which allows Hey to block Wnt transcriptional activation. Additionally, I have found that these two mechanisms are conserved across vertebrates.Together the findings of this thesis improve our understanding of the molecular mechanism underlying the Notch/Wnt crosstalk. In turn, this will give an insight into unravelling how a handful of signalling pathways can generate sufficient diversity in signalling output to specify the hundreds of different cell fates generated to make a mammal. Elucidating these signalling networks will also contribute to our understanding of diseases, both their aetiology, by knowing how changes in one signal can influence another, and their treatment as mimicking points of crosstalk is likely to generate very specific therapeutic agents.
4

Adams, Jason Samuel. "Regulation of Sensory Neurogenesis in the Trigeminal Placode: Notch Pathway Genes, Pax3 Isoforms, and Wnt Ligands." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3144.

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This dissertation is divided into three chapters, each discussing the study of different regulatory molecules involved in sensory neurogenesis occurring in the trigeminal placode. Chapter one is a spatiotemporal description of Notch pathway genes in chick opV placode by stage-specific expression analysis, showing expression of many Notch pathway genes and effectors in the opV placode. Notch pathway gene expression is primarily confined to the ectoderm with highest expression of these genes at the beginning stages of peak neuronal differentiation. This information preceded studies of the functional roles that Notch signaling has in the opV placode and how it may affect the transcription factor, Pax3. Chapter two is a study of the transcription factor Pax3 and its role in opV placode development and sensory neuron differentiation. Pax3 is known to activate or repress gene transcription, and its activity may be dependent on the splice variant or isoform present. We show through RT-PCR that alternative splice forms of Pax3 are present at stages of chick development corresponding to cellular competence, cellular differentiation and ingression, and cellular aggregation. We have named these splice forms, Pax3V1 and Pax3V2. Using quantitative RT-PCR we show that Pax3V2 is consistently expressed at lower levels compared to Pax3 during cellular competence and differentiation. In order to determine the function of the three splice forms, we misexpressed them in the opV placode and analyzed the effect on neurogenesis. We looked at markers for neuronal differentiation of targeted cells after in ovo electroporation of Pax3, Pax3V1, and Pax3V2, which showed a significant difference between the control and each construct, but not between the groups of constructs. To enhance the process of neurogenesis we exposed the electroporated embryos to DAPT, a Notch signaling inhibitor that enhances sensory neurogenesis. Using this method we found that misexpression of Pax3 and Pax3V1 resulted in cells failing to differentiate, while Pax3V2 misexpression more closely resembles the neuronal differentiation seen in controls. These results show that the Pax3V2 isoform allows for neuronal differentiation of opV placodal cells after misexpression, while the Pax3 isoform and the Pax3V1 isoform block neuronal differentiation. Chapter three is a study of the necessity of Wnt signaling originating from the neural tube to induce Pax3 expression in the opV placode. A double knockout of Wnt1 and Wnt3a was produced to determine the necessity of these genes in opV placode development. Pax3 expression in the opV placode at E8.5 and E9.5 was markedly reduced in the double mutants when compared to wild type mice. This study shows that Wnt1 and Wnt3a genes are necessary for normal Pax3 expression, but that other signals may contribute to its induction.
5

Minnis-Lyons, Sarah Elizabeth. "Notch/Wnt signalling and the hepatic progenitor response in hepatocellular regeneration." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23671.

