Добірка наукової літератури з теми "Tbx16"
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Статті в журналах з теми "Tbx16"
Lardelli, Michael. "The evolutionary relationships of zebrafish genes tbx6 , tbx16 / spadetail and mga." Development Genes and Evolution 213, no. 10 (October 1, 2003): 519–22. http://dx.doi.org/10.1007/s00427-003-0348-2.
Повний текст джерелаWells, Simon, Svanhild Nornes, and Michael Lardelli. "Transgenic Zebrafish Recapitulating tbx16 Gene Early Developmental Expression." PLoS ONE 6, no. 6 (June 24, 2011): e21559. http://dx.doi.org/10.1371/journal.pone.0021559.
Повний текст джерелаPayumo, Alexander Y., Lindsey E. McQuade, Whitney J. Walker, Sayumi Yamazoe, and James K. Chen. "Tbx16 regulates hox gene activation in mesodermal progenitor cells." Nature Chemical Biology 12, no. 9 (July 4, 2016): 694–701. http://dx.doi.org/10.1038/nchembio.2124.
Повний текст джерелаMuyskens, Jonathan B., and Charles B. Kimmel. "Tbx16 cooperates with Wnt11 in assembling the zebrafish organizer." Mechanisms of Development 124, no. 1 (January 2007): 35–42. http://dx.doi.org/10.1016/j.mod.2006.09.003.
Повний текст джерелаWarga, Rachel M., Rachel L. Mueller, Robert K. Ho, and Donald A. Kane. "Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity." Developmental Biology 383, no. 1 (November 2013): 75–89. http://dx.doi.org/10.1016/j.ydbio.2013.08.018.
Повний текст джерелаNagel, Stefan, and Corinna Meyer. "Establishment of the TBX-code reveals aberrantly activated T-box gene TBX3 in Hodgkin lymphoma." PLOS ONE 16, no. 11 (November 22, 2021): e0259674. http://dx.doi.org/10.1371/journal.pone.0259674.
Повний текст джерелаEhrlich, Kenneth C., Michelle Lacey, Carl Baribault, Sagnik Sen, Pierre Olivier Esteve, Sriharsa Pradhan, and Melanie Ehrlich. "Promoter-Adjacent DNA Hypermethylation Can Downmodulate Gene Expression: TBX15 in the Muscle Lineage." Epigenomes 6, no. 4 (December 9, 2022): 43. http://dx.doi.org/10.3390/epigenomes6040043.
Повний текст джерелаJahangiri, Leila, and Fiona Wardle. "Co-regulation of mutual target genes by Ntla and Tbx16 in zebrafish mesoderm development." Developmental Biology 356, no. 1 (August 2011): 261. http://dx.doi.org/10.1016/j.ydbio.2011.05.502.
Повний текст джерелаManning, Alyssa J., and David Kimelman. "Tbx16 and Msgn1 are required to establish directional cell migration of zebrafish mesodermal progenitors." Developmental Biology 406, no. 2 (October 2015): 172–85. http://dx.doi.org/10.1016/j.ydbio.2015.09.001.
Повний текст джерелаBouldin, C. M., A. J. Manning, Y. H. Peng, G. H. Farr, K. L. Hung, A. Dong, and D. Kimelman. "Wnt signaling and tbx16 form a bistable switch to commit bipotential progenitors to mesoderm." Development 142, no. 14 (June 10, 2015): 2499–507. http://dx.doi.org/10.1242/dev.124024.
Повний текст джерелаДисертації з теми "Tbx16"
Muyskens, Jonathan B. "Tbx16 and Wnt11 coordinately regulate prechordal plate morphogenesis /." view abstract or download file of text, 2005. http://www.lib.umi.com/cr/uoregon/fullcit?p3201693.
Повний текст джерелаTypescript. Includes vita and abstract. Includes bibliographical references (leaves 55-58). Also available for download via the World Wide Web; free to University of Oregon users.
Burbridge, Sarah. "The role of Tbx18 in axial mesoderm development." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3312/.
