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Artykuły w czasopismach na temat "PTC mutation"
Liu, Xiaoli, Justin Bishop, Yuan Shan, Sara Pai, Dingxie Liu, Avaniyapuram Kannan Murugan, Hui Sun, Adel K. El-Naggar i Mingzhao Xing. "Highly prevalent TERT promoter mutations in aggressive thyroid cancers". Endocrine-Related Cancer 20, nr 4 (13.06.2013): 603–10. http://dx.doi.org/10.1530/erc-13-0210.
Pełny tekst źródłaRusinek, Dagmara, Aleksandra Pfeifer, Jolanta Krajewska, Malgorzata Oczko-Wojciechowska, Daria Handkiewicz-Junak, Agnieszka Pawlaczek, Jadwiga Zebracka-Gala i in. "Coexistence of TERT Promoter Mutations and the BRAF V600E Alteration and Its Impact on Histopathological Features of Papillary Thyroid Carcinoma in a Selected Series of Polish Patients". International Journal of Molecular Sciences 19, nr 9 (6.09.2018): 2647. http://dx.doi.org/10.3390/ijms19092647.
Pełny tekst źródłaClarke, Luka A., Vanessa C. C. Luz, Szymon Targowski, Sofia S. Ramalho, Carlos M. Farinha i Margarida D. Amaral. "Integrity and Stability of PTC Bearing CFTR mRNA and Relevance to Future Modulator Therapies in Cystic Fibrosis". Genes 12, nr 11 (18.11.2021): 1810. http://dx.doi.org/10.3390/genes12111810.
Pełny tekst źródłaHenke, Lauren E., John D. Pfeifer, Thomas J. Baranski, Todd DeWees i Perry W. Grigsby. "Long-term outcomes of follicular variant vs classic papillary thyroid carcinoma". Endocrine Connections 7, nr 12 (grudzień 2018): 1226–35. http://dx.doi.org/10.1530/ec-18-0264.
Pełny tekst źródłaChoi, Yun-Suk, Seong-Woon Choi i Jin-Wook Yi. "Prospective Analysis of TERT Promoter Mutations in Papillary Thyroid Carcinoma at a Single Institution". Journal of Clinical Medicine 10, nr 10 (18.05.2021): 2179. http://dx.doi.org/10.3390/jcm10102179.
Pełny tekst źródłaLiu, Jie, Huizheng Li, Rong Du, Nan Fang, Jingbo Zhang, Yu Tang, Jianwei Wang i Qixi Wu. "Targeted next-generation sequencing in papillary thyroid carcinoma of Chinese Han population." Journal of Clinical Oncology 37, nr 15_suppl (20.05.2019): e17574-e17574. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e17574.
Pełny tekst źródłaChakraborty, Dhritiman, Sunil Shakya, Sanjana Ballal, Shipra Agarwal i Chandrasekhar Bal. "BRAFV600E and TERT promoter mutations in paediatric and young adult papillary thyroid cancer and clinicopathological correlation". Journal of Pediatric Endocrinology and Metabolism 33, nr 11 (26.11.2020): 1465–74. http://dx.doi.org/10.1515/jpem-2020-0174.
Pełny tekst źródłaBarzon, Luisa, Giulia Masi, Isabella Merante Boschin, Enrico Lavezzo, Monia Pacenti, Eric Casal Ide, Antonio Toniato, Stefano Toppo, Giorgio Palù i Maria Rosa Pelizzo. "Characterization of a novel complex BRAF mutation in a follicular variant papillary thyroid carcinoma." European Journal of Endocrinology 159, nr 1 (lipiec 2008): 77–80. http://dx.doi.org/10.1530/eje-08-0239.
Pełny tekst źródłaSiraj, Sarah, Tariq Masoodi, Abdul K. Siraj, Saud Azam, Zeeshan Qadri, Sandeep K. Parvathareddy, Rong Bu i in. "APOBEC SBS13 Mutational Signature—A Novel Predictor of Radioactive Iodine Refractory Papillary Thyroid Carcinoma". Cancers 14, nr 6 (21.03.2022): 1584. http://dx.doi.org/10.3390/cancers14061584.
Pełny tekst źródłaDurand, Stéphanie, Carole Ferraro-Peyret, Mireille Joufre, Annie Chave, Françoise Borson-Chazot, Samia Selmi-Ruby i Bernard Rousset. "Molecular characteristics of papillary thyroid carcinomas without BRAF mutation or RET/PTC rearrangement: relationship with clinico-pathological features". Endocrine-Related Cancer 16, nr 2 (czerwiec 2009): 467–81. http://dx.doi.org/10.1677/erc-08-0081.
Pełny tekst źródłaRozprawy doktorskie na temat "PTC mutation"
Maxwell, Megan Amanda, i n/a. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis". Griffith University. School of Biomolecular and Biomedical Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040219.100649.
