Relevant bibliographies by topics / WNT/ β-CATENIN CASCADE

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Academic literature on the topic 'WNT/ β-CATENIN CASCADE'

Author: Grafiati
Published: 11 September 2023

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Journal articles on the topic "WNT/ β-CATENIN CASCADE"

1

Kumar, Amit, Ravindra B. Chalamalasetty, Mark W. Kennedy, Sara Thomas, Shreya N. Inala, Robert J. Garriock, and Terry P. Yamaguchi. "Zfp703 Is a Wnt/β-Catenin Feedback Suppressor Targeting the β-Catenin/Tcf1 Complex." Molecular and Cellular Biology 36, no. 12 (April 18, 2016): 1793–802. http://dx.doi.org/10.1128/mcb.01010-15.

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The Wnt/β-catenin signaling pathway controls embryonic development and adult stem cell maintenance through the regulation of transcription. Failure to downregulate Wnt signaling can result in embryonic malformations and cancer, highlighting the important role of negative regulators of the pathway. The Wnt pathway activates several negative feedback targets, including axin2 and Dkk1, that function at different levels of the signaling cascade; however, none have been identified that directly target active β-catenin/Tcf1 transcriptional complexes. We show thatZfp703is a Wnt target gene that inhibits Wnt/β-catenin activity in Wnt reporter assays and in Wnt-dependent mesoderm differentiation in embryonic stem cells. Zfp703 binds directly to Tcf1 to inhibit β-catenin/Tcf1 complex formation and does so independently of the Groucho/Tle transcriptional corepressor. We propose that Zfp703 is a novel feedback suppressor of Wnt/β-catenin signaling that functions by inhibiting the association of β-catenin with Tcf1 on Wnt response elements in target gene enhancers.
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Yang, Shengsen, Fei Zhou, Yi Dong, and Fei Ren. "α-Mangostin Induces Apoptosis in Human Osteosarcoma Cells Through ROS-Mediated Endoplasmic Reticulum Stress via the WNT Pathway." Cell Transplantation 30 (January 1, 2021): 096368972110350. http://dx.doi.org/10.1177/09636897211035080.

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α-mangostin has been confirmed to promote the apoptosis of MG-63 cells, but its specific pro-apoptosis mechanism in osteosarcoma (OS) remains further investigation. Here, we demonstrated that α-mangostin restrained the viability of OS cells (143B and Saos-2), but had little effect on the growth of normal human osteoblast. α-mangostin increased OS cell apoptosis by activating the caspase-3/8 cascade. Besides, α-mangostin induced endoplasmic reticulum (ER) stress and restrained the Wnt/β-catenin pathway activity. 4PBA (an ER stress inhibitor) or LiCl (an effective Wnt activator) treatment effectively hindered α-mangostin-induced apoptosis and the caspase-3/8 cascade. Furthermore, we also found that α-mangostin induced ER stress by promoting ROS production. And ER stress-mediated apoptosis caused by ROS accumulation depended on the inactivation of Wnt/β-catenin pathway. In addition, α-mangostin significantly hindered the growth of xenograft tumors, induced the expression of ER stress marker proteins and activation of the caspase-3/8 cascade, and restrained the Wnt/β-catenin signaling in vivo. In short, ROS-mediated ER stress was involved in α-mangostin triggered apoptosis, which might depended on Wnt/β-catenin signaling inactivation.
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Ishitani, Tohru, Satoshi Kishida, Junko Hyodo-Miura, Naoto Ueno, Jun Yasuda, Marian Waterman, Hiroshi Shibuya, Randall T. Moon, Jun Ninomiya-Tsuji, and Kunihiro Matsumoto. "The TAK1-NLK Mitogen-Activated Protein Kinase Cascade Functions in the Wnt-5a/Ca2+ Pathway To Antagonize Wnt/β-Catenin Signaling." Molecular and Cellular Biology 23, no. 1 (January 1, 2003): 131–39. http://dx.doi.org/10.1128/mcb.23.1.131-139.2003.

