Relevant bibliographies by topics / Foxa

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Academic literature on the topic 'Foxa'

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

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Journal articles on the topic "Foxa"

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LIU, Yuanfang, Wei SHEN, Patricia L. BRUBAKER, Klaus H. KAESTNER, and Daniel J. DRUCKER. "Foxa3 (HNF-3γ) binds to and activates the rat proglucagon gene promoter but is not essential for proglucagon gene expression." Biochemical Journal 366, no. 2 (September 1, 2002): 633–41. http://dx.doi.org/10.1042/bj20020095.

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Members of the Forkhead box a (Foxa) transcription factor family are expressed in the liver, pancreatic islets and intestine and both Foxa1 and Foxa2 regulate proglucagon gene transcription. As Foxa proteins exhibit overlapping DNA-binding specificities, we examined the role of Foxa3 [hepatocyte nuclear factor (HNF)-3γ] in control of proglucagon gene expression. Foxa3 was detected by reverse transcriptase PCR in glucagon-producing cell lines and binds to the rat proglucagon gene G2 promoter element in GLUTag enteroendocrine cells. Although Foxa3 increased rat proglucagon promoter activity in BHK fibroblasts, augmentation of Foxa3 expression did not increase proglucagon promoter activity in GLUTag cells. Furthermore, adenoviral Foxa3 expression did not affect endogenous proglucagon gene expression in islet or intestinal endocrine cell lines. Although Foxa3-/- mice exhibit mild hypoglycaemia during a prolonged fast, the levels of proglucagon-derived peptides and proglucagon mRNA transcripts were comparable in tissues from wild-type and Foxa3-/- mice. These findings identify Foxa3 as a member of the proglucagon gene G2 element binding-protein family that, unlike Foxa1, is not essential for control of islet or intestinal proglucagon gene expression in vivo.
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Sharma, Sanjeev K., Ulrike Leinemann, Regine Ratke, Elke Oetjen, Roland Blume, Corinna Dickel, and Willhart Knepel. "Characterization of a novel Foxa (hepatocyte nuclear factor-3) site in the glucagon promoter that is conserved between rodents and humans." Biochemical Journal 389, no. 3 (July 26, 2005): 831–41. http://dx.doi.org/10.1042/bj20050334.

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The pancreatic islet hormone glucagon stimulates hepatic glucose production and thus maintains blood glucose levels in the fasting state. Transcription factors of the Foxa [Fox (forkhead box) subclass A; also known as HNF-3 (hepatocyte nuclear factor-3)] family are required for cell-specific activation of the glucagon gene in pancreatic islet α-cells. However, their action on the glucagon gene is poorly understood. In the present study, comparative sequence analysis and molecular characterization using protein–DNA binding and transient transfection assays revealed that the well-characterized Foxa-binding site in the G2 enhancer element of the rat glucagon gene is not conserved in humans and that the human G2 sequence lacks basal enhancer activity. A novel Foxa site was identified that is conserved in rats, mice and humans. It mediates activation of the glucagon gene by Foxa proteins and confers cell-specific promoter activity in glucagon-producing pancreatic islet α-cell lines. In contrast with previously identified Foxa-binding sites in the glucagon promoter, which bind nuclear Foxa2, the novel Foxa site was found to bind preferentially Foxa1 in nuclear extracts of a glucagon-producing pancreatic islet α-cell line, offering a mechanism that explains the decrease in glucagon gene expression in Foxa1-deficient mice. This site is located just upstream of the TATA box (between −30 and −50), suggesting a role for Foxa proteins in addition to direct transcriptional activation, such as a role in opening the chromatin at the start site of transcription of the glucagon gene.
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Yu, Xiuping, Kichiya Suzuki, Yongqing Wang, Aparna Gupta, Renjie Jin, Marie-Claire Orgebin-Crist, and Robert Matusik. "The Role of Forkhead Box A2 to Restrict Androgen-Regulated Gene Expression of Lipocalin 5 in the Mouse Epididymis." Molecular Endocrinology 20, no. 10 (October 1, 2006): 2418–31. http://dx.doi.org/10.1210/me.2006-0008.

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Abstract Murine epididymal retinoic acid-binding protein [or lipocalin 5 (Lcn5)] is synthesized and secreted by the principal cells of the mouse middle/distal caput epididymidis. A 5-kb promoter fragment of the Lcn5 gene can dictate androgen-dependent and epididymis region-specific gene expression in transgenic mice. Here, we reported that the 1.8-kb Lcn5 promoter confers epididymis region-specific gene expression in transgenic mice. To decipher the mechanism that directs transcription, 14 chimeric constructs that sequentially removed 100 bp of 1.8-kb Lcn5 promoter were generated and transfected into epididymal cells and nonepididymal cells. Transient transfection analysis revealed that 1.3 kb promoter fragment gave the strongest response to androgens. Between the 1.2-kb to 1.3-kb region, two androgen receptor (AR) binding sites were identified. Adjacent to AR binding sites, a Foxa2 [Fox (Forkhead box) subclass A] binding site was confirmed by gel shift assay. Similar Foxa binding sites were also found on the promoters of human and rat Lcn5, indicating the Foxa binding site is conserved among species. We previously reported that among the three members of Foxa family, Foxa1 and Foxa3 were absent in the epididymis whereas Foxa2 was detected in epididymal principal cells. Here, we report that Foxa2 displays a region-specific expression pattern along the epididymis: no staining observed in initial segment, light staining in proximal caput, gradiently heavier staining in middle and distal caput, and strongest staining in corpus and cauda, regions with little or no expression of Lcn5. In transient transfection experiments, Foxa2 expression inhibits AR induction of the Lcn5 promoter, which is consistent with the lack of expression of Lcn5 in the corpus and cauda. We conclude that Foxa2 functions as a repressor that restricts AR regulation of Lcn5 to a segment-specific pattern in the epididymis.
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Bach, Duc-Hiep, Nguyen Long, Thi-Thu-Trang Luu, Nguyen Anh, Sung Kwon, and Sang Lee. "The Dominant Role of Forkhead Box Proteins in Cancer." International Journal of Molecular Sciences 19, no. 10 (October 22, 2018): 3279. http://dx.doi.org/10.3390/ijms19103279.

