Relevant bibliographies by topics / Wnt genes

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Academic literature on the topic 'Wnt genes'

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

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Journal articles on the topic "Wnt genes"

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Nusse, Roel, and Harold E. Varmus. "Wnt genes." Cell 69, no. 7 (June 1992): 1073–87. http://dx.doi.org/10.1016/0092-8674(92)90630-u.

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Parr, Brian A., and Andrew P. McMahon. "Wnt genes and vertebrate development." Current Opinion in Genetics & Development 4, no. 4 (August 1994): 523–28. http://dx.doi.org/10.1016/0959-437x(94)90067-d.

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Brueggmann, Doerthe, Jenny M. Jaque, Celeste Leigh Pearce, and Claire Templeman. "Expression of Wnt-Signaling Pathway Genes and Wnt-Target Genes in Human Endometriosis Tissue [25]." Obstetrics & Gynecology 125 (May 2015): 18S. http://dx.doi.org/10.1097/01.aog.0000465314.25702.ef.

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Girich, A. S., and A. V. Boyko. "Wnt and Frizzled Genes in Echinoderms." Russian Journal of Marine Biology 45, no. 4 (July 2019): 302–12. http://dx.doi.org/10.1134/s1063074019040072.

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Hogvall, Mattias, Bruno C. Vellutini, José M. Martín-Durán, Andreas Hejnol, Graham E. Budd, and Ralf Janssen. "Embryonic expression of priapulid Wnt genes." Development Genes and Evolution 229, no. 4 (July 2019): 125–35. http://dx.doi.org/10.1007/s00427-019-00636-6.

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Krauss, S., V. Korzh, A. Fjose, and T. Johansen. "Expression of four zebrafish wnt-related genes during embryogenesis." Development 116, no. 1 (September 1, 1992): 249–59. http://dx.doi.org/10.1242/dev.116.1.249.

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The wnt gene family codes for a group of cysteine-rich, secreted proteins, which are differentially expressed in the developing embryo and are possibly involved in cellular communication. Here, we describe the polymerase chain reaction based cloning and embryonic expression patterns of four zebrafish wnt-related sequences; wnt[a], wnt[b], wnt[c] and wnt[d]. One of these genes, wnt[a], is a potential homologue of murine Wnt-3, while the other three genes most likely represent new members of the vertebrate wnt gene family. In zebrafish embryos, transcripts of wnt[a] are confined to the dorsal diencephalon, the dorsal midbrain, the rhombic lips and the dorsal portions of the spinal cord. wnt[b] is expressed in the tail bud and at considerably lower levels in the mesoderm of the head. wnt[c] transcripts are present within the diencephalon and the posterior midbrain whereas wnt[d] shows a surprisingly similar expression pattern to zebrafish wnt-1. By analogy to wnt-1, it is likely that the members of the zebrafish wnt gene family play an important role in cell-to-cell signalling during pattern formation in the neural tube and the tail bud.
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Wong, G. T., B. J. Gavin, and A. P. McMahon. "Differential transformation of mammary epithelial cells by Wnt genes." Molecular and Cellular Biology 14, no. 9 (September 1994): 6278–86. http://dx.doi.org/10.1128/mcb.14.9.6278.

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The mouse Wnt family includes at least 10 genes that encode structurally related secreted glycoproteins. Wnt-1 and Wnt-3 were originally identified as oncogenes activated by the insertion of mouse mammary tumor virus in virus-induced mammary adenocarcinomas, although they are not expressed in the normal mammary gland. However, five other Wnt genes are differentially expressed during development of adult mammary tissue, suggesting that they may play distinct roles in various phases of mammary gland growth and development. Induction of transformation by Wnt-1 and Wnt-3 may be due to interference with these normal regulatory events; however, there is no direct evidence for this hypothesis. We have tested Wnt family members for the ability to induce transformation of cultured mammary cells. The results demonstrate that the Wnt gene family can be divided into three groups depending on their ability to induce morphological transformation and altered growth characteristics of the C57MG mammary epithelial cell line. Wnt-1, Wnt-3A, and Wnt-7A were highly transforming and induced colonies which formed and shed balls of cells. Wnt-2, Wnt-5B, and Wnt-7B also induced transformation but with a lower frequency and an apparent decrease in saturation density. In contrast, Wnt-6 and two other family members which are normally expressed in C57MG cells, Wnt-4 and Wnt-5A, failed to induce transformation. These data demonstrate that the Wnt genes have distinct effects on cell growth and should not be regarded as functionally equivalent.
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Wong, G. T., B. J. Gavin, and A. P. McMahon. "Differential transformation of mammary epithelial cells by Wnt genes." Molecular and Cellular Biology 14, no. 9 (September 1994): 6278–86. http://dx.doi.org/10.1128/mcb.14.9.6278-6286.1994.

