Relevant bibliographies by topics / Catenine

Academic literature on the topic 'Catenine'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Catenine":

1

Tao, Y. S., R. A. Edwards, B. Tubb, S. Wang, J. Bryan, and P. D. McCrea. "beta-Catenin associates with the actin-bundling protein fascin in a noncadherin complex." Journal of Cell Biology 134, no. 5 (September 1, 1996): 1271–81. http://dx.doi.org/10.1083/jcb.134.5.1271.

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Catenins were first characterized as linking the cytoplasmic domains of cadherin cell-cell adhesion molecules to the cortical actin cytoskeleton. In addition to their essential role in modulating cadherin adhesivity, catenins have more recently been indicated to participate in cell and developmental signaling pathways. beta-Catenin, for example, associates directly with at least two receptor tyrosine kinases and transduces developmental signals within the Wnt pathway. Catenins also complex with the tumor suppressor protein adenomatous polyposis coli (APC), which appears to have a role in regulating cell proliferation. We have used the yeast two-hybrid method to reveal that fascin, a bundler of actin filaments, binds to beta-catenin's central Armadillo repeat domain. Western blotting of immunoprecipitates from cell line and mouse and rat brain extracts indicate that this interaction exists in vivo. Fascin and beta-catenin's association was further substantiated in vitro using purified proteins isolated from recombinant bacterial and baculoviral sources. Immunoprecipitation analysis indicates that fascin additionally binds to plakoglobin, which is highly homologous to beta-catenin but not to p120cas, a newly described catenin which contains a more divergent Armadillo-repeat domain. Immunoprecipitation, in vitro competition, and domain-mapping experiments demonstrate that fascin and E-cadherin utilize a similar binding site within beta-catenin, such that they form mutually exclusive complexes with beta-catenin. Immunofluorescence microscopy reveals that fascin and beta-catenin colocalize at cell-cell borders and dynamic cell leading edges of epithelial and endothelial cells. In addition to cell-cell borders, cadherins were unexpectedly observed to colocalize with fascin and beta-catenin at cell leading edges. It is conceivable that beta-catenin participates in modulating cytoskeletal dynamics in association with the microfilament-bundling protein fascin, perhaps in a coordinate manner with its functions in cadherin and APC complexes.
2

Zhurinsky, J., M. Shtutman, and A. Ben-Ze'ev. "Plakoglobin and beta-catenin: protein interactions, regulation and biological roles." Journal of Cell Science 113, no. 18 (September 15, 2000): 3127–39. http://dx.doi.org/10.1242/jcs.113.18.3127.

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Beta-catenin can play different roles in the cell, including one as a structural protein at cell-cell adherens junctions and another as a transcriptional activator mediating Wnt signal transduction. Plakoglobin (gamma)-catenin), a close homolog of beta-catenin, shares with beta-catenin common protein partners and can fulfill some of the same functions. The complexing of catenins with various protein partners is regulated by phosphorylation and by intramolecular interactions. The competition between different catenin partners for binding to catenins mediates the cross-talk between cadherin-based adhesion, catenin-dependent transcription and Wnt signaling. Although plakoglobin differs from beta-catenin in its functions and is unable to compensate for defects in Wnt signaling resulting from lack of beta-catenin, recent evidence suggests that plakoglobin plays a unique role in Wnt signaling that is different from that of beta-catenin. The functional difference between catenins is reflected in their differential involvement in embryonic development and cancer progression.
3

Aberle, H., S. Butz, J. Stappert, H. Weissig, R. Kemler, and H. Hoschuetzky. "Assembly of the cadherin-catenin complex in vitro with recombinant proteins." Journal of Cell Science 107, no. 12 (December 1, 1994): 3655–63. http://dx.doi.org/10.1242/jcs.107.12.3655.

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The cytoplasmic domain of classical cadherins is tightly associated with three proteins termed alpha-, beta- and gamma-catenin. These accessory proteins are of central importance for the adhesive properties of this class of cell adhesion molecules. In order to examine the molecular architecture of the cadherin-catenin complex in more detail we have expressed the catenins and the cytoplasmic domain of E-cadherin as fusion proteins in Escherichia coli, and analyzed the interaction of purified recombinant cadherin and catenins in combinatorial protein-protein interaction experiments. The cytoplasmic domain of E-cadherin cannot directly associate with alpha-catenin but interacts with high affinity with beta-catenin, whereas the binding of gamma-catenin (plakoglobin) to E-cadherin is less efficient. alpha- and beta-catenin assemble into a 1:1 heterodimeric complex. The analysis of various truncated beta-catenins revealed that an alpha-catenin binding site in beta-catenin is localized between amino acid positions 120 and 151. The central role of beta-catenin for the assembly of the heterotrimeric E-cadherin/alpha-catenin/beta-catenin complex in mixing experiments with all components was demonstrated. The reconstitution in vitro of the cadherin-catenin complex should allow the study of the interaction with signalling molecules and with the actin-based cytoskeleton.
4

Papkoff, J., B. Rubinfeld, B. Schryver, and P. Polakis. "Wnt-1 regulates free pools of catenins and stabilizes APC-catenin complexes." Molecular and Cellular Biology 16, no. 5 (May 1996): 2128–34. http://dx.doi.org/10.1128/mcb.16.5.2128.

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The Wnt-1 proto-oncogene induces the accumulation of beta-catenin and plakoglobin, two related proteins that associate with and functionally modulate the cadherin cell adhesion proteins. Here we have investigated the effects of Wnt-1 expression on the tumor suppressor protein APC, which also associates with catenins. Expression of Wnt-1 in two different cell lines greatly increased the stability of APC-catenin complexes. The steady-state levels of both catenins and APC were elevated by Wnt-1, and the half-lives of both beta-catenin and plakoglobin associated with APC were also markedly increased. The stabilization of catenins by Wnt-1 was primarily the result of a selective increase in the amount of uncomplexed, monomeric beta-catenin and plakoglobin, detected both by affinity precipitation and size-exclusion chromatography of cell extracts. Exogenous expression of beta-catenin was possible in cells already responding to Wnt-1 but not in the parental cells, suggesting that Wnt-1 inhibits an essential regulatory mechanism for beta-catenin turnover. APC has the capacity to oppose this Wnt-1 effect in experiments in which overexpression of the central region of APC significantly reduced the size of the monomeric pool of beta-catenin induced by Wnt-1. Thus, the Wnt-1 signal transduction pathway leads to the accumulation of monomeric catenins and stabilization of catenin complex formation with both APC and cadherins.
5

Böhm, Jan, Leo Niskanen, Kari Kiraly, Jari Kellokoski, Matti Eskelinen, Sinikka Hollmen, Esko Alhava, and Veli-Matti Kosma. "Expression and Prognostic Value of α-, β-, andγ -Catenins in Differentiated Thyroid Carcinoma." Journal of Clinical Endocrinology & Metabolism 85, no. 12 (December 1, 2000): 4806–11. http://dx.doi.org/10.1210/jcem.85.12.7079.