Повний текст джерелаArribas, Arranz Jéssica. "Los factores de transcripción TBX15 e YY1 en cáncer. Función y regulación de TBX15. Expresión de YY1 en cáncer de tiroides." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/323905.
Повний текст джерелаTBX15 and YY1 are transcription factors; these molecules are able to transduction signals, being essential in the regulation of many basic cellular processes including cell proliferation and apoptosis. Therefore, the anomalous expression and function of these transcription factors is crucial in the beginning and in the development of cancer. Transcription factors act as oncogenes or tumor suppressor genes and their expression is found altered in multiple types of cancer. Specific transcription factors of the thyroid gland have been reported to be associated with thyroid cancer; however there is no information about the implication of general transcription factors, such as TBX15 or YY1. The involvement of YY1 in cancer is well documented; whereas there are scarcely any studies describing the possible implication of TBX15 in cancer. In this context, the present thesis provides knowledge about the role of transcription factor TBX15 in the development of cancer; moreover, it also analyzes the expression of transcription factor YY1 in differentiated thyroid cancer. Our study reveals a novel function of transcription factor TBX15 as an inhibitor of cellular apoptosis, which can contribute to the proliferative potential of cancer cells, and may suggest TBX15 as a potential therapeutic target in cancer treatment. Furthermore, we have also proven that NFkB activates the transcription of TBX15 by binding to the 5’-flanking regulatory region of the gene TBX15. Thus, the interaction between TBX15 and NFkB could prove to be important to understand the function of TBX15 in cancer. Without any previous information regarding the expression of transcription factor YY1 in thyroid cancer, our results represent the first study about the implication of YY1 in this type of cancer. We demonstrate how YY1 is overexpressed in differentiated thyroid cancer, and what’s more, its positive expression has been found to be more frequent in the papillary type rather than in the follicular type. Therefore these results evidence the possible implication of transcription factor YY1 in thyroid cancer.
Cinzia, Caprio. "Tbx1 functions in pharyngeal arch and cardiovascular development." Thesis, Open University, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663223.
Повний текст джерелаMartin, Jody Carl. "TBx18 and the epicardium in cardiac development and regenerative medicine." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3336705.
Повний текст джерелаTitle from first page of PDF file (viewed January 6, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 128-139).
De, Mesmaeker Julie Anne Laurence Nathalie. "Molecular mechanisms connecting genotype and phenotype in Tbx1 deficiency." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:56013dc6-50af-454c-b036-284e5449aa8f.
Повний текст джерелаGiménez, Esteban Mariano. "Expresión y regulación De los genes WDR3 y TBX15 en cáncer." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/121601.
Повний текст джерелаThere are numerous studies dedicated to find out the causes of cancer and its progression and the application of this knowledge to improving the prevention, diagnosis and treatment. In this context our group contributes to these objectives, providing new insights into the processes involved in tumor development of thyroid cancer in particular and carcinogenesis in general. The main objective of this thesis is to study the involvement of the genes WDR3 and TBX15 in cancer. The study of these genes arises from studies conducted in our laboratory that identified two polymorphisms markers of thyroid cancer susceptibility in the chromosomal region 1p12, where these genes have been mapped. Additionally, this chromosomal region has often been associated with many types of cancer. One of the polymorphisms identified is located in WDR3 (intron 24) gene and the other in a region located at 460 Kb from TBX15 gene. The function of these genes has not been completely known, however, it has been proposed that WDR3 is involved in the proliferation of the cell cycle through the disruption of the ribosome biogenesis. In addition, several studies have shown an irregular expression of WD repeat proteins in certain types of cancer. Moreover, the TBX15 gene, like other members of the T-box family, has been related to developmental processes and several evidences suggest a relationship between the T-box genes and tumorigenesis, with effects on cell proliferation, invasion and metastasis. That is why we hypothesize that genes WDR3 and TBX15 may be related to cancer. Numerous studies are conducted in our laboratory to elucidate the role of these genes in the etiology of thyroid cancer in particular and also in cancer in general. In this thesis was performed an association study of genes WDR3 and TBX15 with thyroid cancer