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The mouse Wnt family includes at least 10 genes that encode structurally related secreted glycoproteins. Wnt-1 and Wnt-3 were originally identified as oncogenes activated by the insertion of mouse mammary tumor virus in virus-induced mammary adenocarcinomas, although they are not expressed in the normal mammary gland. However, five other Wnt genes are differentially expressed during development of adult mammary tissue, suggesting that they may play distinct roles in various phases of mammary gland growth and development. Induction of transformation by Wnt-1 and Wnt-3 may be due to interference with these normal regulatory events; however, there is no direct evidence for this hypothesis. We have tested Wnt family members for the ability to induce transformation of cultured mammary cells. The results demonstrate that the Wnt gene family can be divided into three groups depending on their ability to induce morphological transformation and altered growth characteristics of the C57MG mammary epithelial cell line. Wnt-1, Wnt-3A, and Wnt-7A were highly transforming and induced colonies which formed and shed balls of cells. Wnt-2, Wnt-5B, and Wnt-7B also induced transformation but with a lower frequency and an apparent decrease in saturation density. In contrast, Wnt-6 and two other family members which are normally expressed in C57MG cells, Wnt-4 and Wnt-5A, failed to induce transformation. These data demonstrate that the Wnt genes have distinct effects on cell growth and should not be regarded as functionally equivalent.
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Jackstadt, Rene, Michael Charles Hodder, and Owen James Sansom. "WNT and β-Catenin in Cancer: Genes and Therapy." Annual Review of Cancer Biology 4, no. 1 (March 9, 2020): 177–96. http://dx.doi.org/10.1146/annurev-cancerbio-030419-033628.

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The WNT pathway is a pleiotropic signaling pathway that controls developmental processes, tissue homeostasis, and cancer. The WNT pathway is commonly mutated in many cancers, leading to widespread research into the role of WNT signaling in carcinogenesis. Understanding which cancers are reliant upon WNT activation and which components of the WNT signaling pathway are mutated is paramount to advancing therapeutic strategies. In addition, building holistic insights into the role of WNT signaling in not only tumor cells but also the tumor microenvironment is a vital area of research and may be a promising therapeutic strategy in multiple immunologically inert cancers. Novel compounds aimed at modulating the WNT signaling pathway using diverse mechanisms are currently under investigation in preclinical/early clinical studies. Here, we review how the WNT pathway is activated in multiple cancers and discuss current strategies to target aberrant WNT signaling.
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Ding, Xin, Junxia Liu, Lu Zheng, Jiangbo Song, Niannian Li, Hai Hu, Xiaoling Tong, and Fangyin Dai. "Genome-Wide Identification and Expression Profiling of Wnt Family Genes in the Silkworm, Bombyx mori." International Journal of Molecular Sciences 20, no. 5 (March 11, 2019): 1221. http://dx.doi.org/10.3390/ijms20051221.

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Wnt is a family of conserved glycoproteins that participate in a variety of important biological processes including embryo development, cell proliferation and differentiation, and tissue regeneration. The Wnt family is a metazoan novelty found in all animal phyla. Studies have revealed that the number of Wnt genes varies among species, presumably due to reproduction and loss of genes during evolution. However, a comprehensive inventory of Wnt genes in Lepidoptera is lacking. In this study, we identified the repertoire of Wnt genes in the silkworm and seven other species of Lepidoptera and obtained eight Wnt genes (Wnt1, Wnt5–Wnt7, Wnt9–Wnt11, and WntA) in each species. Four of these Wnt genes are clustered in two orientations (5′-Wnt9-Wnt1-Wnt6-Wnt10-3′ and 5′-Wnt10-Wnt6-Wnt1-Wnt9-3′) in both moths and butterflies. Transcript analysis of Wnt in silkworm embryonic stages showed that each BmWnt gene had a unique expression pattern during embryological development. Analysis of a larval stage revealed differential expression of Wnt family members in diverse tissues. Our study provides an overview of the Wnt family in Lepidoptera and will inspire further functional study of the Wnt genes in the silkworm.
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Dissertations / Theses on the topic "Wnt genes"

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Huguet, Emmanuel L. "Wnt genes in human breast biology." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297228.

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Torres, Monica Alexandra. "WNT signaling pathways in Xenopus laevis /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6293.