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Catenins (α, β, and γ) are a group of intracellular cell adhesion molecules that unite cytoskeleton with extracellular adhesion system. Abnormal expression of these molecules may have prognostic relevance in various carcinomas, including differentiated thyroid carcinoma (DTC). We have, therefore, evaluated the prognostic value of α-, β-, andγ -catenins along with traditional risk factors in 206 consecutive DTC patients by immunohistochemistry. Papillary carcinomas showed normal staining pattern for α-, β-, andγ -catenins in 124 (60%), 136 (67%), and 94 (46%) cases, respectively. Follicular carcinomas expressed α-, β-, andγ -catenins normally in 16 (48%), 18 (55%), and 8 (32%) cases, respectively. Follicular type of tumor showed more often reduced staining for all catenins than papillary carcinoma (P = 0.009, P = 0.004, and P = 0.002, respectively). Age (>60 yr) and pTNM-stage were related to reduced α- and β-catenin expression levels (P = 0.027 and P = 0.026, respectively) and larger size of the tumor to reduced β- andγ -catenin expressions (P = 0.039 and P = 0.007, respectively). Nodal metastases at the time of primary treatment related to reduced α-catenin expression and distal metastases to reduced β- and γ-catenin staining signals (P = 0.022, P = 0.014, and P = 0.039, respectively). Reduced α-catenin associated with tumor recurrence (P = 0.002) and reduced β-catenin with cancer-related mortality (P = 0.005). The multivariate analysis for recurrence-free survival showed that α-catenin and serum thyroglobulin level 1 yr after primary treatment were prognostic of recurrent disease (hazards ratio, 3.42, P = 0.022; and hazards ratio, 10.03, P = 0.0001). In addition,α -catenin retained its prognostic significance in low-stage patients (P = 0.0151). We propose that the evaluation ofα -catenin expression by immunohistochemistry in DTC patients has prognostic value in addition to that obtained by traditional prognostic factors.
6

Ozawa, M., and R. Kemler. "Molecular organization of the uvomorulin-catenin complex." Journal of Cell Biology 116, no. 4 (February 15, 1992): 989–96. http://dx.doi.org/10.1083/jcb.116.4.989.

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The Ca(2+)-dependent cell adhesion molecule uvomorulin is a member of the cadherin gene family. Its cytoplasmic region complexes with structurally defined proteins termed alpha-, beta-, and gamma-catenins. Here we show that A-CAM (N-cadherin), another member of this gene family, also associates with catenins suggesting that this complex formation may be a general property of the cadherins. For uvomorulin it has been found that this association with catenins is of crucial importance for the adhesive function, but little is known about the molecular organization of the uvomorulin-catenin complex. Using a combination of biochemical analyses we show that a single complex is composed of one molecule of uvomorulin, one or two molecules of beta-catenin, and one molecule of alpha-catenin. Furthermore, beta-catenin seems to interact more directly with uvomorulin. In pulse-chase experiments beta-catenin is already associated with the 135-kD uvomorulin precursor molecule but the assembly of the newly synthesized alpha-catenin into the complex is only detected around the time of endoproteolytic processing.
7

Staddon, J. M., C. Smales, C. Schulze, F. S. Esch, and L. L. Rubin. "p120, a p120-related protein (p100), and the cadherin/catenin complex." Journal of Cell Biology 130, no. 2 (July 15, 1995): 369–81. http://dx.doi.org/10.1083/jcb.130.2.369.

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Cadherins and catenins play an important role in cell-cell adhesion. Two of the catenins, beta and gamma, are members of a group of proteins that contains a repeating amino acid motif originally described for the Drosophila segment polarity gene armadillo. Another member of this group is a 120-kD protein termed p120, originally identified as a substrate of the tyrosine kinase pp60src. In this paper, we show that endothelial and epithelial cells express p120 and p100, a 100-kD, p120-related protein. Peptide sequencing of p100 establishes it as highly related to p120. p120 and p100 both appear associated with the cadherin/catenin complex, but independent p120/catenin and p100/catenin complexes can be isolated. This association is shown by coimmunoprecipitation of cadherins and catenins with an anti-p120/p100 antibody, and of p120/p100 with cadherin or catenin antibodies. Immunocytochemical analysis with a p120-specific antibody reveals junctional colocalization of p120 and beta-catenin in epithelial cells. Catenins and p120/p100 also colocalize in endothelial and epithelial cells in culture and in tissue sections. The cellular content of p120/p100 and beta-catenin is similar in MDCK cells, but only approximately 20% of the p120/p100 pool associates with the cadherin/catenin complex. Our data provide further evidence for interactions among the different arm proteins and suggest that p120/p100 may participate in regulating the function of cadherins and, thereby, other processes influenced by cell-cell adhesion.
8

Nieset, J. E., A. R. Redfield, F. Jin, K. A. Knudsen, K. R. Johnson, and M. J. Wheelock. "Characterization of the interactions of alpha-catenin with alpha-actinin and beta-catenin/plakoglobin." Journal of Cell Science 110, no. 8 (April 15, 1997): 1013–22. http://dx.doi.org/10.1242/jcs.110.8.1013.

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Cadherins are calcium-dependent, cell surface glycoproteins involved in cell-cell adhesion. To function in cell-cell adhesion, the transmembrane cadherin molecule must be associated with the cytoskeleton via cytoplasmic proteins known as catenins. Three catenins, alpha-catenin, beta-catenin and gamma-catenin (also known as plakoglobin), have been identified. beta-catenin or plakoglobin is associated directly with the cadherin; alpha-catenin binds to beta-catenin/plakoglobin and serves to link the cadherin/catenin complex to the actin cytoskeleton. The domains on the cadherin and betacatenin/plakoglobin that are responsible for protein-protein interactions have been mapped. However, little is known about the molecular interactions between alpha-catenin and beta-catenin/plakoglobin or about the interactions between alpha-catenin and the cytoskeleton. In this study we have used the yeast two-hybrid system to map the domains on alpha-catenin that allow it to associate with beta-catenin/plakoglobin and with alpha-actinin. We also identify a region on alpha-actinin that is responsible for its interaction with alpha-catenin. The yeast two-hybrid data were confirmed with biochemical studies.
9

Ilan, N., S. Mahooti, D. L. Rimm, and J. A. Madri. "PECAM-1 (CD31) functions as a reservoir for and a modulator of tyrosine-phosphorylated beta-catenin." Journal of Cell Science 112, no. 18 (September 15, 1999): 3005–14. http://dx.doi.org/10.1242/jcs.112.18.3005.