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Forkhead box (FOX) proteins are multifaceted transcription factors that are significantly implicated in cancer, with various critical roles in biological processes. Herein, we provide an overview of several key members of the FOXA, FOXC, FOXM1, FOXO and FOXP subfamilies. Important pathophysiological processes of FOX transcription factors at multiple levels in a context-dependent manner are discussed. We also specifically summarize some major aspects of FOX transcription factors in association with cancer research such as drug resistance, tumor growth, genomic alterations or drivers of initiation. Finally, we suggest that targeting FOX proteins may be a potential therapeutic strategy to combat cancer.
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Gosalia, Nehal, Rui Yang, Jenny L. Kerschner, and Ann Harris. "FOXA2 regulates a network of genes involved in critical functions of human intestinal epithelial cells." Physiological Genomics 47, no. 7 (July 2015): 290–97. http://dx.doi.org/10.1152/physiolgenomics.00024.2015.

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The forkhead box A (FOXA) family of pioneer transcription factors is critical for the development of many endoderm-derived tissues. Their importance in regulating biological processes in the lung and liver is extensively characterized, though much less is known about their role in intestine. Here we investigate the contribution of FOXA2 to coordinating intestinal epithelial cell function using postconfluent Caco2 cells, differentiated into an enterocyte-like model. FOXA2 binding sites genome-wide were determined by ChIP-seq and direct targets of the factor were validated by ChIP-qPCR and siRNA-mediated depletion of FOXA1/2 followed by RT-qPCR. Peaks of FOXA2 occupancy were frequent at loci contributing to gene ontology pathways of regulation of cell migration, cell motion, and plasma membrane function. Depletion of both FOXA1 and FOXA2 led to a significant reduction in the expression of multiple transmembrane proteins including ion channels and transporters, which form a network that is essential for maintaining normal ion and solute transport. One of the targets was the adenosine A2B receptor, and reduced receptor mRNA levels were associated with a functional decrease in intracellular cyclic AMP. We also observed that 30% of FOXA2 binding sites contained a GATA motif and that FOXA1/A2 depletion reduced GATA-4, but not GATA-6 protein levels. These data show that FOXA2 plays a pivotal role in regulating intestinal epithelial cell function. Moreover, that the FOXA and GATA families of transcription factors may work cooperatively to regulate gene expression genome-wide in the intestinal epithelium.
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Kohler, Sarah, and Lisa Ann Cirillo. "Stable Chromatin Binding Prevents FoxA Acetylation, Preserving FoxA Chromatin Remodeling." Journal of Biological Chemistry 285, no. 1 (November 5, 2009): 464–72. http://dx.doi.org/10.1074/jbc.m109.063149.

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Kanamoto, Naotetsu, Tetsuya Tagami, Yoriko Ueda-Sakane, Masakatsu Sone, Masako Miura, Akihiro Yasoda, Naohisa Tamura, Hiroshi Arai, and Kazuwa Nakao. "Forkhead Box A1 (FOXA1) and A2 (FOXA2) Oppositely Regulate Human Type 1 Iodothyronine Deiodinase Gene in Liver." Endocrinology 153, no. 1 (January 1, 2012): 492–500. http://dx.doi.org/10.1210/en.2011-1310.

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Type 1 iodothyronine deiodinase (D1), a selenoenzyme that catalyzes the bioactivation of thyroid hormone, is expressed mainly in the liver. Its expression and activity are modulated by several factors, but the precise mechanism of its transcriptional regulation remains unclear. In the present study, we have analyzed the promoter of human D1 gene (hDIO1) to identify factors that prevalently increase D1 activity in the human liver. Deletion and mutation analyses demonstrated that a forkhead box (FOX)A binding site and an E-box site within the region between nucleotides −187 and −132 are important for hDIO1 promoter activity in the liver. EMSA demonstrated that FOXA1 and FOXA2 specifically bind to the FOXA binding site and that upstream stimulatory factor (USF) specifically binds to the E-box element. Overexpression of FOXA2 decreased hDIO1 promoter activity, and short interfering RNA-mediated knockdown of FOXA2 increased the expression of hDIO1 mRNA. In contrast, overexpression of USF1/2 increased hDIO1 promoter activity. Short interfering RNA-mediated knockdown of FOXA1 decreased the expression of hDIO1 mRNA, but knockdown of both FOXA1 and FOXA2 restored it. The response of the hDIO1 promoter to USF was greatly attenuated in the absence of FOXA1. Taken together, these results indicate that a balance of FOXA1 and FOXA2 expression modulates hDIO1 expression in the liver.
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Long, Lingyun, and Brett T. Spear. "FoxA Proteins Regulate H19 Endoderm Enhancer E1 and Exhibit Developmental Changes in Enhancer Binding In Vivo." Molecular and Cellular Biology 24, no. 21 (November 1, 2004): 9601–9. http://dx.doi.org/10.1128/mcb.24.21.9601-9609.2004.