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Nambiar, Roopa. "Zebrafish hdac1 reciprocally regulates the canonical and non-canonical Wnt pathways." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1150313622.

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Lako, Majlinda. "Identifying and characterising novel human WNT genes." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242351.

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Leal, Letícia Ferro. "Via Wnt/?-catenina em tumores adrenocorticais pediátricos." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/17/17144/tde-06012016-181445/.

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Introdução: Em crianças das regiões Sul e Sudeste do Brasil há uma incidência elevada de tumores adrenocorticais (TAC). Anormalidades da ?-catenina tem sido encontradas em TAC em adultos e sugerem a ativação da via Wnt/ -catenina nestes tumores. No entanto, não há estudos avaliando o papel desta via em casuísticas de TAC pediátricos. Objetivos: Avaliar o papel da via Wnt/catenina e mutações do gene CTNNB1 na tumorigênese adrenocortical pediátrica. Indivíduos, Material e Métodos: Foram avaliados 62 pacientes pediátricos com TAC oriundos de dois centros de referência. Controles: córtex adrenal de indivíduos jovens com morte acidental. Avaliou-se a presença de mutação nos genes TP53 e CTNNB1. A expressão de genes da via Wnt (CTNNB1, o ligante WNT4, os inibidores SFRP1, DKK3 e AXIN1, o fator de transcrição TCF7 e os genes-alvo MYC e WISP2) foi avaliada por qPCR, utilizando-se o método de 2-Ct. Adicionalmente, a expressão de proteínas da via Wnt/-catenina e P53 foi avaliada por imunoistoquímica. Avaliou-se a relação entre possíveis anormalidades moleculares com o fenótipo clínico e o desfecho. Resultados: A sobrevida geral foi maior em pacientes menores que 5 anos de idade (p<0.0001) e em pacientes com estágios tumorais menos avançados (p<0.0001). A mutação P53 p.R337H foi encontrada em 87% dos pacientes e não se associou com características clinicopatológicas ou desfecho. Mutações do gene CTNNB1 foram encontradas em 4/62 (6%) TAC, todos carreadores da mutação P53 p.R337H. Houve associação entre óbito e presença de mutações do gene CTNNB1 (p=0,02). Acúmulo difuso da -catenina foi observado em 71% dos TAC, a maioria sem mutações do CTNNB1. Comparados a adrenais normais, os TAC apresentaram aumento da expressão do RNAm de CTNNB1 (p=0.008) e diminuição da expressão de genes inibidores da via Wnt: DKK3 (p<0.0001), SFRP1 (p=0.05) e AXIN1 (p=0.04). Com relação aos genes-alvo da via Wnt/-catenina, TAC apresentaram expressão aumentada de WISP2 e baixa expressão de MYC. Maior sobrevida geral foi associada à expressão baixa de SFRP1 (p=0.01), WNT4 (p=0.004) e TCF7 (p<0.01). Conclusões: Em TAC pediátricos, mutações somáticas ativadoras do gene CTNNB1 são pouco freqüentes e parecem estar associadas à maior ocorrência de óbito. Mesmo na ausência de mutações do gene CTNNB1, estes tumores apresentaram acúmulo de -catenina e do gene-alvo WISP2 e expressão reduzida de inibidores da via Wnt (DKK3, SFRP1 e AXIN1). Estes dados demonstram evidências de anormalidades na via Wnt/-catenina em TAC pediátricos, mesmo na ausência de mutações do gene CTNNB1. É provável que outros eventos genéticos afetando a via Wnt/-catenina estejam envolvidos na tumorigênese adrenocortical pediátrica
Context: CTNNB1 mutations and activation of Wnt/-catenin pathway are frequent in adult adrenocortical tumors (ACTs) but data on childhood ACTs are lacking. Objective: To investigate Wnt/-catenin pathway abnormalities and CTNNB1 mutations in childhood ACTs. Patients and Methods: Clinicopathological findings and outcome of 62 childhood ACTs patients were analyzed regarding to CTNNB1/ -catenin mutations and to the expression of Wnt-related genes (CTNNB1, a Wnt ligand: WNT4, Wnt inhibitors: SFRP1, DKK3 and AXIN1, a transcription factor: TCF7, and target genes: MYC and WISP2) by qPCR and immunohistochemistry. Results: Overall survival (OS) was higher in patients younger than 5 years (p<0.0001) and associated with less advanced tumoral stage (p<0.0001). The p.R337H P53 mutation, found in 87% of the patients, was not associated with clinicopathological findings or outcome. CTNNB1 activating mutations were found in only 4/62 ACTs (6%), all of them harboring TP53 mutation. There was association between the presence of CTNNB1 mutation and death (p=0.02). Diffuse -catenin accumulation was found in 71% of ACTs, most of them without CTNNB1 mutation. CTNNB1 mutated ACTs presented weak/moderate -catenin accumulation. Compared to normal adrenals, ACTs presented increased expression of CTNNB1 (p=0.008) and underexpression of Wnt inhibitor genes: DKK3 (p<0.0001), SFRP1 (p=0.05) and AXIN1 (p=0.04). With regards to Wnt/-catenin target genes, ACTs presented lower expression of MYC but increased expression of WISP2. Higher overall survival was associated with underexpression of SFRP1 (p=0.01), WNT4 (p=0.004) and TCF7 (p<0.01). Conclusions: In childhood ACTs, CTNNB1 mutations are rare and appear to be associated with poor prognosis. Regardless of CTNNB1 mutations, these tumors presented reduced expression of Wnt inhibitor genes (DKK3, SFRP1 and AXIN1) and increased expression of CTNNB1 and a target gene, WISP2. Thus, besides CTNNB1 mutations, additional genetic events affecting the Wnt/-catenin pathway may be involved in childhood adrenocortical tumorigenesis.
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Chow, Hei-man, and 周熙文. "Hormonal, chemical, and transcriptional regulations of Wnt/{221}-catenin signaling in mammary carcinogensis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4589100X.