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Catenins function as regulators of cellular signaling events in addition to their previously documented roles in adherens junction formation and function. Evidence to date suggests that beta and gamma catenins can act as signaling molecules, bind transcriptional factors and translocate to the nucleus. Beta- and gamma-catenin are also major substrates for protein tyrosine kinases, and tyrosine phosphorylation of junctional proteins is correlated with decreased adhesiveness. One way in which catenin functions are modulated is by dynamic incorporation into junctional complexes which controls, in part, the cytoplasmic levels of catenins. Here we show that: (1) vascular endothelial growth factor (VEGF) induces beta-catenin tyrosine phosphorylation in a time-, and dose-dependent manner and that VEGF receptors co-localize to areas of endothelial cell-cell contact in vitro and in vivo. (2) Platelet-endothelial cell adhesion molecule (PECAM)-1 can function as a reservoir for, and modulator of, tyrosine phosphorylated beta-catenin. (3) PECAM-1 can prevent beta-catenin nuclear translocation in transfected SW480 colon carcinoma cells. We suggest that PECAM-1 may play a role in modulating beta-catenin tyrosine phosphorylation levels, localization and signaling and by doing so, functions as an important modulator of the endothelium.
10

Balatskyi, V. V., L. L. Macewicz, T. P. Ruban, and O. O. Piven. "Adhesion proteins are able to controle the proliferation and size of neonatal cardiomoycytes in Mus musculus." Visnik ukrains'kogo tovaristva genetikiv i selekcioneriv 16, no. 1 (September 7, 2018): 5–11. http://dx.doi.org/10.7124/visnyk.utgis.16.1.897.

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Aim. In our present work, we have analyzed the influence of adhesion proteins — catenins on the proliferation of neonatal cardiomyocytes, under there cardiac-specific knockout. Methods. The studies were conducted using mice with a conditional knockout of the β-catenin gene (β-catflox/flox); αE-catenin (αE-catflox/flox) and transgenic animals which express the Crerecombinase under the control of the heavy chain promoter of α-myosin ((αMHC) -Cre). Results. The cardiac ablation of the β-catenin gene results in lower cell proliferation and decreased myocardial size, whereas the knockout of αE-catenin, increased proliferation as well as the size of the newborn heart. Conclusions. Intercellular adhesion genes — β-catenin and αE-catenins have not only an important structural function in maintaining of the myocardium tissue structure, but also involved in controlling of the proliferation, size of neonatal cardiomyocytes and newborn heart. Keywords: β-catenin, αE-catenin, cardiomyocytes, proliferation.
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You might also be interested in the extended bibliographies on the topic 'Catenine' for particular source types:
Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Catenine":

1

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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Ress, Angelika. "Proteininteraktionspartner von Beta-Catenin Identifikation von Protein-Proteininteraktionen, Charakterisierung von Modulatoren des Wnt-Signaltransduktionsweges, Wege zu einem neuen Verständnis des Onkoproteins Bcr-Abl /." [S.l. : s.n.], 2004. http://www.diss.fu-berlin.de/2004/334/index.html.

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3

Levy, Laurence. "Etude des propriétés oncogéniques de la beta-caténine : activité transcriptionnelle et gènes cibles." Paris 6, 2003. http://www.theses.fr/2003PA066194.

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Patricio, Flavia Rezende Pereira. "E-caderina e B-catenina : analise da expressão e relação com a evolução e prognostico nos tumores do cortex de adrenal em crianças." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308380.

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Orientador: Antonio Gonçalves de Oliveira Filho
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-13T04:54:32Z (GMT). No. of bitstreams: 1 Patricio_FlaviaRezendePereira_M.pdf: 2174141 bytes, checksum: 0011ea137b3f271896d984e54bb4f4d6 (MD5) Previous issue date: 2009
Resumo: Tumores do córtex da supra-renal (TCSR) em crianças são raros e correspondem a 0,2% dos tumores da infância. Estes tumores são endocrinologicamente ativos, causando na maioria das vezes, virilização do paciente associada, ou não, a um aumento de cortisol. O tratamento dos TCSR é principalmente cirúrgico, sendo a cirurgia com o procedimento de ressecção completa do tumor e sem ruptura a principal modalidade terapêutica. No entanto, a distinção entre tumores benignos e malignos, baseada exclusivamente na histologia, pode ser difícil de ser realizada. Os fatores prognósticos são baseados quase exclusivamente no estadiamento da doença, o qual leva em conta o peso e volume tumoral e a disseminação metastática do tumor. Estudos clínicos e experimentais sugerem que a propagação metastática em alguns tumores está relacionada aos níveis de E-caderina e ?-catenina, que são moléculas presentes no tecido epitelial normal, estando envolvidas diretamente na adesão intercelular. A análise da expressão destas moléculas pode fornecer dados que permite identificar grupos de pacientes mais propensos à evolução tumoral desfavorável, proporcionando, assim, um tratamento mais adequado e individualizado a estes pacientes. Com o objetivo de analisar a expressão da E-caderina e ?-catenina em crianças com TCSR e sua correlação com a evolução da doença, foi realizada uma revisão retrospectiva dos prontuários de 33 crianças com diagnóstico de TCSR tratadas no Centro Infantil Boldrini (Janeiro de 1998 a Janeiro de 2005). Foram coletados e analisados dados referentes ao sexo, idade, manifestações clínicas, estadiamento, tratamento e evolução dos pacientes. Para a análise imunoistoquímica, foi empregada a técnica de multitissue array com anticorpos específicos para E-caderina e ?-catenina em 30 tumores de crianças com TCSR e uma adrenal normal. Houve predominância do sexo feminino na amostra e a apresentação clínica mais freqüente foi a virilização. Nesta série, observou-se que crianças com idade inferior a dois anos apresentaram melhor prognóstico e, também que a ruptura e recidiva tumoral apresentaram influência negativa na sobrevida dos pacientes. A análise imunoistoquímica mostrou expressão da E-caderina em 73,3% e ?-catenina em 83,3% das crianças que apresentavam TCSR. Além disso, não foi verificada sua expressão na glândula adrenal normal. Quando avaliada a relação da expressão da E-caderina e ?-catenina com os estádios evolutivos da doença, não foi verificada associação significativa entre as variáveis. A positividade da E-caderina e ?-catenina na membrana celular, citoplasma ou núcleo, verificou-se que a expressão na membrana celular mostrou associação significativa com mau prognóstico
Abstract: Adrenal cortical tumor (ACT) in children are rare and they correspond to 0,2% of the tumors of the childhood. They are usually active, causing mainly virilization of patient associate or not with increased levels of corticoids. The treatment of the TCSR is mainly surgical, being the surgery with complete resection of the tumor without spillage the therapeutic mainstay. The distinction between benign and malignant tumors based exclusively on the histology can be difficult and very often uncertain. The prognostic factors are based almost exclusively on the staging of the disease, who takes into account the weight and volume tumoral and the metastatic dissemination. Clinical and experimental studies suggest that metastatic dissemination in some tumors is related with the levels of E-cadherin and ?-catenin. These molecules are found in the normal epithelial tissues and are strongly related with intercellular adhesion. The analysis of the expression of these molecules maybe can allow identifying groups of patients with higher risk of presenting unfavorable outcomes and ensuing appropriate and individualized treatment. With the objective of analyzing the expression of E-cadherin and ?-catenin in children with ACT and its correlation with the evolution of the disease, a retrospective chart review of 33 children with diagnosis of ACT treated at Centro Infantil Boldrini (January of 1998 through January of 2005). Data regarding sex, age, clinical presentation, staging, treatment and outcome were collected and analyzed. Multitissue array technique using specific antibodies for E-cadherin and ?-catenin was done in 30 tumors from children with ACT and 1 normal adrenal tissue. There was predominance of the feminine sex and the most frequent clinical presentation was virilization. In these series children with age bellow two years had a better outcome and tumoral spillage and relapse have had negative influence in the survival of the patients. Immunohistochemical analysis showed expression of E-cadherin in 73,3 % and ?-catenin in 83,3 % of the children who had ACT but showed no expression in the normal adrenal tissue. When the relationship between the expression of E-cadherin and ?-catenin with the stages of the disease was analyzed, no significant association was found. When analyzed the expression of E-cadherin and ?-catenin in the cellular membrane, cytoplasm or nucleus, its presence in the membrane of the cell was found as associated with poor outcome. As far we know, this is the first study to evaluate the expression of E-cadherin and ?-catenin in children with ACT and, although with small number of patients due to the rarity of the disease, it apparently shows some relationship with prognosis. When the relationship between the expression of E-cadherin and ?-catenin with the stages of the disease was analyzed, no significant association was found. When analyzed the expression of E-cadherin and ?-catenin in the cellular membrane, cytoplasm or nucleus, its presence in the membrane of the cell was found as associated with poor outcome. As far we know, this is the first study to evaluate the expression of E-cadherin and ?-catenin in children with ACT and, although with small number of patients due to the rarity of the disease, it apparently shows some relationship with prognosis
Mestrado
Cirurgia
Mestre em Cirurgia
5