susceptibility, and their expression and regulation were analyzed in thyroid cancer, colon cancer and brain tumors. The gene association study of WDR3 with thyroid cancer indicates that this gene is a susceptibility factor for this cancer. The expression analysis shows that the WDR3 is over-expressed in thyroid cancer and colon cancer. The methylation analysis of the promoter region of WDR3 indicates that this epigenetic modification is not involved in the regulation of WDR3 expression at transcriptional level, however, analysis of transcription factors binding to the promoter shows that the c-Myc and CTCF factors could act as regulators of the WDR3 expression. Moreover, the association study of TBX15 gene with thyroid cancer indicates that this gene is not a susceptibility factor for this cancer. The expression analysis of TBX15 shows decreased expression of this gene in thyroid cancer. The methylation analysis of the promoter region of TBX15 in thyroid tissues and brain tissues, indicates that this epigenetic modification is involved in the regulation of TBX15 expression at transcriptional level. This thesis highlights the role of genes WDR3 and TBX15 in the etiology of thyroid cancer and suggests their involvement in carcinogenesis in general.
Briones, Leon Jose Alberto. "Investigating a Tbx1 and Pax9 genetic interaction during cardiovascular development." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2839.
Повний текст джерелаBussen, Markus. "Die funktionelle Analyse des T-box-Transkriptionsfaktors Tbx18 in der Somitogenese der Maus." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976695405.
Повний текст джерелаMarco, Viviani de. "Estudos dos genes Tbx19 e Crhr1 em cães da raça poodle com hipercortisolismo ACTH-dependente." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-28052010-113552/.
Повний текст джерелаThe ACTH-dependent hypercortisolism (ADH), also called Cushing\'s disease, is one of the most commonly diagnosed endocrine diseases in dogs. The symptoms occur due to glucocorticoids excess leading to gluconeogenic, catabolic, anti-inflammatory and immunosuppressive effects in multiple organs and systems. There is a high incidence of Cushing\'s disease in Poodles and familial disease has been identified suggesting a genetic involvement. The molecular changes that lead to the development of ACTH-dependent hypercortisolism in dogs remain undefined. Among genes implicated in corticotroph development and in corticotropic axis regulation, we would like to point out Tbx19 and Crhr1, respectively. Tbx19 gene is a transcription factor required for transcription of the proopiomelanocortin gene and for terminal differentiation of the corticotroph. Inactivating mutations in that gene are associated with human isolated ACTH deficiency. Since Tbx19 is present exclusively in normal and adenomatous corticotroph cells, its involvement in the secretion of ACTH in Cushing\'s disease was proposed. The presence of CRHR1 in corticotrophinomas in humans and dogs raised the possibility of its involvement in pituitary tumorigenesis, promoting prolonged cell stimulation, even in the absence of hypothalamic hormones. An increased expression of the CRHR1 mRNA was demonstrated in human and canine ACTH-secreting pituitary adenomas, despite the autonomous ACTH secretion and the low portal levels of CRH. The aim of this study was to investigate Tbx19 and Crhr1 coding region mutations in Poodle dogs with ACTH-dependent hypercortisolism. We studied 50 Poodle dogs with ADH (33 females and 17 males) with a mean age of 8.71 years and 50 control dogs of the same breed (32 females and 18 males) older than 6 years (mean 9.38 years) and without endocrinopathies. Genomic DNA was extracted from peripheral blood, amplified by the polymerase chain reaction (PCR) using specific intronic primers and submitted to automatic sequence. We identified a new allelic variant in the Tbx19 and Crhr1 coding regions. The allelic variant p. S343G in the Tbx19 gene was found in two unrelated dogs, but also in two normal controls, suggesting that this is a new polymorphism. The Crhr1 allelic variant p. V97M was found in heterozygosity in one animal with ACTH-dependent hypercortisolism, but was not observed in one hundred normal alleles. The codon 97 is located in the extracellular amino terminal domain of the Crhr1 and is extremely important for high affinity ligand binding. The molecular analysis of the quaternary structure of normal and mutated proteins, followed by evaluation of the binding energy of the contact surface between the hormone and the receptor showed a structural rearrangement of the mutated protein by changing the contact surface between the CRH and its receptor CRHR1, resulting in a binding energy 17% higher than the wild type. In conclusion, this study did not identify Tbx19 mutations associated with canine ACTH-dependent hypercortisolism, but on the other hand, we first identified a Crhr1 gain-of-function mutation probably responsible for ACTH-dependent hypercortisolism in a Poodle dog of our cohort.