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Ng, Chun-laam, and 吳圳嵐. "Wnt inhibitory factor 1 (Wif-1) coordinates Shh and Wnt signaling activities in urorectal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48329629.

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In vertebrates, the urogenital sinus and the hindgut are connected at a hollow region called cloaca. A midline mesenchymal structure known as urorectal septum (urs) descends from the ventral body wall to separate the urogenital sinus from the hindgut before the formation of an anal opening. Subsequent cloaca membrane regression at the ventral midline of the genital tubercle (GT) is crucial for the formation of an anal opening. These two events are important during cloaca septation in urorectal development. Mice with defective Shh or Wnt signaling displayed similar urorectal defects such as GT agenesis, un-partitioned cloaca (persistent cloaca) and proximal urethral opening that are attributable to increased cell apoptosis. Furthermore, Shh and Wnt signal transduction coordinate with each other and regulate cell survival of the developing urorectum. However, the molecular mechanisms by which these two signaling pathways coordinate in urorectal development remain unclear. We previously identified Wnt inhibitory factor1 (Wif1) from Affymetrix array analysis for genes/pathways that is implicated in urorectal development. Wif1 is a secreted protein that binds directly to Wnt ligands preventing Wnts from binding to receptors. This leads to -catenin degradation and thereby inhibits their activities. It is known that Wif1 binds to Wnt3a and Wnt5a with high affinity and deletion of Wnt3a, Wnt5a and -catenin in mice caused GT agenesis, persistent cloaca and proximal hypospadias. Using ETU-induced anorectal malformations model, I found out that Wif1 is ectopically expressed in the un-tubularized and un-septated urorectum. Wif1 is mainly expressed at the fusing endoderm that associates with programmed cell death during cloaca septation. Exogenous addition of Wif1 protein in urorectum culture also caused cloaca membrane disintegration, and proximal urethral opening that may be due to aberrant apoptosis. Shh and Wif1 are differentially expressed at the cloaca endoderm. In normal mice, Shh is highly expressed at the cloaca endoderm except those Wif1-expressing endodermal cells. Blockage of Shh pathway by cyclopamine in urorectum culture induced ectopic expression of Wif1, concomitant with genital tubercle hypoplasia and un-septated cloaca. More importantly, deletion of Shh in mice hastened Wif1 expression at the cloaca membrane endoderm and elicited increased cell death in the Wif1 expressing endoderm. Wif1-/- embryos display urorectal defects including delayed genital outgrowth and proximal hypospadias. Therefore, disruption of spatiotemporal expression of Wif1 could lead to defective Wnt signaling and contributes to abnormal urorectal development in Shh-/- mutant. Current study revealed that Wif1 is involved in urorectal development and is implicated in urorectal defects. It may function as a pro-apoptotic factor to regulate endodermal cell death which is essential for the septation process. Its specific expression is restricted at the midline cloaca endoderm by Shh signaling to inhibit local Wnt--catenin activities during cloaca septation. I proposed novel hypothetical models to explain (1) the significance of the tempo-spatial expression of Wif1; (2) the significance of cell death; and (3) the molecular mechanism that Shh signaling regulates Wnt signaling activities through Wif1 in urorectal development.
published_or_final_version
Surgery
Doctoral
Doctor of Philosophy
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Railo, A. (Antti). "Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514261534.