Milord, Sandrine. "Contribution à l’étude du rôle et de la régulation de Fra-1 dans le cancer." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON13505/document.

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Fra-1 appartient à la famille des facteurs de transcription AP-1. Son expression est particulièrement élevée dans les cellules de cancer du sein qui n'expriment pas le récepteur aux œstrogènes (RE-), c'est-à-dire les cellules les plus agressives. L'inhibition de Fra-1 dans ces cellules entraîne une diminution de la motilité, de l'invasion et de la prolifération, mais elle entraîne aussi de profonds changements de morphologie. Les cellules RE-, qui présentent un phénotype mésenchymateux s'arrondissent et établissent un plus grand nombre de contacts cellule-cellule après l'inhibition de Fra-1. Dans les cellules RE-, la β-caténine est localisée au noyau ou dans le cytoplasme, ce qui est un marqueur de mauvais pronostic. Au cours de cette thèse, j'ai montré que Fra-1 régule la localisation nucléaire de la β-caténine et ainsi régule son activité transcriptionelle en agissant très tardivement sur la voie Wnt. J'ai également mis en évidence une interaction physique directe entre Fra-1 et la β-caténine qui pourrait être responsable de cet effet. De plus, l'analyse de microarrays par RT-QPCR a révélé la régulation d'autres gènes comme la mœsine, la fibronectine et l'extracellular matrix protein 1, qui pourraient également jouer un rôle dans la régulation de l'agressivité tumorale par Fra-1. Par ailleurs, Fra-1 est une protéine instable et nous avons montré qu'elle est phosphorylée et stabilisée par PKCθ. Fra-1 est d'ailleurs nécessaire à l'effet de la kinase sur la motilité cellulaire
Fra-1 is a member of the AP-1 transcription factor family. It is aberrantly expressed in breast cancer cells lacking Estrogen Receptor (ER-) expression, which are the most aggressive ones. Fra-1 inhibition in these cells leads to a decreased in motility, invasion and proliferation, but also to deep morphologic changes. ER- cells, which present a mesenchymal phenotype, become rounder and establish a greater number of cell-cell contacts after Fra-1 inhibition. In ER- cells, β-catenin is nuclear or cytoplasmic, which is considering as a poor prognosis marker. During this PhD, I demonstrate that Fra-1, which acts very downstream in the Wnt/β-catenin signaling pathway, regulates the nuclear localization of β-catenin leading to up-regulation transcriptional activity of β-catenin. I also found that Fra-1 directly interacts with β-catenin. In addition, RT-QPCR microarrays analysis has revealed the regulation of other genes such as mœsin, fibronectin and extracellular matrix protein 1, which might also take part in the tumoral aggressiveness regulated by Fra-1. Moreover, we show that Fra-1, which is an unstable protein, is phosphorylated and stabilized by PKCθ. Furthermore, Fra-1 is necessary to mediate the kinase effect on cell motility
6

Désert, Romain. "Effets phénotypiques de deux mécanismes d’activation de la voie Wnt/beta caténine dans le carcinome hépatocellulaire." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B044/document.