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ABSTRACT Multiple enhancers govern developmental and tissue-specific expression of the H19-Igf2 locus, but factors that bind these elements have not been identified. Using chromatin immunoprecipitation, we have found two FoxA binding sites in the H19 E1 enhancer. Mutating these sites diminishes E1 activity in hepatoma cells. Additional chromatin immunoprecipitations show that FoxA binds to E1 in fetal liver, where H19 is abundantly expressed, but that binding decreases in adult liver, where H19 is no longer transcribed, even though FoxA proteins are present at both times. FoxA proteins are induced when F9 embryonal carcinoma cells differentiate into visceral endoderm (VE) and parietal endoderm (PE). We show that FoxA binds E1 in VE cells, where H19 is expressed, but not in PE cells, where H19 is silent. This correlation between FoxA binding and H19 expression indicates a role for FoxA in regulating H19, including developmental activation in the yolk sac and liver and postnatal repression in the liver. This is the first demonstration of a tissue-specific factor involved in developmental control of H19 expression. These data also indicate that the presence of FoxA proteins is not sufficient for binding but that additional mechanisms must govern the accessibility of FoxA proteins to their cognate binding sites within the H19 E1 enhancer.
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Thanan, Raynoo, Waleeporn Kaewlert, Chadamas Sakonsinsiri, Timpika Chaiprasert, Napat Armartmuntree, Duangkamon Muengsaen, Anchalee Techasen, et al. "Opposing Roles of FoxA1 and FoxA3 in Intrahepatic Cholangiocarcinoma Progression." International Journal of Molecular Sciences 21, no. 5 (March 5, 2020): 1796. http://dx.doi.org/10.3390/ijms21051796.

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Cholangiocarcinoma (CCA), a malignancy of biliary epithelium, is related to liver stem cell deregulation. FoxAs are a group of transcription factors that play critical roles in liver stem cell differentiation. In this study, the expression levels of FoxAs (i.e., FoxA1, FoxA2 and FoxA3) were detected in intrahepatic CCA tissues and the functions of FoxAs were studied in CCA cell lines. FoxA1 and FoxA2 were mainly localized in the nuclei of normal bile duct (NBD) cells and some of the cancer cells. Low expression of FoxA1 in CCA tissues (72%) was significantly correlated with poor prognosis. FoxA3 expression of CCA cells was localized in the nucleus and cytoplasm, whereas it was slightly detected in NBDs. High expression of FoxA3 in cancer tissues (61%) was significantly related to high metastasis status. These findings suggest the opposing roles of FoxA1 and FoxA3 in CCA. Moreover, the FoxA1-over-expressing CCA cell line exhibited a significant reduction in proliferative and invasive activities compared to control cells. Knockdown of FoxA3 in CCA cells resulted in a significant decrease in proliferative and invasive activities compared with control cells. Taken together, in CCA, FoxA1 is down-regulated and has tumor suppressive roles, whereas FoxA3 is up-regulated and has oncogenic roles.
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Rausa, Francisco M., Yongjun Tan, and Robert H. Costa. "Association between Hepatocyte Nuclear Factor 6 (HNF-6) and FoxA2 DNA Binding Domains Stimulates FoxA2 Transcriptional Activity but Inhibits HNF-6 DNA Binding." Molecular and Cellular Biology 23, no. 2 (January 15, 2003): 437–49. http://dx.doi.org/10.1128/mcb.23.2.437-449.2003.

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ABSTRACT In previous studies we used transgenic mice or recombinant adenovirus infection to increase hepatic expression of forkhead box A2 (FoxA2, previously called hepatocyte nuclear factor 3β [HNF-3β]), which caused diminished hepatocyte glycogen levels and reduced expression of glucose homeostasis genes. Because this diminished expression of FoxA2 target genes was associated with reduced levels of the Cut-Homeodomain HNF-6 transcription factor, we conducted the present study to determine whether there is a functional interaction between HNF-6 and FoxA2. Human hepatoma (HepG2) cotransfection assays demonstrated that HNF-6 synergistically stimulated FoxA2 but not FoxA1 or FoxA3 transcriptional activity, and protein-binding assays showed that this protein interaction required the HNF-6 Cut-Homeodomain and FoxA2 winged-helix DNA binding domains. Furthermore, we show that the HNF-6 Cut-Homeodomain sequences were sufficient to synergistically stimulate FoxA2 transcriptional activation by recruiting the p300/CBP coactivator proteins. This was supported by the fact that FoxA2 transcriptional synergy with HNF-6 was dependent on retention of the HNF-6 Cut domain LXXLL sequence, which mediated recruitment of the p300/CBP proteins. Moreover, cotransfection and DNA binding assays demonstrated that increased FoxA2 levels caused a decrease in HNF-6 transcriptional activation of the glucose transporter 2 (Glut-2) promoter by interfering with the binding of HNF-6 to its target DNA sequence. These data suggest that at a FoxA-specific site, HNF-6 serves as a coactivator protein to enhance FoxA2 transcription, whereas at an HNF-6-specific site, FoxA2 represses HNF-6 transcription by inhibiting HNF-6 DNA binding activity. This is the first reported example of a liver-enriched transcription factor (HNF-6) functioning as a coactivator protein to potentiate the transcriptional activity of another liver factor, FoxA2.
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Dissertations / Theses on the topic "Foxa"

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Mourad-Agha, Hanna. "Molecular analysis of the role of FoxR in regulation of the foxA gene of Salmonella enterica serovar Typhimurium." Thesis, University of Reading, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518217.