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ABSTRACT Wnt signaling controls a variety of developmental processes. The canonical Wnt/β-catenin pathway functions to stabilize β-catenin, and the noncanonical Wnt/Ca2+ pathway activates Ca2+/calmodulin-dependent protein kinase II (CaMKII). In addition, the Wnt/Ca2+ pathway activated by Wnt-5a antagonizes the Wnt/β-catenin pathway via an unknown mechanism. The mitogen-activated protein kinase (MAPK) pathway composed of TAK1 MAPK kinase kinase and NLK MAPK also negatively regulates the canonical Wnt/β-catenin signaling pathway. Here we show that activation of CaMKII induces stimulation of the TAK1-NLK pathway. Overexpression of Wnt-5a in HEK293 cells activates NLK through TAK1. Furthermore, by using a chimeric receptor (β2AR-Rfz-2) containing the ligand-binding and transmembrane segments from the β2-adrenergic receptor (β2AR) and the cytoplasmic domains from rat Frizzled-2 (Rfz-2), stimulation with the β-adrenergic agonist isoproterenol activates activities of endogenous CaMKII, TAK1, and NLK and inhibits β-catenin-induced transcriptional activation. These results suggest that the TAK1-NLK MAPK cascade is activated by the noncanonical Wnt-5a/Ca2+ pathway and antagonizes canonical Wnt/β-catenin signaling.
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Wang, Xiaohong, Neeta Adhikari, Qinglu Li, and Jennifer L. Hall. "LDL receptor-related protein LRP6 regulates proliferation and survival through the Wnt cascade in vascular smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 6 (December 2004): H2376—H2383. http://dx.doi.org/10.1152/ajpheart.01173.2003.

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Initial studies have established expression of low-density lipoprotein (LDL) receptor-related protein 6 (LRP6) in vascular smooth muscle cells (VSMCs). We hypothesized that LRP6 is a critical mediator governing the regulation of the canonical Wnt/β-catenin/T cell factor 4 (Tcf-4) cascade in the vasculature. This hypothesis was based on our previous work demonstrating a role for the β-catenin/Tcf-4 pathway in vascular remodeling as well as work in other cell systems establishing a role for LRP family members in the Wnt cascade. In line with our hypothesis, LRP6 upregulation significantly increased Wnt-1-induced Tcf activation. Moreover, a dominant interfering LRP6 mutant lacking the carboxyl intracellular domain (LRP6ΔC) abolished Tcf activity. LRP6-induced stimulation of Tcf was blocked in VSMCs harboring constitutive expression of a dominant negative Tcf-4 transgene lacking the β-catenin binding domain, suggesting that LRP6-induced activation of Tcf was mediated through a β-catenin-dependent signal. Expression of the dominant interfering LRP6ΔC transgene was sufficient to abolish the Wnt-induced survival as well as cyclin D1 activity and cell cycle progression. In conclusion, these findings provide the first evidence of a role for an LDL receptor-related protein in the regulation of VSMC proliferation and survival through the evolutionary conserved Wnt signaling cascade.
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Palchevska, O. L., V. V. Balatskyi, L. L. Macewicz, and O. O. Piven. "Cardiospecific deletion of β-catenin gene associated with an activity violation of signaling cascades involved in the development of myocardial hypertrophy." Visnik ukrains'kogo tovaristva genetikiv i selekcioneriv 15, no. 2 (February 28, 2018): 181–86. http://dx.doi.org/10.7124/visnyk.utgis.15.2.877.

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The aim of our study was to investigate the molecular mechanisms of hypertrophy response under cardiospecific β-catenin haploinsufficiency condition. Materials and methods. Studies were done with β-catenin condtional knockout mice (β-catflox/flox) and α-MHC-Cre-transgenic mice. To induce hypertrophy we used swimming test during 6 weeks. Using western-blot, we have analyzed the level of studied proteins. Results. It has been shown that the β-catenin haploinsufficiency is associated with increased signaling activity of MAPK, PI3-kinase-mTOR-dependent signaling cascades in both: with prolonged physical activity and without it. However, even with an increased activity of this signalling, β-catenin haploinsufficient mice expressed weaker hypertrophic response. Conclusions. The transcriptional activity of β-catenin is necessary for the proper interaction of signaling cascades during heart maturation and adaptation to stress. Keywords: β-catenin, hypertrophy, Wnt-signalling, MAPK signalling, PI3-kinase-mTOR-dependent cascade, PKA-signalling, myocardium.
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Quarta, Santina, Andrea Cappon, Cristian Turato, Mariagrazia Ruvoletto, Stefania Cannito, Gianmarco Villano, Alessandra Biasiolo, et al. "SerpinB3 Upregulates Low-Density Lipoprotein Receptor-Related Protein (LRP) Family Members, Leading to Wnt Signaling Activation and Increased Cell Survival and Invasiveness." Biology 12, no. 6 (May 26, 2023): 771. http://dx.doi.org/10.3390/biology12060771.