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Le carcinome hépatocellulaire (CHC) est une des principales causes de mortalité par cancer dans le monde. Dans environ 50% des tumeurs, on observe les signes d’une activation de la voie Wnt/β-caténine, causée par une mutation de l’exon 3 du gène CTNNB1 ou par stimulation du récepteur FRZD. Des études transcriptomiques du CHCs ont montré que ces deux modes d’activation étaient associés à des sous-types de tumeurs différents. Nous avons cherché à mieux comprendre les caractéristiques cliniques et le phénotype moléculaire de ces deux sous-types de CHCs. Dans un premier temps, nous avons fait le lien entre l'activation Wnt extracellulaire, un phénotype de cellules cancéreuses souches ou progénitrices et la présence de foyers de fibrose discrète intra-tumorale, observable par examen histopathologique, que nous avons appelés "nids fibreux". Nous avons également mis en évidence HAPLN1, une protéine de la matrice extracellulaire dont l’expression est stimulée par Wnt3a dans un modèle de cellules hépatiques progénitrices HepaRG, comme un nouveau marqueur d’agressivité du CHC. Ces résultats montrent une association entre l’activation Wnt extracellulaire et une agressivité tumorale passant par un remodelage matriciel. Dans un second temps, une Méta-analyse de données publiques de transcriptomique a permis de mettre évidence 4 sous-types de CHCs. La mutation CTNNB1, prédite par l’expression de 5 marqueurs par une méthode développée durant la thèse, était associée à un de ces sous-types et à un bon pronostic clinique. Nous avons également isolé un nouveau sous-type de CHC de bon pronostic exprimant un phénotype de tumeur différenciée et des signatures de métabolisme hépatique périportales. Ce sous-type a probablement été un facteur confondant dans les études précédentes mesurant l’association de la mutation CTNNB1 avec un bon pronostic. Enfin, nous avons mis en évidence une forte association négative entre la mutation CTNNB1 et l’inflammation ainsi que la fibrose tumorale dans trois cohortes indépendantes. Cet effet pourrait être provoqué par une inhibition de NF-κB par la β-caténine mutée, comme suggérée par des résultats préliminaires issue d’un modèle in vitro d’HepaRG mutés T41 stimulés par LPS. Nos résultats suggèrent donc que les deux modes d’activation de la voie Wnt/β-caténine sont associés à des mécanismes moléculaires, des profils d’expression, des phénotypes et des pronostics cliniques très différents
Hepatocellular carcinoma (HCC) is the third cause of cancer-related death worldwide. Half of them show activation of Wnt/β-catenin pathway, caused by activating CTNNB1 exon 3 mutation of by stimulation of FRZD receptor. Transcriptomic based HCC classifications showed that this two types of activation were associated with distinct tumor subtypes. We tried to better understand the molecular phenotypes and the clinical features associated with these subtypes. In a first part, we linked extracellular Wnt activation with a stem/progenitor phenotype and with fibrous hotspot in HCC. Fibrous hotspot, which were called “fibrous nest”, can be detected by routine anatomic pathology analyses. We also showed that HAPLN1, an extracellular matrix protein induced by Wnt3a in progenitor HepaRG cells, was a new marker of stemness and bad outcome in HCC. Those results shows the associations between extracellular Wnt activation, extracellular matrix remodeling and tumor aggressiveness. In a second part, a transcriptome meta-analysis of 1133 HCCs highlighted 4 robust subclasses. CTNNB1 mutation, predicted by a 5-genes score based method, was associated with one of these subclasses and with good clinical features. We also highlighted a new subclass of CTNNB1 wild type HCCs associated with tumor differentiation, signatures of periportal metabolism and good outcome. This subclass was probably a confounding factor in survival studies comparing HCCs carrying mutant versus those carrying wild-type CTNNB1. Finally, we highlighted strong negative associations between CTNNB1 mutation and inflammation as well as tumor fibrosis in three independent cohorts. Preliminary results of in vitro HepaRG cells mutated for CTNNB1 in T41 and stimulated by LPS suggest an inhibitory effect of β-caténine on NF-κB. In conclusion, our results show that the two types of Wnt activation in HCC are associated with very distinct molecular phenotypes and clinical features
7

Ruggiero, Antonella. "Impact of Wnt signalling on multipotent stem cell dynamics during Clytia hemisphaerica embryonic and larval development." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066561/document.

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Le but de ce travail était d’accroitre notre connaissance des mécanismes qui gouvernent la formation, la spécification et la différentiation des cellules souches, à l’aide du modèle métazoaire non-bilatérien Clytia hemisphaerica. Clytia possède une population particulière de cellules multipotentes appelées cellules interstitielles (i-cells). Ces cellules, présentes au cours du développement larvaire et chez la méduse adulte, sont capables de donner naissances a des cellules somatiques et aux gamètes. Chez les bilatériens, la signalisation Wnt/β-caténine (Wntβc) régule les processus développementaux fondamentaux ainsi que la prolifération, la spécification et la différenciation des cellules souches. Mon travail s’est porté sur l’implication de la signalisation Wntβc dans les dynamiques des i-cells. Mes résultats suggèrent que la signalisation Wntβc est impliquée dans la dernière étape de la différenciation de certains neurones, mais pas pour la spécification du destin cellulaire. D’autre part, j’ai aussi observé qu’en condition contrôle, la formation des i-cells est Wntβc-indépendante et probablement entraînée par le héritage de plasma germinatif contenant les ARNm localisées au pôle animal. Cependant, suite à des expériences de microdissection, j’ai observe que la reformation des i-cells dans la moitie végétative des embryons requérait l’activation de la voie Wntβc. En conclusion, deux mécanismes distincts peuvent conduire à la formation des i-cell pendant l'embryogenèse. Globalement, les résultats obtenus ont fourni une meilleure idée de la façon dont i- cellules et leurs dérivés se posent lors de l'embryogenèse et le développement larvaire
The aim of this work was to extend our understanding of the mechanisms regulating stem cell formation, specification and differentiation by studies in the non-bilaterian metazoan model Clytia hemisphaerica. Clytia, like other hydrozoan cnidarians, possess a particular population of multipotent stem cells called interstitial cells (i-cells), present during larval development and in the adult medusa, which are able to give rise both to somatic cell types and to gametes.In bilaterian animals Wnt/β-catenin signalling regulates fundamental developmental processes such primary body axis specification, but also regulates stem cell proliferation, lineage specification and differentiation. I investigated the role of Wnt/β-catenin signalling in i-cell specification and differentiation. The results obtained suggest that Wnt/β-catenin signalling is involved in the last step of differentiation for certain neuronal cell types, but not for somatic cell fate choice. In the second part of my study I investigated the role of Wnt/β-catenin signalling in i-cell formation during embryogenesis. The results indicated that during normal development i-cell formation is Wnt/β-catenin independent and probably driven by inheritance of germ plasm containing localised mRNAs from the egg animal pole. In contrast in embryo re-patterning following embryo bisection, Wnt/β-catenin signalling appears to be necessary for de novo i-cell formation in the absence of germ plasm. Thus two distinct mechanisms can lead to i-cell formation during embryogenesis. Overall the results obtained provided a better picture of how i-cells and their derivatives arise during embryogenesis and larval development
8

Soler, Christophe. "Étude d'un complexe protéique impliqué dans l'adhésion kératinocyte-kératinocyte : le complexe cadhérine-caténines : régulation de l'adhésion par les phosphorylations et rôle du complexe dans la viabilité, la différenciation et la prolifération cellulaire." Lyon 1, 1997. http://www.theses.fr/1997LYO1T305.

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Amaddeo, Giuliana. "Altérations génomiques des carcinomes hépatocellulaires liées au virus de l'hépatite B." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05S012.