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Slebe, Concha Juan Felipe 1981. "The FoxA1/FoxA2-LIPG axis regulates beast cancer growth through changes in lipid metabolism." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/299798.

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The Fox transcription factor family comprises FoxA1, FoxA2 and FoxA3, which regulate tissue development and metabolism. In breast cancer, FoxA1 together with estrogen receptor regulates tumor growth and luminal specification. However, it is still unclear whether other members of the FoxA family participate in breast cancer pathogenesis and whether they contribute to tumor metabolic dependence. Here we show that FoxA1 and FoxA2 expression is mutually exclusive across different human breast cancer cell lines. Although both transcription factors regulate different set of genes and biological responses, they promote in vitro and in vivo tumor growth through the expression of endothelial lipase (LIPG). LIPG is ubiquitously expressed across various breast cancer subtypes, as seen in human cell lines and primary tumors. Furthermore, it has the capacity to rescue the loss of FoxA factors regulating a network enriched in oncogenic and structural lipids known to mediate proliferation. These findings collectively reveal how the FoxA1/FoxA2-LIPG axis regulates a central hub of lipids required for the growth of breast cancer.
La familia de factores de transcripción FoxA está compuesta por FoxA1, FoxA2 y FoxA3. Estos factores regulan el desarrollo y el metabolismo de diversos tejidos. En cáncer de mama, FoxA1 media la acción de estrógenos y andrógenos regulando la especificación y el crecimiento del subgrupo luminal. No obstante, aún es desconocida la participación de los otros miembros de la familia en el desarrollo tumoral o su posible función en la dependencia metabólica de éstos. En esta tesis se describió que la expresión de los factores de transcripción FoxA1 y FoxA2 es mutualmente exclusiva en diferentes líneas celulares de cáncer de mama humanas. A pesar de que FoxA1 y FoxA2 controlan diferentes programas génicos y diferentes respuestas biológicas, ambos promueven el crecimiento tumoral in vitro e in vivo regulando la expresión de la enzima lipasa endotelial (LIPG). LIPG se expresa ubícuamente en líneas celulares humanas y tumores primarios de diferentes subgrupos de cáncer de mama. Además, LIPG es capaz de rescatar la pérdida de los factores FoxA regulando una red de lípidos oncogénicos y estructurales que median proliferación. Estos hallazgos revelan colectivamente que el eje FoxA1/FoxA2-LIPG regula un nicho central de lípidos que son necesarios para el crecimiento de cáncer de mama.
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Makki, Rana M. K. "Characterisation of the role of the FoxA gene in Salmonella iron acquisition and virulence." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29842.

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FoxA is an iron-regulated outer membrane receptor protein of Salmonella enterica serovar Typhimurium that is required for utilisation of the trihydroxamate siderophore ferrioxamines, which acts as source of iron. In this study various approaches were attempted in order to clone the entire foxA gene. This was successfully achieved by use of a homologous recombination using a suicide vector strategy. Three different S. Typhimurium foxA mutant strains, SL2MK (this study), RK102 and TML/nr, were tested for growth responsiveness to ferrioxamine B using a plate bioassay. No response was observed for any of the mutant strains while of growth was clearly observed for both of the wild type strains. Mutant strains carrying the complementing foxA+ plasmid showed restored growth stimulation by ferrioxamine, confirming that the observed phenotypes were dependent on the presence or absence of the functional foxA gene. An analysis of the role of FoxA in Salmonella virulence was undertaken. An in vitro assay involving bacterial interaction with human dendritic cells demonstrated that, while mutation of the foxA gene had little or no effect on the ability of S. Typhimurium to invade and survive within dendritic cells, the foxA mutant was significant attenuated in its ability to damage these cells. However, investigations of the involvement of the foxA gene in Salmonella virulence using a murine model of infection yielded consistent evidence which suggested that the foxA gene is not critical for the pathogenesis of Salmonella . The foxA mutant strain SL2MK was able to infect and reside in the liver and spleen of mice infected intravenously to an extent similar to the wild type parent strain SL1344/nr and to the complemented mutant strain CSL2MK. In addition the foxA mutant and its wild type parent strain were recovered in similar numbers from the Peyer's patches, mesenteric lymph nodes, spleens and livers of mice infected by the oral route with these strains.
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Panowski, Siler Hubbell. "PHA-4/Foxa is essential and specific for dietary restriction induced longevity in C. elegans." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3398882.

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Thesis (Ph. D.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed May 19, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (leaves 123-131).
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Rosains, Jacqueline. "Modulation of pha-4/FoxA and C. elegans Foregut Development by the Novel Gene smg-8." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10379.

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FoxA transcription factors are central regulators of gut development in all species. In C. elegans, pha-4/FoxA is necessary to generate cells of the foregut, or pharynx. FoxA factors need to be precisely regulated for proper development, yet we know very little about FoxA regulation. To look for potential genes that act as pha-4 regulators, the Mango lab previously conducted two screens for suppressors of the lethality associated with a partial loss of pha-4 activity. Both screens uncovered smg-8, a novel gene that is highly conserved amongst metazoans. Interestingly, the human homolog of smg-8 is amplified in some breast cancers, which also depend on FoxA1. This observation makes smg-8 a very exciting gene to investigate. The goal of my thesis is to analyze smg-8 to better understand its function and potential role as a candidate regulator of pha-4/FoxA, using C. elegans as a model system. In this thesis, I show that C. elegans smg-8 does not have a role in the Nonsense Mediated Decay pathway. I find that smg-8 modulates pha-4 protein levels during embryonic development. This work is the first direct evidence that smg-8 is a modulator of pha-4. I used biochemical and bioinformatic approaches to uncover possible partners of smg-8. These approaches identified several interesting candidates that will help place C. elegans smg-8 in a functional pathway. This work has expanded our understanding of smg-8 function and lays the foundation for further investigation of the role of this novel gene as a regulator of pha-4/FoxA in C. elegans.
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Gabriel, Frédéric. "Etude fonctionnelle de la β-oxydation chez la levure pathogène opportuniste Candida lusitaniae : caractérisation d’une voie mitochondriale et peroxysomale Fox2p-dépendante et mise en évidence d’une voie peroxysomale alternative Fox2p-indépendante de catabolisme des acides gras." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21896/document.