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Abstract Wnt genes encode secreted signalling molecules that control embryonic development including organogenesis, while dysregulated Wnt signalling is connected to many diseases such as cancer. Specifically, Wnts control a number of cellular processes such as proliferation, adhesion, differentiation and aging. Many Wnt proteins activate the canonical β-catenin signalling pathway that regulates transcription of a still poorly characterized set of target genes. Wnts also transduce their signaling in cells via β-catenin-independent “non-canonical” pathways, which are not well understood. In this study, Wnt-11 signalling mechanisms in a mammalian model cell line and roles of Wnt-11 in heart development were analyzed in detail. In addition the aim was to identify new Wnt target genes by direct chromatin immunoprecipitation and Affymetrix GeneChip assays in the model cells exposed to Wnt-3a. Our studies reveal that Wnt-11 signalling coordinates the activity of key cell signalling pathways, namely the canonical Wnt/β-catenin, the JNK/AP-1, the NF-κB and PI3K/Akt pathways in the CHO cells. Analysis of the Wnt-11-deficient embryos revealed a crucial role in heart organogenesis. Wnt-11 signalling coordinates cell interactions during assembly of the myocardial wall and Wnt-11 localizes the expression of N-cadherin and β-catenin to specific cellular domains in the embryonic ventricular cardiomyocytes. Collectively these studies reveal that the mammalian Wnt-11 behaves as a non-canonical Wnt and that it is a critical factor in the coordination of heart development. Specifically, it controls components of the cell adhesion machinery. Analysis of the Wnt target genes revealed a highly context-dependent profile in the Wnt-regulated genes. Several new putative target genes were discovered. Out of the candidate Wnt target genes, Disabled-2 was identified as a potential new direct target for Wnt signalling.
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Sobreira, Debora Rodrigues 1981. "Identificação de uma nova variante do gene Dapper1 gerada por splicing alternativo durante o desenvolvimento de vertebrados e sua analise numa abordagem evolutiva." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317676.