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Chronic liver disease remains a significant cause of morbidity and mortality globally. Transplantation is the only effective treatment for end-stage disease but is limited by organ availability, surgical complications and risks of long term immunosuppression. Novel therapies for advanced disease are therefore required. The liver has a remarkable capacity to regenerate through division of mature hepatocytes, however in chronic or severe disease hepatocyte replication fails, senescence occurs and liver failure ensues. Ductular reactions (DRs), containing hepatic progenitor cells capable of repopulating the parenchyma, arise in chronic liver injury when hepatocyte regeneration is impaired. Enhancing this endogenous repair mechanism is a key therapeutic goal. Notch and Wnt are key signals required for liver regeneration, however to date they have principally been characterised in end-point disease and the temporal kinetics of these signalling pathways not known. I sought to identify if these signals control expansion of DRs after hepatocyte injury and whether they can be therapeutically manipulated. I examined the dynamics of Notch and Wnt activity using a genetic model of hepatocellular injury and ductular-mediated regeneration whereby induction of injury could be timed, synchronising the regenerative response. Using lineage tracing, small molecules, blocking antibodies and genetic loss of function experiments I defined distinct time-sensitive Notch and Wnt signatures where early regeneration is driven by Notch and the later response by Wnt. I demonstrated that inhibition of Notch1 and Notch3 but not Notch2 reduces the generation of DRs. I identified that DRs were a source of potent growth hormone IGF1 and this production was Wnt driven. Notch driven expression of IGF1-receptor within DRs identified this axis as a node for cooperation between Notch and Wnt signals. Blocking the IGF1 axis prevented DR expansion, which conversely could be enhanced by administration of recombinant IGF1. Here, I functionally defined complex temporal dynamics controlling of DRs and identified therapeutic pathways to enhance liver regeneration.
6

Jarero, Francesca. "Wnt, Hedgehog and Notch signalling in relation to tapeworm anteroposterior polarity and segmentation." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10044881/.

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Tapeworms are a group of parasitic flatworms whose uniquely segmented body plan has raised questions regarding their anteroposterior polarity and homology to other animals for more than a century. The Wnt, Hedgehog and Notch pathways are conserved developmental signalling pathways involved in embryonic patterning and segmentation in the Metazoa. In this thesis, these three pathways were explored in a tapeworm for the first time. Spatial expression patterns for components belonging to each of the pathways were investigated in the mouse bile duct tapeworm, Hymenolepis microstoma. Wnt pathway factors showed polarised, conserved patterns of expression of ‘posterior’ ligands (Wnts) and ‘anterior’ inhibitors (Sfrps). The expression of Wnt inhibitors, in particular, identified the true developmental anterior of H. microstoma larvae, answering a previously unresolved question of tapeworm development. In adult worms, expression patterns of these Wnt inhibitors confirmed the scolex (a region of the worm presumed to be anterior) as truly anterior. Expression of inhibitors and ‘posterior’ Wnts during strobilation shows polarised patterns along the anteroposterior boundaries of individual segments. These expression patterns indicate that the role of the Wnt pathway in specifying anteroposterior axes is conserved amongst tapeworms. Furthermore, a tapeworm-­specific Wnt11 paralog is hypothesised to have taken on a novel function during adult development, likely acting as the effector of strobilation. The expression of Hmic-­Wnt11a is highly restricted between the neck and strobila and defines a newly recognised region of the adult body, dubbed the ‘transition zone’. Hedgehog signalling in adult H. microstoma is linked with the nervous system (as it is in free-­living flatworms). During larval development Hedgehog shows canonical specification of the midline. Notch signalling was found to be involved in a number of developmental processes. The expression pattern of Hmic-­Notch1 was of particular interest as it showed polarised posterior expression within all segments. Finally, this study developed single and double fluorescent in situ hybridisation techniques using tyramide signal amplification and lead the first steps towards an in vivo approach to RNA interference method in H. microstoma.
7

Cheung, L. "Genetic manipulation of the Wnt and Notch signalling pathways in the pituitary gland in vivo." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1408913/.