Частини книг з теми "Tbx16"
Melby, Alan K. "TBX: A terminology exchange format for the translation and localization industry." In Handbook of Terminology, 393–424. Amsterdam: John Benjamins Publishing Company, 2015. http://dx.doi.org/10.1075/hot.1.tbx1.
Повний текст джерелаTsuchihashi, Takatoshi, Reina Ishizaki, Jun Maeda, Akimichi Shibata, Keiko Uchida, Deepak Srivastava, and Hiroyuki Yamagishi. "Modification of Cardiac Phenotype in Tbx1 Hypomorphic Mice." In Etiology and Morphogenesis of Congenital Heart Disease, 215–17. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_28.
Повний текст джерелаYamagishi, Hiroyuki, and Deepak Srivastava. "Molecular Mechanisms Regulating Tissue-Specific Expression of Tbx1." In Cardiovascular Development and Congenital Malformations, 128–31. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch32.
Повний текст джерелаOkubo, Tadashi. "Tbx1/Ripply3/Retinoic Acid Signal Network That Regulates Pharyngeal Arch Development." In New Principles in Developmental Processes, 97–108. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54634-4_8.
Повний текст джерелаXu, Huansheng, Masae Morishima, and Antonio Baldini. "Tbx1 and Digeorge Syndrome: A Genetic Link between Cardiovascular and Pharyngeal Development." In Cardiovascular Development and Congenital Malformations, 132–34. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch33.
Повний текст джерелаKochilas, Lazaros, Jun Liao, Sandra Merscher-Gomez, Raju Kucherlapati, Bernice Morrow, and Jonathan A. Epstein. "New Insights into the Role of Tbx1 in the Digeorge Mouse Model." In Cardiovascular Development and Congenital Malformations, 135–36. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch34.
Повний текст джерелаBaldini, A., F. G. Fulcoli, and E. Illingworth. "Tbx1." In Current Topics in Developmental Biology, 223–43. Elsevier, 2017. http://dx.doi.org/10.1016/bs.ctdb.2016.08.002.
Повний текст джерелаMorrow, Bernice E., Donna M. Mcdonald-Mcginn, and Beverly S. Emanuel. "The 22q11.2 Deletion Syndrome and TBX1." In Epstein's Inborn Errors of Development, 827–31. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199934522.003.0120.
Повний текст джерелаTurnpenny, Peter D., Kenro Kusumi, and Sally L. Dunwoodie. "DLL3, MESP2, LFNG, HES7, TBX6, RIPPLY2 and Spondylocostal Dysostosis." In Epstein's Inborn Errors of Development, 559–70. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199934522.003.0074.
Повний текст джерелаHannan, Fadil M., Bart L. Clarke, and Rajesh V. Thakker. "Hypocalcaemic Disorders, Hypoparathyroidism, and Pseudohypoparathyroidism." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 685–98. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0085.
Повний текст джерелаТези доповідей конференцій з теми "Tbx16"
Yue Zhang, Kuanquan Wang, Henggui Zhang, and Wei Wang. "Simulation of effects of TBX18 on the pacemaker activity of human ventricular cells." In 2015 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2015. http://dx.doi.org/10.1109/bibm.2015.7359906.
Повний текст джерела