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Orientadores: Lucia Elvira Alvares, Jose Xavier Neto
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-13T10:17:43Z (GMT). No. of bitstreams: 1 Sobreira_DeboraRodrigues_M.pdf: 2481929 bytes, checksum: 2cb1105ccc78322b5f11f4528108d2fc (MD5) Previous issue date: 2009
Resumo: Splicing Alternativo é um mecanismo importante para expandir a diversidade protéica em eucariotos. Este processo permite a produção de diferentes mRNAs a partir de uma mesma molécula de pré-RNA e é freqüentemente utilizado pelos genes envolvidos no desenvolvimento embrionário. O gene Oapper1 (Opr1) é um importante modulador da via de sinalização Wnt, atuando em diversos processos como especificação do tecido neural, morfogênese cefálica e desenvolvimento do coração e olho. Entre seus parceiros estão as '1lOléculas Dishevelled, o fator de transcrição TCF-3 (ambas as moléculas envolvidas na sinalização Wnt) e Dbf-4 (regulador do ciclo celular). Considerando que Dpr1 possui uma estrutura modular e interage com diferentes parceiros moleculares através de diferentes domínios estruturais, esta molécula poderia utilizar a maquinaria de Splicing Alternativo para combinar diferentes domínios e conseqüentemente ampliar suas funções biológicas. Neste estudo, descrevemos uma nova Variante do gene Opr1, identificada inicialmente no transcriptoma de camundongo utilizando ferramentas de Bioinformática. Esta nova Variante é maior em 111 pb em relação à codificada pela seqüência referência de RNAm para Dpr1 RefSeq, as quais são denominadas, respectivamente, como Variante A e Variante B. Estes transcritos variantes são gerados por dois sítios aceptores de Splicing distintos presentes no início do exon 4. O segmento exclusivo da Variante A codifica 37 aminoácidos localizados na região onde Opr1 se associa ao fator transcricional TCF-3. Uma análise comparativa do lócus de Opr1 entre diversos vertebrados (peixe, anfíbio, galinha, camundongo e humano) revelou que ambos os sítios aceptores de Splicing são conservados nos tetrápodas, enquanto que em peixe apenas um sítio é encontrado. Ensaios de RT-PCR confirmaram nossos resultados obtidos em Bioinformática. Além disso, demonstramos que ambas as Variantes são co-expressas ao longo do desenvolvimento de galinha, sugerindo que a concentração relativa dessas moléculas pode ser importante para a sua função. Finalmente, análises de pressão seletiva foram realizadas para a molécula de Dpr1. Apesar de não se confirmar a presença de seleção positiva ao longo da proteína Dpr1, o exon 4 parece estar sob pressão seletiva mais relaxada quando comparado aos outros exons. Nossos resultados são consistentes com a hipótese de que o mecanismo de Splicing Alternativo atua acelerando a evolução, reduzindo a seleção negativa.
Abstract: Alternative splicing is an important mechanism to expand protein diversity in eukaryotes. This process allows the production of different mRNAs from a single coding sequence and is frequentfy used by genes involved in development. Oapper 1 (Opr1) is an important rnodulator of Wnt signalling, working in several developmental processes, such as neural tissue specification, head morphogenesis, heart and eye development. While its interaction with Oishevelled is known to modulate Wnt signalling both in vivo and in vitre, the interaction wrth other molecules is required to mediate its multiple biological functions. Considering that Dpr1 has a modular structure that mediates its interaction with different partners through different structural domains, this molecule could greatly benefit from alternative splicing in order to combine different domains and consequently amplify its biological functions. In the present study we describe a new Opr1 isoform that was initially identified in the mouse transcriptome using bioinformatic tools. This isoform is 111 pb longer than the one encoded by the RefSeq mRNA for Opr1, here named O and E isoforms, respectively. The variant transcripts are generated through two distinct acceptor splice sites in exon 4. The segment exclusive of the O isoform is in frame and encodes 37 residues located in a variable region of Oprl exon 4, known to be necessary for the interaction with the transcriptional factor Tcf3. comparative analysis of the Opr1 locus among fish, frog, chicken, mouse and human revealed that in tetrapods two acceptor splice sites are conserved in the beginning of the exon 4, while in fish a single acceptor splice site is found. RT-PCR using species-specific primers confirmed the expression of the O and E isoforms in tetrapods while in fish only the O isoform was detected. In addition, we showed that the Opr1 isoforms are coexpressed throughout chicken development, suggesting that the relative concentration of these molecules may be important for their functionality. Finally, even though no evidence of positive selection was detected for the entire Dpr1 protein, exon 4 seems to be under more relaxed selective pressure than the other exons. These results are consistent with the notion that alternative splicing can act as a mechanism for opening accelerated paths of evolution by reducing negative selection pressure.
Mestrado
Histologia
Mestre em Biologia Celular e Estrutural
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Ho, Sze-hang, and 何思恆. "Differential expression of Wnt inhibitors Dickkopf-1 (Dkk-1) and Wnt inhibitory factor-1 (Wif1) in the regulation of urorectal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207999.

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In mammals, the external genitalia, urinary tract and anorectal tract are developed from a common embryonic primordium, the urorectum. Cloaca is the hollow space inside the urorectum that connects the hindgut and the urogenital sinus. During the urorectal development, the external genitalia is formed from the outgrowth of genital tubercle (GT) protruding from the urorectum, while the future urinary tract and anorectal tract are formed by the partition of cloaca during cloacal septation. GT outgrowth and cloacal septation are important developmental events for the formation of genitourinary and anorectal system. In human, dysregulation of these developmental events results in congenital anorectal malformations (ARM). Wnt signaling is one of the key signaling pathways that regulates urorectal development. The activity of Wnt signaling is initiated by the binding of Wnt ligands to cell surface receptors, which can be antagonized by secretory Wnt inhibitors. Dickkopf1 (Dkk1) and Wnt inhibitory factor 1 (Wif1) are secretory Wnt inhibitors implicated in urorectal development. However, the functions of other secretory Wnt inhibitors during urorectal developments remain to be elucidated. In this study, expression analyses showed that Dkk1, Dickkopf2 (Dkk2), Dickkopf4 (Dkk4), Secreted Frizzled-related Protein 1 (Sfrp1) and Wif1 were expressed in the developing urorectum. The dynamic, overlapping and restricted expression patterns of these Wnt inhibitors were closely associated with the GT outgrowth and the cloacal septation events, implying that these Wnt inhibitors functioned in a coordinated manner in defining the field of Wnt signaling activities in the developing urorectum. Wif1 knockout mice (〖Wif1〗^(-/-)) was used as the model to investigate the functions of and the interplay between secretory Wnt inhibitors in urorectal development. GT outgrowth and cloacal septation defects were observed in 〖Wif1〗^(-/-) embryos. Most of the 〖Wif1〗^(-/-) embryos displayed varying degrees of GT outgrowth defects, while septation defects were only occasionally observed. This suggested that GT outgrowth and cloacal septation were regulated by Wif1 via different regulatory mechanisms. In the urorectum of 〖Wif1〗^(-/-) embryos, Dkk1 was significantly upregulated in the peri-cloacal mesenchyme. Further expression analysis suggested that Dkk1 was sufficient to rescue cloacal septation defects but not GT outgrowth defects in 〖Wif1〗^(-/-)embryos. In the 〖Wif1〗^(-/-) embryos with severe GT outgrowth defects, the Fgf8-expressing distal urethral epithelium, the signaling center in the urorectum, was absent, suggesting that the GT outgrowth defects could be contributed by the loss of dUE-expressing signals such as Fgf8. This study demonstrated the importance of secretory Wnt inhibitors in the GT outgrowth and cloacal septation and suggested that secretory Wnt inhibitors played partially overlapping roles in urorectal development. A rescue mechanism for cloacal septation performed by Dkk1 upon Wif1 deletion was proposed. Such auto-regulatory mechanism within the Wnt signaling pathway indicated that Wnt inhibitors play essential regulatory roles in the urorectal development and a balanced Wnt signaling activity modulated by Wnt inhibitors is crucial to the development of urorectum.
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Books on the topic "Wnt genes"