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The Wnt and Notch signal transduction pathways are two important regulators of pituitary organogenesis. Wnt signalling regulates maintenance, proliferation and differentiation of the progenitor pool during early pituitary development, whilst Notch signalling prevents the premature specification of endocrine cell-types. Components of the Wnt and Notch pathways are downregulated in the pituitary as development proceeds. Furthermore, their expression is detected in the mature, adult gland. Our studies investigate the role of Wnt and Notch signalling in the adult and developing pituitary gland through genetic manipulation of signalling mediators in vivo. We investigate the function of Wnt signalling in committed POU1F1-expressing cells through the conditional deletion of the canonical Wnt signalling mediator Ctnnb1. We find that the loss of β-catenin from adult POU1F1-expressing cells does not dramatically affect adult pituitary hormone production, suggesting that the canonical Wnt pathway is not required for normal function of POU1F1- expressing cells. In parallel, we studied the role of Notch signalling in POU1F1-expressing cells through conditional overexpression of the constitutively activated Notch receptor. We find that, in contrast to previous studies, constitutive Notch signalling in POU1F1-expressing cells also does not affect their differentiation or function. At the same time, we do not find any pituitary-specific functions for the Notch signalling ligand Delta-like 1 homologue (DLK1). We therefore conclude that downregulation of Notch signalling is not required for normal development or function of POU1F1-expressing cells. Finally, our studies investigated the temporal specificity of Notch signalling throughout pituitary organogenesis through constitutive Notch activation in celltypes ranging from early progenitors to committed endocrine cells. Our results indicate that Notch signalling is especially important for specification of embryonic progenitors into melanotrophs. We also find evidence suggesting non-redundant functions for NOTCH receptor paralogues, and we ultimately propose a model for Notch signalling function during pituitary development.
8

Ungerbäck, Jonas. "Notch signalling in carcinogenesis : With special emphasis on T-cell lymphoma and colorectal cancer." Licentiate thesis, Linköping University, Linköping University, Cell Biology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-51692.

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The Notch signalling pathway is an evolutionary conserved pathway, named after the Notch receptors, Notch1-4 in mammals, which upon cell-cell contact and ligand binding releases the intracellular domain (NICD). NICD translocates into the nucleus where it binds the transcriptional repressor RBP-Jk, which together with co-activators belonging to the Mastermind-like family of proteins form a transcriptional activation complex. This complex activates genes controlling cell fate decision, embryonic development, proliferation, differentiation, adult homeostasis and stem cell maintenance. On the other hand, disrupted Notch signalling may result in pathological conditions like cancer, although the mechanisms behind the disruption are often complex and in many cases largely unknown.

Notch1 drives the lymphocyte differentiation towards a T-cell fate and activating mutations in the gene have been suggested to be involved in T-cell lymphoma. In paper I, genetic alterations in Notch1 and the Notch1 regulating gene CDC4 were investigated in tumours from murine T-cell lymphoma induced with phenolphthalein, 1,3-butadiene or 2’,3’-dideoxycytidine. We identified activating Notch1 mutations in 39% of the lymphomas, suggesting that Notch1 is an important target gene for mutations in chemically induced lymphomas.

While it is known that constitutively activated Notch signalling has a clear oncogenic function in several solid malignancies as well, the molecular mechanisms are less known in this context. Unpublished data of our lab, together with other recent studies, suggest that mutations of Notch and Notch-related genes per se are uncommon in solid malignancies including colorectal cancer, while a growing body of evidence indicates that aberrant Wnt/b-catenin signalling may result in pro-tumoural Notch activation in these contexts. In paper II, we therefore investigated potential transcriptional interactions between the Notch and Wnt signalling pathways in colorectal cancer cell lines. The proximal Notch and Wnt pathway gene promoters were bioinformatically identified and screened for putative TCF/LEF1 and RBP-Jk sites. In canonical Wnt signalling, Apc negatively regulates b-catenin leading to repression of TCF/LEF1 target genes. Upon repression of the Wnt pathway we observed that several genes in the Notch pathway, including Notch2, were transcriptionally downregulated. We also confirmed binding of Lef1 to Notch2 as well as other Notch pathway gene promoters and luciferase assays showed an increased activity for at least one LEF1/TCF-site in the Notch2 promoter upon co-transfection of HT29 or HCT116 cells with mutated b-catenin. HT29 cell lines were also treated with the g-secretase inhibitor DAPT, leading to inactivation of the Notch pathway by preventing release of NICD. However, results showed no effects on Apc, b-catenin or their target cyclin D1. Taken together, these results indicate that the Wnt pathway may function as a regulator of the Notch pathway through the TCF/LEF1 target gene program in colon cancer cell lines.

In summary, Notch pathway deregulation is of importance in both murine T-cell lymphoma and human colorectal cancer, although the mechanisms differ. The current results give new insights in Notch pathway alterations as well as the signalling networks in which the Notch pathway interacts, and thus increase the understanding of Notch’s involvement in malignant diseases.