Pełny tekst źródłaMaxwell, Megan Amanda. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis". Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366184.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Full Text
Panton, Nicola. "Mutation analysis of four genes implicated in iron homeostasis in porphyria cutanea tarda (PCT) patients". Thesis, Link to the online version, 2008. http://hdl.handle.net/10019/888.
Pełny tekst źródłaAjlani, Ghada. "Détermination des sites de mutation responsables de résistance aux herbicides chez des mutants de la cyanobactérie Synechocystis PCC 6714 : étude de l'effet de ces mutations sur le transfert d’électrons du photosystème II". Paris 11, 1989. http://www.theses.fr/1989PA112130.
Pełny tekst źródłaMohamed-Uvaize, Musfira. "The Effects of Dilated Cardiomyopathy and Atrial Fibrillation Lamin A/C Mutations on Phosphorylated Kinase C Alpha Cellular Distribution and Activity". Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30545.
Pełny tekst źródłaLemonnier, François. "Mutations d'IDH2, TET2 et DNMT3A dans les lymphomes T périphériques : de la biologie à la clinique". Thesis, Paris Est, 2016. http://www.theses.fr/2016PESC0082.
Pełny tekst źródłaTET2, IDH2 and DNMT3A, 3 genes involved in the regulation of DNA methylation, are frequently mutated in Peripheral T Cell Lymphomas (PTCL). However, the consequences of these mutations are poorly understood. Focusing on IDH2 mutation, we demonstrated that this mutation is restricted to tumor T cells within angioimmunoblastic lymphoma (AITL) tumor tissue. We also demonstrated that, in AITL, IDH2 mutated T cells had the ability to produce D-2 hydroxyglutarate (D-2HG), a metabolite that has oncogenic effect. Using transgenic mouse models, we showed that IDH2R172K was the only IDH mutation that, when expressed in T cells, produced enough D-2HG to inhibit TET proteins and impairing lymphoid differentiation. This likely explains why IDH2R172 is the only IDH mutation found in AITL. As IDH2 mutation results in TET2 inhibition, which impairs 5hmC formation, we assessed the level of 5hmC in AITL, and described 5hmC loss, compared to normal TFH, in all AITL, regardless of the TET2, IDH2 and DNMT3A mutational status. We extended these finding to main nodal and extranodal PTCL entities, showing that 5hmC loss was a general mechanism present in all PTCL, with the exception of hepatosplenic T cell lymphoma. In a translational approach, we saw that the high frequency of TET2, DNMT3A and RHOA mutations in TFH like PTCL suggest a common molecular basis shared with AITL that could argue, in addition to phenotypic and histological similarities, to group these 2 entities into a single category. Finally, we described the first complete remission of a patient with a TET2 mutated AITL with 5 azacytidine, suggesting that hypomethylating agents could be active in PTCL
Kallassy-Awad, Mireille. "Étude de gènes impliqués dans la cancerogénèse de la peau chez l'homme : implications des gènes p21WAF1, ptch, smoh et cdc27HS/h-nuc". Lyon 1, 1998. http://www.theses.fr/1998LYO1T051.
Pełny tekst źródłaRusso, Chantal. "De l'assurance de responsabilité à l'assurance directe : contribution à l'étude d'une mutation de la couverture des risques". Nice, 1999. http://buadistant.univ-angers.fr/login?url=https://www.dalloz-bibliotheque.fr/pvurl.php?r=http%3A%2F%2Fdallozbndpro-pvgpsla.dalloz-bibliotheque.fr%2Ffr%2Fpvpage2.asp%3Fpuc%3D5442%26nu%3D48.
Pełny tekst źródłaKarimi, Gilda. "Etude de l'assemblage de la NADPH oxydase du phagocyte". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112025.
Pełny tekst źródłaThe NADPH oxidase of phagocytes is an enzyme involved in the innate defense of organisms against pathogens. After phagocyte activation, this enzyme produces superoxide ions by reduction of dioxygen by NADPH. It is constituted of four cytosolic sub-units (p47phox ; p67phox ; p40phox et Rac) and two membrane proteins (gp91 ; p22phox). Its activation takes place through a complex process that involves protein-protein interaction changes leading to assembly and functionning of the catalytic core. In order to obtain information on this process, I have reconstituted the enzyme in a cell free systeme using recombinant proteins, to be able to fully control all the measurement conditions. In this work, we have compared different activation modes of p47phox i) phosphorylation; ii) substitution serine - aspartate by mutations at positions S303, S304 and S328 to mimic phosphorylation; iii) addition of arachidonic acid (AA), a well known activator molecule in vitro. It has been shown that these three activating methods transform p47phox to an open configuration with similar characteristics. However, we have found that the effects of these methods are significantly different. Indeed, the conformational changes observed by circular dichroism are different. For p47phox, the addition of AA destructures the protein. Its phosphorylation induces a bathochromic displacement of the bands, whereas the mutations S-D lead to an opposite displacement. For the dimer p47phox-p67phox , the addition of AA destructures the proteins while mutations induce hardly no changes. We have measured the dissociation constant Kd of the complex p47phox-p67phox. For wild type proteins, Kd value is low (4±2 nM), while mutations of p47phox as well as addition of AA increase its value up to 50 nM, showing a decrease of affinity between p47phox and p67phox. Moreover, on the whole complex, the effect of phosphorylation of p47phox is different from mutations. We have shown that the EC50 values relative to p67phox are sensitive to the various modifications of p47phox. Phosphorylation of p47phox decreases EC₅₀, while double or triple mutations increase its value. We have confirmed that phosphorylation and mutation are not sufficient to activate the enzyme. The presence of AA is a prerequisite for the functionning of the complex, i.e. production of superoxide. The binding order of the cytosolic proteins seems random but it is necessary that all the components be present during the activation by AA. Finally, deletion of the C terminal part of p47phox (aa 343 to 390, interaction domain with p67phox) leads to the absence of dimer formation but does not affect the enzyme activity. These results bring new information on the role of dimerisation of p47-p67 and on that of phosphorylation in the activation of NADPH oxidase in vitro
Bettignies, Geoffroy de. "Analyse fonctionnelle de la Rho GAP codée par le gène RGD1 chez la levure Saccharomyces cerevisiae : mise en évidence de relations avec la "voie PKC"". Bordeaux 2, 2000. http://www.theses.fr/2000BOR28740.