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Abnormal activation of the Wnt-β-catenin signaling cascade is involved in tumor growth and dissemination. SerpinB3 has been shown to induce β-catenin, and both molecules are overexpressed in tumors, particularly in those with poor prognoses. The aim of this study was to evaluate the ability of SerpinB3 to modulate the Wnt pathway in liver cancer and in monocytic cells, the main type of inflammatory cells in the tumor microenvironment. The Wnt cascade, Wnt co-receptors, and low-density lipoprotein receptor-related protein (LRP) members were analyzed in different cell lines and human monocytes in the presence or absence of SerpinB3. The Wnt-β-catenin axis was also evaluated in liver tumors induced in mice with different extents of SeprinB3 expression. In monocytic cells, SerpinB3 induced a significant upregulation of Wnt-1/7, nuclear β-catenin, and c-Myc, which are associated with increased cell lifespan and proliferation. In liver tumors in mice, the expression of β-catenin was significantly correlated with the presence of SerpinB3. In hepatoma cells, Wnt co-receptors LRP-5/6 and LRP-1, implicated in cell survival and invasiveness, were upregulated by SerpinB3. The LRP pan-inhibitor RAP not only induced a decrease in LRP expression, but also a dose–dependent reduction in SerpinB3-induced invasiveness. In conclusion, SerpinB3 determines the activation of the Wnt canonical pathway and cell invasiveness through the upregulation of LRP family members.
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Grishanova, Alevtina Y., Lyubov S. Klyushova, and Maria L. Perepechaeva. "AhR and Wnt/β-Catenin Signaling Pathways and Their Interplay." Current Issues in Molecular Biology 45, no. 5 (May 2, 2023): 3848–76. http://dx.doi.org/10.3390/cimb45050248.

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As evolutionarily conserved signaling cascades, AhR and Wnt signaling pathways play a critical role in the control over numerous vital embryonic and somatic processes. AhR performs many endogenous functions by integrating its signaling pathway into organ homeostasis and into the maintenance of crucial cellular functions and biological processes. The Wnt signaling pathway regulates cell proliferation, differentiation, and many other phenomena, and this regulation is important for embryonic development and the dynamic balance of adult tissues. AhR and Wnt are the main signaling pathways participating in the control of cell fate and function. They occupy a central position in a variety of processes linked with development and various pathological conditions. Given the importance of these two signaling cascades, it would be interesting to elucidate the biological implications of their interaction. Functional connections between AhR and Wnt signals take place in cases of crosstalk or interplay, about which quite a lot of information has been accumulated in recent years. This review is focused on recent studies about the mutual interactions of key mediators of AhR and Wnt/β-catenin signaling pathways and on the assessment of the complexity of the crosstalk between the AhR signaling cascade and the canonical Wnt pathway.
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Langhammer, Tina-Susann, Catrin Roolf, Saskia Krohn, Christin Kretzschmar, Rayk Huebner, Arndt Rolfs, Mathias Freund, and Christian Junghanss. "PI3K/Akt Signaling Interacts With Wnt/β-Catenin Signaling But Does Not Induce An Accumulation Of β-Catenin In The Nucleus Of Acute Lymphoblastic Leukemia Cell Lines." Blood 122, no. 21 (November 15, 2013): 4886. http://dx.doi.org/10.1182/blood.v122.21.4886.4886.