1

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

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

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Hagens, Olivier. An investigation of two novel genes associated with Wnt signalling in Drosophila melanogaster. Brighton, UK: University of Sussex, 2000.

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Nusse, Roel, Xi He, and Renee van Amerongen. Wnt signaling: A subject collection from Cold Spring harbor perspectives in biology. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2012.

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Kahn, Michael. Targeting the Wnt pathway in cancer. New York: Springer, 2011.

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Derkx, Peter, and Felix van de Laar. Genen, wat willen we ermee?: 21 wetenschappers over de consequenties van genomics. Antwerpen: Garant, 2012.

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Jameson, Richard T. They went thataway: Redefining film genres : a National Society of Film Critics video guide. San Francisco: Mercury House, 1994.

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Bauernsatiren: Entstehung und Entwicklung des bäuerlichen Genres in der deutschen und niederländischen Kunst ca. 1470-1570. Niederzier: Lukassen, 1986.

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Schröder, Martin. Humor und Dialekt: Untersuchungen zur Genese sprachlicher Konnotationen am Beispiel der niederdeutschen Folklore und Literatur. Neumünster: K. Wachholtz, 1995.

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We all want to change the world: Rock and politics from Elvis to Eminem. Lanham, MD: Taylor Trade Pub., 2005.

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Book chapters on the topic "Wnt genes"

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Bergstein, Ivan, and Anthony M. C. Brown. "WNT Genes and Breast Cancer." In Breast Cancer, 181–98. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-456-6_8.

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Sun, Zijie, and Suk Hyung Lee. "Androgen Action, Wnt Signaling, and Prostate Tumorigenesis." In Androgen-Responsive Genes in Prostate Cancer, 101–16. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6182-1_7.

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Bordet, Guillaume, and Vincent Bertrand. "Zic Genes in Nematodes: A Role in Nervous System Development and Wnt Signaling." In Advances in Experimental Medicine and Biology, 59–68. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7311-3_4.

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Edwards, Paul A. W., Clare Abram, Susan E. Hiby, Christina Niemeyer, Trevor C. Dale, and Jane M. Bradbury. "The Role of erbB-Family Genes and Wnt Genes in Normal and Preneoplastic Mammary Epithelium, Studied by Tissue Reconstitution." In Intercellular Signalling in the Mammary Gland, 57–66. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_6.

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Planutis, Kestutis, Marina Planutiene, and Randall F. Holcombe. "In Situ Hybridization to Evaluate the Expression of Wnt and Frizzled Genes in Mammalian Tissues." In Methods in Molecular Biology, 231–41. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-249-6_18.

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Aoki, Koji, and Makoto M. Taketo. "Tissue-Specific Transgenic, Conditional Knockout and Knock-In Mice of Genes in the Canonical Wnt Signaling Pathway." In Methods in Molecular Biology, 307–31. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-249-6_24.

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Zhang, Chen U., and Ken M. Cadigan. "An Overview of Gene Regulation by Wnt/β-Catenin Signaling." In Wnt Signaling in Development and Disease, 51–71. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118444122.ch4.

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Bryant, J. "Introduction: Part II–Genomes, genes and proteins." In WIT Transactions on State-of-the-art in Science and Engineering, 13–27. Southampton UK: WIT Press, 2006. http://dx.doi.org/10.2495/978-1-85312-853-0/02.