Studies on molecular genetic alterations in colorectal cancer
9

Chabanais, Julien. "Contribution de la protéine O-fucosyltransférase 1( POFUT1) à la différenciation myogénique et à la tumorigenèse colorectale." Thesis, Limoges, 2019. http://www.theses.fr/2019LIMO0039.

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La protéine O-fucosyltransférase 1 (POFUT1) réticulaire, dont le gène est localisé dans la région chromosomique 20q11.21 chez l’Homme, catalyse le transfert d’un fucose qui sera O-lié sur la sérine ou la thréonine présente dans la séquence consensus (C2X4S/TC3), portée par un domaine EGF-like d’une glycoprotéine membranaire ou sécrétée. Le knockdown de Pofut1 (Po -) dans la lignée myoblastique murines C2C12 conduit à la formation de myotubes allongés et minces, à faible nombre de noyaux ainsi qu’à une sous-expression du marqueur myogénique tardif Myf6, suggérant des défauts significatifs dans la fusion secondaire. La signalisation NFATc2/IL-4 est décrite comme la voie principale associée à cette étape. Nous montrons que la moindre expression de Nfatc2 dans les myotubes Po - est corrélée à une baisse de l'IL-4 sécrétée et à une faible quantité de son récepteur (IL-4Rα) présent chez les cellules de réserve qui doivent participer à la fusion avec les myotubes naissants. La neutralisation de l’IL-4Rα sur les C2C12 sauvages provoque des défauts d'accrétion myonucléaire, semblables à ceux observés pour les Po -. Ainsi, POFUT1 pourrait être un nouveau médiateur de la croissance des myotubes au cours du processus myogénique, notamment par la signalisation NFATc2/IL-4. La glycoprotéine WIF1, cible potentielle de POFUT1, est un antagoniste de la signalisation WNT via sa fixation aux protéines WNT. Cette voie est connue pour être impliquée dans la prolifération et la différenciation des myoblastes. Néanmoins, aucune donnée ne concerne le rôle de WIF1 dans le processus myogénique. Par un apport exogène de WIF1, nous avons montré l’augmentation de la prolifération et l’altération de la différenciation myoblastique des C2C12. Lors de la prolifération, une augmentation de l’expression de Myf5 et une diminution de MyoG sont observées. A 7 jours de différenciation, les myotubes Po - ont un diamètre plus petit que les myotubes sauvages et ils sont plus nombreux à avoir un faible nombre de noyaux, traduisant des défauts de fusion. Nous démontrons pour la première fois, l’implication de la protéine WIF1 dans le processus myogénique. Récemment, POFUT1 a aussi été proposé comme nouveau biomarqueur pour certains cancers, mais pas évalué dans le cancer colorectal (CCR). Nous avons donc collecté des données issues de 626 tumeurs et 51 tissus adjacents non tumoraux disponibles dans FireBrowse, celles de lignées cellulaires cancéreuses colorectales et de prélèvements tumoraux provenant du Centre de Ressources Biologiques du CHU de Limoges. Une surexpression de POFUT1 est observée dès le stade I, majoritairement due à une amplification de la région 20q11.21. Elle est significativement associée aux adénocarcinomes non mucineux et à une localisation rectale. De plus, l’expression de POFUT1 est corrélée à celles des récepteurs NOTCH ainsi qu’au processus métastatique, probablement par activation de la voie NOTCH. A ce titre, POFUT1 pourrait être considéré comme un nouveau biomarqueur pour le diagnostic du CCR
The ER protein O-fucosyltransferase 1 (POFUT1), whose gene is located at the 20q11.21 chromosomic region in humans, catalyzes O-linked fucose addition to serine or threonine present in the consensus sequence (C2X4S/TC3) carried by EGF-like domain of membrane or secreted glycoprotein. Pofut1 knockdown (Po -) in murine myoblast C2C12 cell line leads to formation of elongated and thin myotubes, with a low number of nuclei and to downexpression of the late myogenic marker Myf6, suggesting significant defects in secondary fusion. NFATc2/IL-4 signaling is described as the main pathway associated to this step. We showed that the slightest expression of Nfatc2 in Po - myotubes is correlated with a decrease in IL-4 secretion and a lower quantity of IL 4Rα in reserve cells, which had to fuse with nascent myotubes. IL-4Rα neutralization on wild-type C2C12 causes myonuclear accretion defects, similar to those observed in Po -. Then, POFUT1 could be a new mediator of myotube growth during myogenic process, particularly through NFATc2/IL-4 signaling. The glycoprotein WIF1, potential POFUT1 target, is an antagonist of WNT signaling via its binding to WNT proteins. This pathway is involved in proliferation and differentiation of myoblasts. However, no data are available on WIF1 role in the myogenic process. Through exogenous WIF1 treatment, we showed a proliferation increase and a myoblast differentiation impairment in C2C12. During proliferation, increase in Myf5 and decrease in MyoG expressions are observed. At 7 days of differentiation, Po - myotubes have a smaller diameter than wild-type ones and are more numerous to have a small number of nuclei, reflecting fusion defects. For the first time, we demonstrate the involvement of WIF1 in the myogenic process. Recently, POFUT1 was proposed to be a new biomarker for several cancers, but not evaluated in colorectal cancer (CRC). We used data from 626 tumors and 51 adjacent non-tumor tissues available at FireBrowse, colorectal cancer cell lines and tumor samples from the Biological Resource Centre of Limoges hospital. A POFUT1 overexpression is observed from stage I, mainly due to amplification of 20q11.21 region. It is significantly associated to non-mucinous adenocarcinoma and to rectum location. Moreover, POFUT1 expression is correlated with those of NOTCH receptors as well as the metastatic process, probably by activation of the NOTCH pathway. POFUT1 could therefore be considered as a new biomarker for CRC diagnosis
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Angbohang, Angshumonik. "Role of Wnt and Notch signalling pathways on the neural differentiation of human Müller stem cells and their modulation by growth factors." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1530890/.