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Abstract Signaling pathways play essential roles in biological processes as development, cell proliferation and homeostasis. The accurate modulation of signaling pathways, their adapted interaction and their time- and tissue-specific adjusted regulation are required for normal cell development. PI3K/Akt and Wnt/β-Catenin signaling pathways act as key regulators in cell proliferation, differentiation and growth. Both signaling pathways include GSK3β as a common protein, which may mediate an interaction and cross-talk between the pathways. Aberrant activation of PI3K/Akt signaling has been linked to different types of leukemia while Wnt/β-Catenin signaling is known to be deregulated in some solid tumors. However, a potential role of Wnt/β-Catenin signaling for pathogenesis of acute lymphoblastic leukemia (ALL) has not yet been analyzed. In our study we analyzed both signaling pathways in different B- and T-ALL cell lines (RS4;11, SEM, REH, CEM, Jurkat, MOLT-4), thereby focusing mainly on their potential interaction via the protein GSK3β. Western Blot experiments were performed to evaluate the expression of specific PI3K/Akt and Wnt/β-Catenin key proteins. To evaluate the activation status of Wnt signaling immunofluorescence and protein fractionation experiments were performed, analyzing the activation linked nucleic localization of β-Catenin. The effect of pathway activation and inhibition on cell proliferation via chemical compounds was analyzed by WST-1 test. High pAkt levels were detected in B-ALL cell line SEM and T-ALL cell line CEM, indicating a hyperactive PI3K/Akt signaling, whereas other analyzed cell lines diplayed lower pAkt status. Among all cell lines analyzed SEM and CEM also showed the highest cytoplasmic β-Catenin levels, indicating a direct interaction of both signaling pathways. However, immunofluorescence and fractionation experiments revealed that a translocation of β-Catenin into the nucleus did not occur. To further investigate the role and interaction of PI3K/Akt and Wnt/β-Catenin signaling, pathway inhibiting and stimulating experiments were performed. Treatment of cells with Wnt3a led to activation of the Wnt/β-Catenin signaling cascade, characterized by nuclear β-Catenin accumulation. Inhibition of cell proliferation was detected after treatment with high concentrations Wnt3a (≥ 500 ng/ml). PI3K inhibition by LY294002 led to decreased phosphorylation of GSK3β at Ser9 and an increased decay of β-Catenin. Stimulation of PI3K/Akt signaling using activating ligand FLT3L induced GSK3β phosphorylation at Ser9 and accumulation of cytoplasmic β-Catenin. However a translocation of β-Catenin into the nucleus seems not to occur. In summary our results indicate that PI3K/Akt and Wnt/β-Catenin signaling can interact through their common protein GSK3β, but stimulation of the PI3K/Akt signaling pathway by addition of PI3K/Akt specific activators does not fully activate Wnt/β-Catenin signaling in ALL cells. Complete activation of the Wnt cascade characterized by translocation of β-Catenin into the nucleus can only be induced by use of specific Wnt effectors. Disclosures: No relevant conflicts of interest to declare.
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Banerjee, Anwesha, Mamta Chawla-Sarkar, and Anupam Mukherjee. "Rotavirus-Mediated Suppression of miRNA-192 Family and miRNA-181a Activates Wnt/β-Catenin Signaling Pathway: An In Vitro Study." Viruses 14, no. 3 (March 9, 2022): 558. http://dx.doi.org/10.3390/v14030558.

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The significance of the Wnt/β-catenin signaling cascade in Rotavirus (RV) infection has not been elucidated. In this study, we attempt to elucidate the importance of the Wnt/β-catenin pathway in the RV pathogenesis and investigate a miRNA-mediated approach to regulate the pathway to repress the RV infection in the host. The regulation of the Wnt signaling pathway in terms of β-catenin accumulation and activation was analyzed by Western blotting and Confocal imaging analysis. The expression levels of miR-192 family members and miR-181a were enquired into using qPCR assays, whereas their targets in the Wnt pathway were confirmed using the Luciferase Reporter Assays. Members of the miR-192 family and miR-181a, which target the components of the pathway, were also found to be considerably decreased in expression during RV infection. Ectopic expression of these miRNAs could restrict the RV pathogenesis by targeting the intermediates of the Wnt signaling pathway. The miR-192 family and miR-181a were capable of suppressing the RV infection via targeting of the Wnt/β-catenin pathway. The study not only highlights the role of the Wnt signaling cascade in RV infection but also suggests that miRNAs can synergistically decrease RV replication by a significant amount. Thus, the miR-192 family and miR-181a present themselves as prospective antivirals against RV infection.
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Wang, Zhongyuan, Bo Li, Liang Zhou, Shubin Yu, Zijie Su, Jiaxing Song, Qi Sun, et al. "Prodigiosin inhibits Wnt/β-catenin signaling and exerts anticancer activity in breast cancer cells." Proceedings of the National Academy of Sciences 113, no. 46 (October 31, 2016): 13150–55. http://dx.doi.org/10.1073/pnas.1616336113.