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Les levures Candida sont des pathogènes opportunistes émergents. Après phagocytose macrophagique, C. albicans reprogramme son métabolisme pour faire face à une carence carbonée et induit 2 voies métaboliques, le cycle du glyoxylate et la β-oxydation. Notre objectif est d’étudier le lien entre β-oxydation, capacité de résistance à la phagocytose et virulence dans notre modèle biologique C. lusitaniae. Chez les levures Ascomycètes la β-oxydation, essentielle pour dégrader les acides gras (AG), est présumée être exclusivement peroxysomale.Nous avons construit 3 mutants nuls chez C. lusitaniae : icl1Δ, fox2Δ et pxa1Δ, respectivement défectifs pour l’isocitrate lyase (enzyme clé du cycle du glyoxylate), pour la protéine multifonctionnelle de la β-oxydation et pour une protéine responsable de l’import peroxysomal des AG à longue chaîne. L’étude de l’assimilation des AG et du catabolisme du 14Calpha-palmitoyl-CoA a révélé que les acyl-CoA à longue chaîne étaient toujours dégradés chez fox2Δ. L’étude du catabolisme des AG dans les fractions peroxysomale et mitochondriale des souches sauvage et fox2Δ, l’immunolocalisation de la protéine Fox2p et la mesure de la respiration mitochondriale nous ont permis de montrer pour la première fois chez une levure Ascomycète l’existence d’une β-oxydation Fox2p-dépendante dans la mitochondrie. C’est aussi la première démonstration chez un organisme eucaryote de la double localisation peroxysomale et mitochondriale de Fox2p. L’invalidation des gènes FOX1 et FOX3 (acyl-CoA oxydase et kétoacyl-CoA thiolase) a confirmé pour la première fois chez les champignons l’existence d’une voie peroxysomale alternative de catabolisme des AG, Fox2p-indépendante
The Candida spp. are emerging opportunistic pathogens. Phagocytic cells are a primary line of defense against these opportunistic pathogens. Upon phagocytosis by macrophages, C. albicans reprograms its metabolism because genes involved in the peroxisomal metabolism, such as glyoxylic acid cycle and beta-oxidation pathway, are overexpressed. The objective of this study was to study the relation between fatty acid beta-oxidation, resistance to phagocytosis and virulence in the biological model Candida lusitaniae. In ascomycetous yeasts, the fatty acid β-oxidation is assumed to be exclusively located to peroxisomes.We constructed three null-mutants in C. lusitaniae: icl1Δ, fox2Δ et pxa1Δ, respectively lacking the isocitrate lyase (a key enzyme of the glyoxylate cycle), the multifunctional fatty acid beta-oxidation protein (essential in C. albicans to the β-oxidation pathway), and a protein involved in the peroxisomal import of long-chain fatty acids. The study of fatty acid assimilation and 14Calpha-palmitoyl-CoA catabolism revealed that long-chain fatty acids were still catabolized in fox2Δ. The observation of 14Calpha-palmitoyl-CoA catabolism in mitochondrial and peroxisomal fractions of wild-type and fox2Δ strains, the immunolocalization of Fox2p and mitochondrial respiration measurements yielded to the first demonstration in ascomycetous yeast of a mitochondrial Fox2p-dependent fatty acid β-oxidation pathway. We also demonstrated for the first time in Eucaryota that Fox2p co-localized in both peroxisomes and mitochondria. The invalidation of FOX1 and FOX3 genes (acyl-CoA oxidase and ketoacyl-CoA thiolase, respectively) confirmed for the first time in Fungi the existence of an alternative peroxisomal pathway for fatty acid catabolism, Fox2p-independently
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Kaufmann, Anna-Kristin. "Functional properties of the intact and compromised midbrain dopamine system." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:8769a453-aa91-4509-b06e-48f25e88f15a.