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Contexte: Le carcinome hépatocellulaire (CHC) est la plus fréquent des tumeurs primitives du foie. Près de 50% des CHC sont causés par une infection par le virus de l'hépatite B (VHB). Au cours des différents stades de l’infection par le VHB, des multiples altérations génétiques et/ou chromosomiques s'accumulent et favorisent ainsi le développement tumoral. Objectives: a) étudier, in vitro et in vivo, le rôle potentiel d’un nouveau gène susceptible d’être impliqué dans la carcinogénèse hépatique : IRF-2 (Interferon regulatory factor 2). Ce gène a été identifié comme fréquemment délété par analyse CGH-SNP dans les CHC liés à l’infection par le VHB. b) caractériser une série de CHC liés au VHB en étudiant le statut viral, les altérations génétiques et l’expression de différents gènes afin de mieux comprendre le rôle du VHB dans l’hépato-carcinogenèse et comparer ces différents paramètres avec une série de CHC non liés au VHB. Résultats : a) Dans une série de 125 CHC, Sandrine Imbeaud, au sein du laboratoire, a effectué une analyse CGH-SNP microarray et a identifié une région commune de délétion homozygote localisée en 4q34.3-35 comprenant le gène IRF-2 dans 4 échantillons. Nous avons ensuite mis en évidence par séquençage des mutations somatiques inactivatrices dans 2 autres tumeurs. In vitro, la sousexpression d’IRF-2 a entrainé une augmentation de la prolifération cellulaire et sa sur-expression a induit une promotion de l'apoptose cellulaire. In vivo, l’extinction d’IRF-2 était responsable de la formation de tumeurs de grande taille. Les 6 tumeurs inactivées pour IRF-2 étaient associées au VHB (p = 0.0003), et les mutations de TP53 et d’IRF-2 étaient mutuellement exclusives. La sousexpression de IRF-2 induisait une sous-expression de TP53 et une forte corrélation entre les expressions protéiques de p53 et de IRF-2 a été observée (r2 = 0,72, p = 0,004). En plus, on a observé que l’expression des gènes cibles directs de TP53 était modulée par le niveau d‘expression d’IRF-2. Nous avons émise l'hypothèse que IRF-2 pourrait altérer la fonction de p53 car IRF-2 est connue pour se lier à MDM2, un régulateur négatif de l’expression de p53. Le traitement des cellules inactivées pour IRF-2 avec MG132, un inhibiteur du protéasome, a induit la restauration de l'expression de p53. In vivo, le traitement avec bortézomib, un inhibiteur du proteasome utilisé en oncologie, a entrainé une régression des tumeurs inactivées pour IRF-2. b) Nous avons caractérisé sur le plan clinique et moléculaire une série de CHC liés au VHB et, ensuite, nous avons comparé nos résultats avec ceux d’une série de CHC liés à autres étiologies. Nous avons montré que les CHC liés au VHB présentaient des caractéristiques cliniques et pathologiques différentes de celles des CHC non liés au VHB : ils survenaient chez des patients plus jeunes (P < 0.0001), d'origine Africaine ou Asiatique (P < 0.0001), avec un taux sérique d'alpha-foeto protéine élevé (P = 0.008) et étaient sur le plan histologique des tumeurs peu différenciés (P = 0.04). Nous avons identifié des mutations inactivatrices du gène HBX dans 71% des tumeurs et dans 33% des tissus non tumoraux adjacents (P < 0.0001). Dans 63% des cas, le nombre de copies virales dans les tumeurs était plus faible que dans les tissus non tumoraux adjacents (P < 0.0001). Le gène TP53 était le gène le plus fréquemment muté dans les CHC liés au VHB (41%, P = 0.0002), avec des mutations R249S présentes dans 14 échantillons (16%, p < 0.0001). Ce type de mutation est classiquement associé à l'aflatoxine B1. Nous avons observé que les mutations de TP53 étaient un prédicteur indépendant de survie uniquement pour les patients infectés par le VHB. Enfin,
Pas de résumé en anglais
Introduzione: Il carcinoma epatocellulare (HCC) è il tumore primitivo più comune del fegato. Nel mondo, quasi il 50% di tutti gli HCC sono causati dal virus dell'epatite B (HBV). Durante le fasi dell’ infezione da HBV, si possono accumulare alterazioni genetiche e / o cromosomiche e quindi promuovere lo sviluppo del tumore. Obiettivi: a) analizzare in vitro e in vivo il ruolo potenziale di un nuovo gene potenzialmente coinvolto nella carcinogenesi epatica: IRF-2 (Interferon regulatory factor 2). Questo gene è stato identificato mediante l’analisi CGH-SNP come frequentemente deleto negli HCC correlati all’ HBV. b) caratterizzare una cohorte di HCC correlati all’HBV studiandone lo stato virale, le alterazioni genetiche e l’espressione di differenti geni al fine di comprendere meglio il ruolo di HBV nella carcinogenesis epatocellulare e confrontare questi parametri con una cohorte di HCC a diversa eziologia. Risultati: a) In laboratorio, Sandrine Imbeaud ha condotto un'analisi SNP-CGH microarray su una cohorte di 125 HCC che ha evidenziato una regione deleta in maniera omozigote localizzata sul braccio lungo del cromosoma 4 (4q34.3-35) in 4 campioni tumorali. La regione comprende un unico gene: IRF2. In altri due campioni sono state identificate mutazioni somatiche inattivatrici mediante sequenziamento della regione codante di IRF-2. In vitro, la soppressione di IRF-2 ha indotto un aumento della proliferazione cellulare, al contrario, la sua sovra-espressione ha causato un aumento dell’apoptosi cellulare. In vivo, la soppressione di IRF-2 è responsabile della formazione di tumori più grandi nei topi nude. I 6 tumori mutati per IRF2 sono tutti correlati all’ HBV (p = 0,0003. Nella cohorte di tumori studiati, le mutazioni di TP53 e di IRF-2 erano vicendevolmente esclusive. Inoltre, la soppressione dell’espressione della proteina IRF-2 induceva una riduzione dell’espressione della proteina p53 ed una stretta correlazione tra l’espressione delle due proteine è stata osservata (r2 = 0,72, p = 0,004). Inoltre, abbiamo dimostrato che il livello di espressione di IRF-2 è in grado di modulare l'espressione di alcuni geni target di TP53. Abbiamo, quindi, ipotizzato che IRF2 possa alterare la funzione di p53. Come è noto IRF2 può legarsi a MDM2, un regolatore negativo di p53 che induce la sua degradazione proteasomica. Il trattamento di cellule inattivate per IRF2 con MG132, un inibitore del proteasoma, induceva il restauro dell’espressione di p53. In vivo, il trattamento con bortezomib, chemioterapico inibitore del proteasoma, ha determinato la regressione del tumore inattivato per IRF2. b) 86 HCC correlati all’HBV sono stati caratterizzati dal punto di vista clinico e molecolare ed in seguito sono stati confrontati una serie di 90 HCC correlati ad altre eziologie. Gli HCC correlati all’HBV hanno delle caratteristiche cliniche e patologiche diverse da quelle degli HCC d’altra eziologia: insorgenza in pazienti più giovani (p <0,0001), di origine africana o asiatica (P <0.0001), alfa-fetoproteina sierica elevata (P = 0.008) e scarsa differenziazione istologica (P = 0,04). Mutazioni inattivatrici del gene HBX sono state identificate nel 71% dei tumori e il 33% dei tessuti non tumorali adiacenti (P <0.0001). Nel 63% dei casi, il numero di copie virali nel tessuto tumorale era inferiore rispetto al tessuto non tumorale adiacente (p <0,0001). Il gene TP53 è stato il gene più frequentemente mutato nella serie di HCC correlati a HBV (41%, p = 0,0002), con una considerevole presenza di mutazioni al codone 249 (R249S) (16%, p <0,0001). Questo tipo di mutazione è associate classicamente all’ aflatossina B1. Abbiamo osservato, inoltre, che TP53 mutato era un predittore indipendente di sopravvivenza solo per i pazienti infetti da HBV. Infine,
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Mialhe, Agnès. "Expression du complexe d'adhérence E-cadhérine/caténines dans les cellules tumorales vésicales." Université Joseph Fourier (Grenoble ; 1971-2015), 1998. http://www.theses.fr/1998GRE10100.