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Prodigiosin, a natural red pigment produced by numerous bacterial species, has exhibited promising anticancer activity; however, the molecular mechanisms of action of prodigiosin on malignant cells remain unclear. Aberrant activation of the Wnt/β-catenin signaling cascade is associated with numerous human cancers. In this study, we identified prodigiosin as a potent inhibitor of the Wnt/β-catenin pathway. Prodigiosin blocked Wnt/β-catenin signaling by targeting multiple sites of this pathway, including the low-density lipoprotein-receptor-related protein (LRP) 6, Dishevelled (DVL), and glycogen synthase kinase-3β (GSK3β). In breast cancer MDA-MB-231 and MDA-MB-468 cells, nanomolar concentrations of prodigiosin decreased phosphorylation of LRP6, DVL2, and GSK3β and suppressed β-catenin–stimulated Wnt target gene expression, including expression of cyclin D1. In MDA-MB-231 breast cancer xenografts and MMTV-Wnt1 transgenic mice, administration of prodigiosin slowed tumor progression and reduced the expression of phosphorylated LRP6, phosphorylated and unphosphorylated DVL2, Ser9 phosphorylated GSK3β, active β-catenin, and cyclin D1. Through its ability to inhibit Wnt/β-catenin signaling and reduce cyclin D1 levels, prodigiosin could have therapeutic activity in advanced breast cancers.
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Book chapters on the topic "WNT/ β-CATENIN CASCADE"

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Lai, Keane K. Y., and Michael Kahn. "Pharmacologically Targeting the WNT/β-Catenin Signaling Cascade: Avoiding the Sword of Damocles." In Pharmacology of the WNT Signaling System, 383–422. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_523.

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Conference papers on the topic "WNT/ β-CATENIN CASCADE"

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Šeklić, Dragana, Milena Jovanović, Nevena Milivojević, and Marko Živanović. "PLATINUM(IV) COMPLEX AND ITS CORRESPONDING LIGAND SUPPRESS CELL MOTILITY AND PROMOTE EXPRESSION OF FRIZZLED-7 RECEPTOR IN COLORECTAL CANCER CELLS." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.288s.

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Suppression of cell movement is an imperative in the effectiveness of future generations of chemotherapeutics. Frizzled 7 receptor (FZD7), as the first protein of Wnt/β-catenin signaling cascade, plays a significant role in regulation of cell differentiation, proliferation, and cell migration. This study aimed to investigate the potential effects of platinum (IV) complex: [PtCl4 (dbu-S, S-eddp)] – C1, and its corresponding ligand – L1 on cell movement, as well as the FZD7 expression and localization after treatments on two human colorectal carcinoma cell lines (HCT-116, SW-480). A Wound healing assay was used to examine cell migration, while FZD7 protein expression was examined by immunofluorescence. Chemical compounds, especially L1, reduced cell motility of both tested cell lines. They showed a particularly good effect on HCT-116 cells, increasing protein expression of the antimigratory marker FZD7 whose localization was observed on the cell membrane of HCT-116 cells. Suppression of cell movement was significantly lower in SW-480 cells after treatments, when compared to HCT-116, with an obvious decrease of FZD7 receptor expression and its localization in the cytoplasm of these cells. Our results indicate that among the examined treatments, the ligand showed more significant results in the suppression of HCT-116 cell movement, most likely through the stimulation of differentiation, which is indicated by the promotion of FZD7 expression.
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Nava, Miguel, Nwamaka A. Amobi, Yanyuan Wu, Robin Farias-Eisner, and Jay Vadgama. "Abstract 1333: Cross talk between mitogen-activated protein kinase signaling cascades and Wnt/β-catenin in HER2+ overexpressing breast cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1333.

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