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Weber-Hall, Stephen, Deborah Phippard, Christina Niemeyer, and Trevor Dale. "Developmental and Hormonal Regulation of Wnt Gene Expression in the Mouse Mammary Gland." In Intercellular Signalling in the Mammary Gland, 105–6. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_26.

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Tanner, Matthew J., Elina Levina, Michael Shtutman, Mengqian Chen, Patrice Ohouo, and Ralph Buttyan. "Unique Effects of Wnt Signaling on Prostate Cancer Cells: Modulation of the Androgen Signaling Pathway by Interactions of the Androgen Receptor Gene and Protein with Key Components of the Canonical Wnt Signaling Pathway." In Androgen Action in Prostate Cancer, 569–86. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-69179-4_24.

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Conference papers on the topic "Wnt genes"

1

Phillip, Cornel J., and Carlos S. Moreno. "Abstract 4932: Genistein Can Induce Demethylation Of Wnt Negative Regulatory Genes In Prostate Cancer Cells." 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.am10-4932.

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Bernabe-Dones, Raul D., Sharon C. Fonseca-Williams, Mercedes Y. Lacourt-Ventura, Cristina Muñoz, Maribel Tirado-Gomez, and Marcia R. Cruz-Correa. "Abstract 4783: Expression of genes panel related to WNT- signaling in colorectal cancer Human Papillomavirus-positive colorectal cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4783.

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Komatsu, Hisateru, Atsushi Niida, Masami Ueda, Hidenari Hirata, Ryutaro Uchi, Sho Nambara, Tomoko Saito, et al. "Abstract 1948: In silico screening for novel Wnt/β-catenin pathway target and regulator genes in human hepatocellular carcinoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1948.

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Ripple, Michael J., Amanda Struckhoff, Robin McGoey, and Luis Del Valle. "Abstract 4774: JC virus T-antigen-dependent activation of Wnt target genes and cell cycle progression in colon cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4774.

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Bobbs, Alexander, William Morgan Hallas, Katrina Gellerman, Stancy Joseph, and Karen Cowden Dahl. "Abstract POSTER-BIOL-1303: ARID3B alters tumor cell adhesion by binding to the promoter regions in fzd5 and other wnt pathway genes." In Abstracts: 10th Biennial Ovarian Cancer Research Symposium; September 8-9, 2014; Seattle, WA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.ovcasymp14-poster-biol-1303.

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Januskevicius, Andrius, Simona Lavinskiene, Reinoud Gosens, Ieva Janulaityte, Deimante Hoppenot, Raimundas Sakalauskas, and Kestutis Malakauskas. "LSC Abstract – Eosinophils enhance WNT-5a and TGF-β1 genes expression in airway smooth muscle cells and promote their proliferation in asthma." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa632.

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Januskevicius, Andrius, Simona Lavinskiene, Reinoud Gosens, Ieva Janulaityte, Deimante Hoppenot, Raimundas Sakalauskas, and Kestutis Malakauskas. "LSC Abstract – Eosinophils enhance WNT-5a and TGF-β1 genes expression in airway smooth muscle cells and promote their proliferation in asthma." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pp222.

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Linnekamp, Janneke, Raju Kandimalla, Louis Vermeulen, Hanneke van Laarhoven, and Jan Paul Medema. "Abstract 5273: Role of methylation of Wnt target genes in tumorigenesis and effect of re-expression with demethylating agent decitabine in colon cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5273.

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Sarkar, Dipak K., Shaima Jabbar, and Omkaram Gangisetty. "Abstract 1125: Developmental pluripotency associated 4 oncogene interacts with Wnt/β-catenin signaling and stem cells regulatory genes to control pituitary tumor cells invasiveness." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1125.

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Luo, Li Z., Ewa Krawczyk, Anbarasu Lourdusamy, Lisa C. Storer, Lingling Xian, Kenneth J. Cohen, Richard Schlegel, Richard Grundy, and Linda Resar. "Abstract LB-224: A novel model of pediatric spinal ependymoma using conditionally reprogrammed cells from a primary tumor demonstrates aberrant expression ofHMGA, HOX, MYCand other Wnt target genes." 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-lb-224.

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Reports on the topic "Wnt genes"

1

Wang, Xianshu. Analysis of Human AXIN2 and Other Wnt Signal Pathway Genes in Human Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada415833.

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Huang, Shixia, and Harold Varmus. The Use of cDNA Microarray to Study Gene Expression in Wnt-1 Induced Mammary Tumors. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411264.

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