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Dans les cancers epitheliaux ou carcinomes, la perte d'adherence intercellulaire est probablement une des premieres etapes des mecanismes d'invasion et de formation des metastases. De recentes avancees demontrent que la e-cadherine, molecule d'adherence intercellulaire specifique des cellules epitheliales, mais egalement les catenines, groupe de proteines cytoplasmiques interagissant avec la cadherine, sont particulierement alterees dans les carcinomes invasifs. Ce travail de these a ete consacre a l'etude des anomalies d'expression du complexe e-cadherine-catenines dans le carcinome vesical, dont le comportement recidivant et l'evolution vers des tumeurs tres infiltrantes en font un modele d'etude interessant. Dans un premier temps, nous avons mis en evidence une frequence importante des anomalies d'expression de la e-cadherine et des catenines alpha et beta dans les carcinomes vesicaux les plus invasifs, montrant ainsi le role essentiel de ces molecules dans la progression tumorale vesicale. L'expression de la e-cadherine a en outre une valeur pronostique, ce qui renforce l'interet clinique de son etude. La deuxieme etape de ce travail a consiste a etudier, dans differentes lignees tumorales de vessie, l'expression du complexe e-cadherine-catenines, les interactions proteiques entre ses differents constituants et sa regulation. Nous avons observe une diminution d'expression de la e-cadherine dans les lignees les moins differenciees et demontre qu'une diminution de la transcription des arnm de la e-cadherine est sans doute un mecanisme majeur conduisant a cette baisse d'expression proteique. En fait, dans certaines lignees tres agressives, mais egalement dans certaines tumeurs, les catenines peuvent encore etre exprimees au niveau membranaire, meme en absence de e-cadherine transmembranaire, ce qui suggere la presence d'autres cadherines dans ces cellules. En effet, la detection de n-cadherine membranaire dans ces lignees semble indiquer que cette autre cadherine pourrait jouer un role non negligeable dans la tumorigenese vesicale.
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Books on the topic "Catenine":

1

Pintacuda, Nicolò. Catene di Markov. Pisa: ETS, 2000.

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Disertori, Sandro. Mondi in catene. Rovereto (Tn) [i.e. Trento, Italy]: Stella, 2007.

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Gillard, R. E. The self-assembly of catenanes. Birmingham: University of Birmingham, 1997.

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Allen, Garrick V., Shari Boodts, Lukas J. Dorfbauer, Gilles Dorival, Carla Falluomini, John Gram, Susan B. Griffith, et al., eds. Commentaries, Catenae and Biblical Tradition. Piscataway, NJ, USA: Gorgias Press, 2016. http://dx.doi.org/10.31826/9781463236908.

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Evangelisti, Valerio. Le catene di Eymerich. Milano: Mondadori, 2006.

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Lagarde, Paul de, ed. Catenae in Evangelia Aegyptiacae quae supersunt. Piscataway, NJ, USA: Gorgias Press, 2010. http://dx.doi.org/10.31826/9781463225131.

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Nasreen, R. Template synthesis and dynamic properties of novel catenanes. Manchester: UMIST, 1996.

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Marquis, Damien Jean-Franco̧is. Molecular meccano: Catenanes and rotaxanes made to order. Birmingham: University of Birmingham, 1992.

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Conte, Domenico. Catene di civiltà: Studi su Spengler. Napoli: Edizioni scientifiche italiane, 1994.

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Capodivacca, Silvia. Danzare in catene: Saggio su Nietzsche. Milano: Mimesis, 2009.

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Book chapters on the topic "Catenine":

1

Behrens, Jürgen. "Cadherins/Catenins." In Encyclopedia of Molecular Pharmacology, 1–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_32-1.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, Antoine Galmiche, Ken-Ichi Takemaru, Xingwang Chen, Feng-Qian Li, et al. "Beta-Catenin." In Encyclopedia of Signaling Molecules, 192–96. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_528.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Catenin Beta." In Encyclopedia of Signaling Molecules, 256. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100168.

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Takemaru, Ken-Ichi, Xingwang Chen, and Feng-Qian Li. "Beta-Catenin." In Encyclopedia of Signaling Molecules, 545–49. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_528.

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Pettitt, Jonathan. "β-Catenin." In Wnt Signaling in Development and Disease, 217–24. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118444122.ch16.

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Morin, Pat J. "APC/β-Catenin Pathway." In Encyclopedia of Cancer, 236–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_348.

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Ringwald, Martin. "The Uvomorulin—Catenin Complex." In Cellular Adhesion, 77–92. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2466-3_5.

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Morin, Pat J. "APC/β-Catenin Pathway." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_348-2.

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Morin, Pat J. "APC/β-Catenin Pathway." In Encyclopedia of Cancer, 321–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_348.

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Hargitai, Henrik. "Catena, Catenae." In Encyclopedia of Planetary Landforms, 1–2. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9213-9_35-1.

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Conference papers on the topic "Catenine":

1

Shiraishi, Toshihiko, and Akitoshi Nishijima. "A Study of a Mechanism of Cell Proliferation Promotion of Cultured Osteoblasts by Mechanical Vibration." In ASME 2018 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/imece2018-87364.