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The midbrain dopamine system is involved in many aspects of purposeful behaviour and, when compromised, can have devastating effects on movement and cognition as seen in diseases like Parkinson's. In the healthy brain, dopamine neurons are thought to play particularly important roles in learning by signalling errors in reward prediction. The objective of this thesis was to investigate the diversity in the functional properties of the midbrain dopamine system, and how this is altered through genetic variation of relevance to Parkinson's and development of cell phenotype. This objective was addressed with a combination of behavioural experiments, in vivo single-cell recording and labelling (both in anaesthetised as well as awake rodents), immunofluorescence labelling, retrograde tracing and stereology. In a first set of experiments, it was demonstrated that chronic as well as acute genetic challenges can alter the firing patterns of midbrain dopamine neurons. Using a novel bacterial artificial chromosome-transgenic rat model, it was shown that the R1441C mutation in human leucine-rich repeat kinase 2, which is linked to Parkinson's, leads to motor deficits and an age-dependent reduction in the in vivo firing variability and burst firing of substantia nigra pars compacta (SNc) dopamine neurons. These findings help reveal processes of early, pre-degenerative dysfunction in dopamine neurons in Parkinson's. Similar effects on firing variability and burst firing of SNc dopamine neurons were found in a mouse model with conditional knock- out of the transcription factors Forkhead box A1 and A2 (FoxA1/2) in midbrain dopamine neurons. These findings indicate that FoxA1/2 are not only crucial for the early development of dopamine neurons, but also their function in the mature brain. In a second set of experiments in wildtype mice, it was demonstrated that midbrain dopamine neurons (located in SNc and ventral tegmental area) show diverse expression of the molecular markers Calbindin, Calretinin, Aldh1a1, Sox6, Girk2, SatB1 and Otx2. It was found that selective expression of these markers is of use for discriminating between midbrain dopamine neurons that project to dorsal striatum or nucleus accumbens. To elucidate whether the diverse molecular marker expression would map onto dopamine neurons whose firing correlates with distinct behavioural events, midbrain dopamine neurons were recorded and labelled in head-fixed awake mice either exposed to neutral sensory stimuli or performing a classical conditioning paradigm. The population activity of midbrain dopamine neurons was not modulated by neutral sensory stimuli. Interestingly, fewer than 50% of identified dopamine neurons showed phasic firing increases following reward- predicting cue and/or reward delivery, despite the common assumption that most (if not all) midbrain dopamine neurons signal reward prediction errors. Instead, firing was modulated by other explanatory factors, such as licking, or showed no modulation during the task. Response types of midbrain dopamine neurons were not correlated with their anatomical location nor the selective or combinatorial expression of the markers Aldh1a1, Calbindin and Sox6. In conclusion, the first set of experiments identified how different genetic burdens can alter the in vivo firing of midbrain dopamine neurons, and provide new insights into how circuits can change in pathological or compensatory ways at early disease stages in Parkinson's. The second set of experiments revealed striking heterogeneity of midbrain dopamine neurons in the intact system, and established further a functional diversity in the response types of identified midbrain dopamine neurons that is only partially consistent with canonical reward prediction error signalling.
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Kim, Eujin 1963. "Functional relationshipp between FoxA2 and its closely related family member FoxA1." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80303.

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The transcription factor FoxA2 and its closely related family member FoxA1 have been shown to both be expressed in the visceral and definitive endoderm, node, notochord and floor plate. Both factors have been shown to function as transcriptional activators and recognize the same DNA elements in vitro, suggesting that they may be functionally equivalent. However, there is increasing evidence, which suggest that they may play different roles in vivo. In order to begin to address whether FoxA1 is equivalent to FoxA2 in vivo, I used a gene targeting approach to replace the FoxA2 gene with the coding region of FoxA1, thus placing FoxA1 under the control of the FoxA2 regulatory elements. Screening of over 1600 clones allowed the identification of two correctly targeted ES cell lines. These ES cell lines will be an essential tool to address the functional equivalence of FoxA1 and FoxA2 in vivo.
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Sirigu, Giulia. "Continuity and change in Mexican foreign policy under Fox : a strategic-relational analysis." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/continuity-and-change-in-mexican-foreign-policy-under-foxa-strategicrelational-analysis(1181d7bb-a332-4793-8200-ccd37b8809b5).html.

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This thesis presents a Strategic-Relational (SR) analysis of the processes ofchange and continuity in Mexican foreign policy during the Fox government. In2000, the election of President Fox determined the victory of a new party after71 years of Partido Revolucionario Institucional (PRI) rule, producing thedemocratisation of the country. Domestic and international changes generatedby the end of the Cold War, and the presence of new actors in the Mexicanscenario created momentum for the country, helped also by the introduction ofa new foreign policy paradigm. Despite the significance of these elements, thestudy of their reciprocal influence in foreign policy has been neglected. Thesetransformations and the discrepancy between the discourse of change and itsimplementation are considered an ideal scenario for the study of continuity andchange in foreign policy-making. This research focuses on the application ofJessop and Hay’s Strategic-Relational Approach (SRA), considered able togenerate an understanding of this complex process of interaction. However,although the SRA theorises the impact of these interplays in policy-making,scarce consideration has been given to this approach in the study of foreignpolicy change. Therefore, the thesis aims to understand the dynamicsgrounding Fox’s foreign policy, employing the SRA to identify those conditionsnecessary for the implementation of change and appreciate how the interplayamong different elements was manifest. After explaining the SRA and its relevance to the study of change in foreignpolicy, the thesis provides a historical framework explaining Mexico’s evolutionin the years up to 2000. Building on these chapters, three empirical casestudies presenting different degrees of foreign policy change are then analysedthrough the SRA. They respectively consider Mexico’s approach topeacekeeping operations, its participation in the United Nations SecurityCouncil and its refusal to support the Iraq War, and Mexico’s internationalapproach to human rights. The thesis compares how, in the presence ofconsistent general conditions, the processes of change and continuity weredifferently implemented. The interplay established among the fundamental SRelements is interpreted as pivotal in every empirical chapter for its capacity toaccount for the complexity of the foreign policy process and the generation ofconcrete change in foreign policy.
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Forneck, K?ri L?cia. "Met?fora ?... : uma abordagem metate?rica da met?fora." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2016. http://tede2.pucrs.br/tede2/handle/tede/7112.