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Müller glia mediates retina regeneration in zebrafish. Despite exhibiting Müller glial with stem cell (hMSC) characteristics in vitro by the human retina, retinal regeneration mediated by Müller glia following disease or injury has not been demonstrated. Notch, Wnt, TGFβ and HBEGF signalling is well known to regulate retinal neurogenesis and inflammation, but the roles of these molecules in the neural differentiation of hMSC are not known. This thesis aimed to establish whether there is an interaction between these signalling pathways and the role that these factors play during retinal ganglion cell (RGC) and photoreceptor differentiation of hMSC. The research showed that inhibition of Notch signalling caused downregulation of components of the canonical Wnt signalling pathway in these cells, as demonstrated by a decrease in mRNA expression of the Wnt ligand WNT2B and its target genes WISP-1 and AXIN2. Addition of TGFβ1 did not significantly change the expression of the Notch signalling target HES1 or the RGC marker BRN3A/B. Culture of hMSC with a combination of factors that induce their photoreceptor differentiation (FGF2, taurine, retinoic acid and Insulin growth factor; collectively called FTRI), markedly upregulated the expression of components of the canonical Wnt signalling pathway, including WNT2B, DKK1 and active β-catenin. Although FTRI did not modify mRNA expression of WNT5B, a component of the non-canonical/planar cell polarity Wnt pathway, it upregulated its secretion. Furthermore, TGFβ1 not only decreased WNT2B expression, but inhibited FTRI-induced photoreceptor differentiation of hMSC, as determined by expression of the photoreceptor markers NR2E3, rhodopsin and recoverin. Inhibition of TGFβ1 signalling by an ALK5 inhibitor prevented TGFβ1 induced changes in the expression of the two Wnt ligands examined. More importantly, inhibition of the canonical Wnt signalling by XAV-939 prevented FTRI-induced photoreceptor differentiation. Similarly, HBEGF, a factor shown to be upregulated by FTRI also decreased Wnt signalling components such as WNT2B, WISP-1, DKK1 and AXIN2. Inhibition of HBEGF by its specific inhibitor CRM197 prevented photoreceptor differentiation. These observations suggest that both Notch and Wnt signalling pathways can regulate the neurogenicity of hMSC in vitro and that TGFβ as well as HBEGF play important roles in mediating key pathways leading to either RGC or photoreceptor differentiation of hMSC. Targeting components of both Notch and Wnt pathways may constitute targets for potential induction of endogenous regeneration of the human retina and this merits further studies.
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Books on the topic "Wnt and Notch signaling":

1

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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Yasutomo, Koji, ed. Notch Signaling. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2.