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This paper describes a mechanism of cell proliferation promotion of cultured osteoblasts by mechanical vibration focusing on β-catenin. 12.5 Hz and 0.5 G mechanical vibration was reported to promote the cell proliferation of cultured osteoblasts in plane culture. That is because the mechanical vibration weakens cell-cell adhesion, promotes to pile up cells, and allows cells to form multilayer structure. However, it has not been clarified why cells continue cell division after their monolayer confluent state. Here we show that mechanical vibration not only weakens cell-cell adhesion bound by β-catenin but also promotes to move β-catenin from the cytoplasm to the nuclei, where β-catenin associates with DNA-binding members of the Tcf/LEF family and other associated transcription factors including cell division. After osteoblastic cells were cultured under 12.5 Hz and 0.5 G mechanical vibration, cells were fractionated into nuclear and cytoplasmic fractions using a centrifugation method. β-catenin in each fraction was detected by a western blot experiment. The protein bands from western blot films were quantified with an image processing and analysis software, ImageJ. As a result, the vibration group gave higher expression of β-catenin in nuclear fraction than the non-vibration group just after the vibration group reached the saturated cell density. It indicates that 12.5 Hz and 0.5 G mechanical vibration may promote to move β-catenin into the nuclei and the cell division.
2

Takagi, Yuta, Toshihiko Shiraishi, Shin Morishita, Ryohei Takeuchi, Tomoyuki Saito, and Yuko Mikuni-Takagaki. "Effects of Mechanical Vibration on Matrix Production and Proliferation of Three-Dimensional Cultured Chondrocytes." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-66805.

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This paper describes the effects of vibration stimulation on chondrocytes in three-dimensional culture in relation to the production of regenerative cartilage tissue, using collagen artificial skin as a carrier and supplementation with hyaluronic acid (used in the conservative treatment of osteoarthritis), and the mechanism of the adaptive response of chondrocytes to mechanical loading. The experimental condition imitates an environment of articular cartilage in vivo that chondrocytes are completely surrounded by the extracellular matrix and receives mechanical stimulation for the weight-bearing mechanics. Chondrocytes were isolated from articular cartilage of porcine metatarsophalangeal joints. Experiments were performed under four different culture conditions: control condition, in which chondrocytes were cultured with atelocollagen gel and collagen artificial skins, and no vibration (HA−Vib−); HA−Vib+, in which chondrocytes were cultured in atelocollagen gel and collagen artificial skins with vibration treatment for 2 weeks; HA+Vib−, in which chondrocytes were cultured in medium containing 0.1% hyaluronic acid; and HA+Vib+, in which chondrocytes were cultured in medium containing 0.1% hyaluronic acid with vibration treatment for 2 weeks. Histologic analysis was conducted at 14 days of culture. The proliferation of chondrocytes was obtained by counting the number of cells with a hemocytometer after 3, 7, 10, and 14 days of culture. The expression of Sox 9 and β-catenin was detected by western blotting analysis. Sox 9 has been reported of involvement in transcription of type IX collagen that binds cartilage-specific type II collagen fibrils. β-catenin plays an important role of signaling pathways of cell proliferation although the relationship between β-catenin and mechanical vibration stimulation has not been clarified yet. The obtained results are as follows. The mechanical vibration enhanced the thickness of extracellular matrix of chondrocytes in histologic section at 14 days of culture and increased the expression of Sox 9. In addition, the mechanical vibration significantly increased the number of chondrocytes after 10 days of culture and promoted the expression of β-catenin. These results show that mechanical vibration promotes the matrix production and proliferation of chondrocytes and that a part of important signaling pathways in relation to mechanical vibration stimulation and proliferation of chondrocytes has been revealed.
3

Jansen, Sepp R., Marieke van Ziel, Hoeke A. Baarsma, and Reinoud Gosens. "²-catenin Regulates Airway Smooth Muscle Contraction." 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.a5292.

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Joiner, Danese M., Bryan T. MacDonald, Xi He, Peter V. Hauschka, and Steven A. Goldstein. "Reduction of the Wnt Inhibitor Dkk1 Correlates With Improved Bone Mechanical and Morphological Properties in Mice." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175478.

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Abstract:
The Wnt/β-Catenin signaling pathway is a key regulator in bone development and bone homeostasis. Inactivating mutations in the Wnt co-receptor Low density lipoprotein Receptor related Protein 5 (LRP5) results in osteoporosis while “activating” mutations in LRP5 results in high bone mass. Dickkopf-1 (Dkk1) is a secreted Wnt inhibitor that binds to LRP5 and LRP6 reducing their availability to form a complex with Wnt and Frizzled and resulting in unrestrained Wnt signaling. It is expected that a decrease in Dkk1 will result in an increase in Wnt activity and ultimately a high bone mass phenotype. An allelic series of Dkk1 mutant mice were generated to examine the affects of reduced Dkk1 levels on bone density, morphology, and mechanical properties.
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Chen, Xi, Paul M. Evans, Wen Zhang, and Chunming Liu. "Abstract 998: KLF4 interacts with β-catenin/TCF4 and blocks p300/CBP recruitment by β-catenin." 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.am10-998.

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Russell, Susan R., Anna Lam, Annette Flozak, and Cara J. Gottardi. "Wnt/²-catenin Pathway Activation In Lung Injury." 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.a2713.

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Nurmemmedov, Elmar, Anton Cheltsov, and Peter K. Vogt. "Abstract 2520: Novel inhibitors of β-catenin." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2520.

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Clark, Alison D., Nicholas F. Dybdal-Hargreaves, and Susan L. Mooberry. "Abstract 349: Eribulin induces cortical localization of E-cadherin, p120-catenin and beta-catenin in 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.am2017-349.

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Zhang, Yixian, Steven Kim, Victoria Shi, Zhengxing Qu, Stephen Castaneda, Maoliang Wang, Peifang Zhu, David Filpula, Lee M. Greenberger, and Ivan D. Horak. "Abstract 601:In vitroandin vivoinhibition of β-catenin by two novel β-catenin RNA antagonists, EZN-3889 and 3892." 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.am10-601.

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Lin, Hsiao-Hui, Wen-Chi Feng, LI-Chun Lu, Ta-Wen Hsu, Ann-Lii Cheng, and Chih-Hung Hsu. "Abstract 2625: Increased sensitivity to Wnt/beta-catenin inhibitors in hepatocellular carcinoma cells harboring activating mutation of beta-catenin." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2625.

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Reports on the topic "Catenine":

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Rana, Basabi. Beta Catenin in Prostate Cancer Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada609572.

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Baswaran, Vijay, and Stephen W. Byers. Beta-Catenin Stability in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada375157.

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Rana, Basabi. Beta Catenin in Prostate Cancer Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580101.

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Rana, Basabi. Beta Catenin in Prostate Cancer Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada544420.

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Feltes, Carolyn. Beta Catenin-Regulated Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada381197.

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Feltes, Carolyn. Beta Catenin-Regulated Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2000. http://dx.doi.org/10.21236/ada396038.

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Teo, Marissa. IKK and Beta-Catenin in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407807.

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Byers, Stephen, and Keith Orford. Characterization of a beta-Catenin-Associated Kinase. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada405220.

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Byers, Stephen W. Characterization of a BETA-Catenin-Associated Kinase. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada375103.

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Byers, Stephen W. Characterization of a B-Catenin-Associated Kinase. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada375192.

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