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Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior - CAPES
Considering the diversity of theories available on the treatment of metaphor, we have two methodological options of study: either we approach it under the foundations of one area and analyze the object from the constructed properties within the scope of the approach; or we construct an interface repackaging, in which we put into play complex properties that delimit a third object built on the borderlines of disciplines in dialogue (CAMPOS, 2007). In the study that we propose, we illustrate this second approach, putting into dialogue the foundations of Linguistics, especially Pragmatics - via Grice's Theory of Implicatures (1967; 1975) and via Relevance Theory, by Sperber and Wilson (1986; 2008) and Wilson and Sperber, (2012) - and Psicolinguistics (GLUCKSBERG et al., 2007; BOWDLE and GENTNER, 2005), on the one hand; and, on the other, Neuroscience, through a qualitative meta-analysis constructed by the study of twenty fMRI experiments, from which the circuitry of the neurological processing of the metaphor is described. In this meta-analysis, we have tried to elucidate the nature of the theoretical approach and its implications in the design of the experiments and in the results achieved, in order to collect elements to compose the meta-theoretical approach of the interface that we proposed. In a second moment, then, we elevate the properties constructed in the scope of each area to the condition of meta-theoretical properties of the metaphor, with the purpose of putting into dialogue theories with distinct granularity and of proposing an alternative to the mapping problem (POEPPEL, 2012) resulting from a study of this nature. We thus have constructed a third, more complex object by deepening the descriptive and explanatory potential of the treatment given to the metaphor. Therefore, we see that, from an interface approach, two consequences emerge: the first, epistemological, because we contribute in the debate about the properties of the metaphor theories in interface, from whose dialogue the revitalization of the foundations in dialogue results; the second, theoretical, because we also contribute to the debate about the properties of the metaphor itself. The proposed interface emphasizes the potential of such approaches by extending possibilities for new treatments of different objects of linguistic research, including the metaphor itself.
Considerando a diversidade de teorias que temos ? disposi??o sobre o tratamento da met?fora, temos duas op??es metodol?gicas de estudo: ou a abordamos sob os fundamentos de uma ?rea e analisamos o objeto a partir das propriedades constru?das dentro do escopo da abordagem; ou constru?mos uma roupagem de interface, em que colocamos em jogo propriedades complexas que delimitam um objeto terceiro constru?do nas fronteiras das disciplinas em di?logo (CAMPOS, 2007). No estudo que propomos, ilustramos essa segunda abordagem, colocando em di?logo fundamentos da Lingu?stica, em especial da Pragm?tica ? via Teoria das Implicaturas de Grice (1967; 1975) e via Teoria da Relev?ncia, de Sperber e Wilson (1986; 2008) e Wilson e Sperber, (2012) ? e da Psicolingu?stica (GLUCKSBERG et al., 2007; BOWDLE e GENTNER, 2005), de um lado; e, de outro, da Neuroci?ncia, por meio de uma meta-an?lise qualitativa constru?da pelo estudo de vinte experimentos com fMRI, a partir dos quais descreve-se a circuitaria do processamento neurol?gico da met?fora. Nessa meta-an?lise, procuramos elucidar a natureza da abordagem te?rica e suas implica??es no design dos experimentos e nos resultados alcan?ados, no intuito de recolhermos elementos para compor a abordagem metate?rica da interface que propusemos. Num segundo momento, ent?o, al?amos ? condi??o de propriedades metate?ricas da met?fora as propriedades constru?das no escopo de cada ?rea, com o prop?sito de colocar em di?logo teorias com granularidade distinta e de propor uma alternativa ao mapping problem (POEPPEL, 2012) decorrente de um estudo dessa natureza. Constru?mos, assim, um objeto terceiro, mais complexo, ao aprofundarmos o potencial descritivo e explanat?rio do tratamento dado ? met?fora. Dessa forma, verificamos que de uma abordagem na interface emergem duas consequ?ncias: a primeira, epistemol?gica, porque contribu?mos no debate sobre as propriedades das teorias da met?fora em interface, de cujo di?logo decorre a revitaliza??o dos pr?prios fundamentos em di?logo; a segunda, te?rica, porque tamb?m contribu?mos no debate sobre as propriedades da met?fora em si. A interface proposta evidencia o potencial de abordagens dessa natureza por ampliarem possibilidades de novos tratamentos a diferentes objetos de investiga??o lingu?stica, entre os quais a pr?pria met?fora.
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Books on the topic "Foxa"

1

Foxy. New York: Beech Tree, 1997.

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Fosa. Warszawa: Wydawnictwo W.A.B. - Grupa Wydawnicza Foksal, 2015.

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Foxy! London: Frances Lincoln Children's, 2012.

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Foxy. London: HarperCollins Children's, 2012.

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Foxy. London: Walker Books, 1990.

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Griffith, Helen V. Foxy. London: MacRae, 1985.

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Anton, Ion. Foka. Chișinău: Silvius Libris, 2012.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. FOBA. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1.

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Foxy. New York: Harper, 2012.

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Walsh, Haley. Foxe tail: A Skyler Foxe mystery. Albion, NY: MLR Press, 2010.

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Book chapters on the topic "Foxa"

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DeGraff, David J., Xiuping Yu, Qian Sun, Janni Mirosevich, Ren Jie Jin, Yongqing Wang, Aparna Gupta, et al. "The Role of Foxa Proteins in the Regulation of Androgen Receptor Activity." In Androgen Action in Prostate Cancer, 587–615. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-69179-4_25.

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Umebayashi, Katsu. "Nesting: Beyond Objects to the Bodily Experience of Space." In FOBA, 9–11. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_1.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. "Organ." In FOBA, 119–32. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_10.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. "Myougei." In FOBA, 135–42. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_11.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. "Asphodel." In FOBA, 145–56. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_12.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. "Orient." In FOBA, 159–67. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_13.

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Daniell, Thomas. "FOB Homes: Brand Recognition." In FOBA, 169–71. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_14.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. "FOB Homes Typologies." In FOBA, 172–76. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_15.