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Bellen, Hugo J., and Shinya Yamamoto, eds. Notch Signaling. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1139-4.

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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, Tex: Landes Bioscience/Eurekah.com, 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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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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Borggrefe, Tilman, and Benedetto Daniele Giaimo, eds. Molecular Mechanisms of Notch Signaling. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89512-3.

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Book chapters on the topic "Wnt and Notch signaling":

1

Tang, Su-Ni, Sharmila Shankar, and Rakesh K. Srivastava. "Cross Talks Among Notch, Wnt, and Hedgehog Signaling Pathways Regulate Stem Cell Characteristics." In Stem Cells and Human Diseases, 593–606. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2801-1_27.

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Horvay, Katja, and Helen E. Abud. "Regulation of Intestinal Stem Cells by Wnt and Notch Signalling." In Transcriptional and Translational Regulation of Stem Cells, 175–86. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6621-1_10.

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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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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, 1–13. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_230-1.

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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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Hozumi, Katsuto. "Notch Ligands for Lymphocyte Development." In Notch Signaling, 3–20. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_1.

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Maekawa, Yoichi, Takahide Ikeda, and Piyarat Srinontong. "Notch Controls the Differentiation and Function of Cytotoxic CD8 T Cells." In Notch Signaling, 21–33. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_2.

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Conference papers on the topic "Wnt and Notch signaling":

1

McGlothen, TZ, C. Gillespie, L. Colbert, D. Blaylock-Hogans, S. Guo, and Perez RR Gonzalez-. "P5-06-10: Leptin Signaling Impacts Notch and Wnt Crosstalk in Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p5-06-10.

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Dhawan, Punita, Jillian Pope, Ashok Sharma, Mary Kay Washington, and Amar B. Singh. "Abstract 1334: Overexpression of claudin-1 induces Notch and Wnt signaling to regulate colon carcinogenesis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1334.

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Brilliant, A., Y. Brilliant, and S. Sazonov. "PO-270 Signalling pathways WNT, hedgehog and NOTCH in breast cancer with presence and absence of cancer stem cells." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.301.

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Pudi, Renuka, Peter A. Pinto, and Jonathan C. Vogel. "Abstract LB-266: Identification and enrichment of tumor-initiating cells from human prostate cancers using lentiviral vectors that can detect activated Wnt, Notch, or Hedgehog signaling." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-266.

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Varisco, B. M., M. Oria, E. Aydin, R. Joshi, N. Cabanas, R. Schmidt, C. Schroeder, M. Marotta, and J. Peiro. "Proteomic Profiling of Tracheal Fluid in Ovine Model of Congenital Diaphragmatic Hernia with Fetal Tracheal Occlusion Identifies Dysregulation of Epithelial PI3K/AKT, Wnt, and Notch Signaling." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4438.

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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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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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Chen, Jihua, Daniel J. Moloney, and Pamela Stanley. "GLYCAN FUNCTIONS IN NOTCH SIGNALING." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.374.

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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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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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Reports on the topic "Wnt and Notch signaling":

1

Mehta, Samir, and Kurt Hankenson. Notch Signaling in Bone Regeneration. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada564010.

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2

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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3

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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4

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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5

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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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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7

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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8

Supsavhad, Wachiraphan. Wnt Signaling in Prostate Cancer Bone Metastases. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada623452.

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9

Jeffries, Shawn. Molecular Mechanisms of Notch Signaling in Neoplasia. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411237.

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10

Robling, Alexander G. Secreted Wnt Signaling Inhibitors in Disuse-Induced Bone Loss. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada613318.

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