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Allison, Peter. "Prototypes in Suburbia." In FOBA, 177–84. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_16.

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Umebayashi, Katsu, Thomas Daniell, Michael Webb, Peter Allison, and Kazuhiro Kojima. "FOB Homes Examples." In FOBA, 186–217. New York, NY: Princeton Archit.Press, 2005. http://dx.doi.org/10.1007/1-56898-635-1_17.

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Conference papers on the topic "Foxa"

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Koenig, Michael J., Joseph Amann, Bernice Agana, Jacob Kaufman, Vicki Wysocki, Christopher Oakes, and David P. Carbone. "Abstract 824: LKB1 loss in lung adenocarcinoma leads to global hypomethylation and altered FOXA binding." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-824.

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Koenig, Michael J., Joseph Amann, Bernice Agana, Jacob Kaufman, Vicki Wysocki, Christopher Oakes, and David P. Carbone. "Abstract 824: LKB1 loss in lung adenocarcinoma leads to global hypomethylation and altered FOXA binding." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-824.

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Li, Zhaoyu. "Abstract A1-08: Comparative genomics study of FOXA/ER dual regulation in breast cancer and liver cancer." In Abstracts: AACR Special Conference: Translation of the Cancer Genome; February 7-9, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.transcagen-a1-08.

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Milan, Marta, and Gioacchino Natoli. "Abstract LB-202: Role of the FOXA transcription factors in shaping distinct transcriptional programs in human pancreatic cancers." 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-lb-202.

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Verhaeghe, C., S. Park, LT Nguyenvu, C. Eisley, and DJ Erle. "Distinct Roles of FOXA2 and FOXA3 in Allergic Airway Disease." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6297.

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Li, Zhaoyu, Geetu Tuteja, Jonathan Schug, and Klaus H. Kaestner. "Abstract 5112: Foxa1 and Foxa2 are essential for gender dimorphism in liver cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5112.

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Wang, Sibo, Renchi Yang, Xiaokui Xiao, Zhewei Wei, and Yin Yang. "FORA." In KDD '17: The 23rd ACM SIGKDD International Conference on Knowledge Discovery and Data Mining. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3097983.3098072.

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Hulden, Mans. "Foma." In the 12th Conference of the European Chapter of the Association for Computational Linguistics: Demonstrations Session. Morristown, NJ, USA: Association for Computational Linguistics, 2009. http://dx.doi.org/10.3115/1609049.1609057.

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"Urs Ziegler, FOCA." In 9th AIAA Aviation Technology, Integration, and Operations Conference (ATIO). Reston, Virigina: American Institute of Aeronautics and Astronautics, 2009. http://dx.doi.org/10.2514/6.2009-7132.

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Marton, Fabio, Marco Agus, Giovanni Pintore, and Enrico Gobbetti. "FOX." In the 10th International Conference. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2087756.2087767.

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Reports on the topic "Foxa"

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Aldrich, William F. Fox Conner. Fort Belvoir, VA: Defense Technical Information Center, April 1993. http://dx.doi.org/10.21236/ada264549.

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St-Onge, M. R., M. Sanborn-Barrie, and M. D. Young. Geology, Foxe Peninsula, Baffin Island, Nunavut. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2007. http://dx.doi.org/10.4095/224222.

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Kang, Kyo C., Sholom G. Cohen, James A. Hess, William E. Novak, and A. S. Peterson. Feature-Oriented Domain Analysis (FODA) Feasibility Study. Fort Belvoir, VA: Defense Technical Information Center, November 1990. http://dx.doi.org/10.21236/ada235785.

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Seus, Sarah, and Susanne Buehrer. How to Evaluate a Transition-Oriented Funding Programme? Lessons Learned from the Evaluation of FONA, the German Framework Programme to Promote Sustainability Research. Fteval - Austrian Platform for Research and Technology Policy Evaluation, July 2021. http://dx.doi.org/10.22163/fteval.2021.515.

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This article is based on the evaluation of the German research funding programme “FONA - Forschung für Nachhaltigkeit” (Research for Sustainability.) It reflects upon the methodological challenges confronting the evaluation. These challenges result from the specific objectives and design of the FONA programme (a strategic portfolio of heterogenious interventions). FONA’s ambition is to fund activities under the emerging field of ‘sustainability research’. The core characteristics of sustainability research are: interdisciplinary and trans-disciplinary research processes; orientation towards transferring the research results (into society) and the interdependency with a wider system and global perspective.
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Mason, John Jeffrey. TOA/FOA geolocation error analysis. Office of Scientific and Technical Information (OSTI), August 2008. http://dx.doi.org/10.2172/957215.

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Belaguli, Narasimhaswamy S. Forkhead Box Protein 1 (Foxa1) and the Sumoylation Pathway that Regulates Foxa1 Stability are Potential Targets for Breast Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada489768.

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Huot-Vézina, G., V. Brake, N. Pinet, and D. Lavoie. GIS compilation of the Hudson Bay / Foxe sedimentary basins. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2013. http://dx.doi.org/10.4095/292800.

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Yu, Xiuping. Wnt/beta-Catenin, Foxa2, and CXCR4 Axis Controls Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada609497.

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Brembs, Björn. What is the function of FoxP in operant self-learning? [proposal]. ThinkLab, November 2015. http://dx.doi.org/10.15363/thinklab.a8.

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Brembs, Björn. What is the function of FoxP in operant self-learning? [project]. ThinkLab, November 2015. http://dx.doi.org/10.15363/thinklab.11.

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