Pełny tekst źródłaKsiążki na temat "PTC mutation"
Derks, Allen Kimbell. Synechococcus sp. PCC 7002 CpcB lyase null mutations alter phycocyanin chromophore function and, consequently, affect the redistribution of excitation energy via the light state transition. St. Catharines, Ont: Brock University, Dept. of Biological Sciences, 2007.
Znajdź pełny tekst źródłaMatthew Kynes, J. Hemophilia (Presentation in Emergency Surgery). Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0085.
Pełny tekst źródłaCzęści książek na temat "PTC mutation"
Enoiu, Eduard P., Daniel Sundmark, Adnan Čaušević, Robert Feldt i Paul Pettersson. "Mutation-Based Test Generation for PLC Embedded Software Using Model Checking". W Testing Software and Systems, 155–71. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-47443-4_10.
Pełny tekst źródłaBuzby, J. S., R. O. Mumma, D. A. Bryant, J. Gingrich, R. H. Hamilton, R. D. Porter, C. A. Mullin i S. E. Stevens. "Genes with Mutations Causing Herbicide Resistance from the Cyanobacterium Synechococcus PCC 7002". W Progress in Photosynthesis Research, 757–60. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-017-0519-6_157.
Pełny tekst źródłaShari, Ummi Syuhada Halmi, Azlin Suhaida Azmi i Azura Amid. "Chemical Mutation Method for High CO2-Requiring-Mutants of the Cyanobacterium Synechococcus sp. PCC 7002". W Multifaceted Protocol in Biotechnology, 53–62. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2257-0_5.
Pełny tekst źródłaGingrich, Jeffrey C., Jeffrey S. Buzby, Veronica L. Stirewalt i Donald A. Bryant. "Genetic analysis of two new mutations resulting in herbicide resistance in the cyanobacterium Synechococcus sp. PCC 7002". W Molecular Biology of Photosynthesis, 353–69. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-2269-3_16.
Pełny tekst źródłaSchulz, R., L. B. Smart, J. Yu i L. McIntosh. "A New Set of Site-Directed Mutations in Photosystem I Core Reaction Center from Synechocystis sp. PCC 6803". W Photosynthesis: from Light to Biosphere, 1097–100. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0173-5_259.
Pełny tekst źródłaZeng, Mingtao, Irit Sagi, Michael C. W. Evans, Nathan Nelson i Chanoch Carmeli. "Site Directed and Suppressor Mutations of Ex Ligands in Psab of Photosystem I in Synechocystis SP PCC 6803". W Photosynthesis: Mechanisms and Effects, 643–46. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-3953-3_152.
Pełny tekst źródłaMeng, Xiangxiu, Xuejun Zhu, Yunpeng Ding i Dengrong Qi. "Application of Image Recognition in Precise Inoculation Control System of Pleurotus Eryngii". W Proceeding of 2021 International Conference on Wireless Communications, Networking and Applications, 988–1005. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2456-9_100.
Pełny tekst źródłaAstier, C., G. Ajlani, I. Perewoska, M. Picaud i C. Vernotte. "Expected and Unexpected Effects of Mutations Conferring Herbicide Resistance on Photosystem II Activity in Synechocystis PCC 6714 and 6803". W Research in Photosynthesis, 575–78. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-009-0383-8_126.
Pełny tekst źródłaChu, Hsiu-An, Anh P. Nguyen i Richard J. Debus. "An Improved Host Strain of Synechocystis sp. PCC 6803 for Introducing Site-Directed Mutations into the D1 Protein of Photosystem II". W Photosynthesis: from Light to Biosphere, 1417–20. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0173-5_334.
Pełny tekst źródłaErmakova-Gerdes, Svetlana, Sergey Shestakov i Wim Vermaas. "Development of a Photosystem I-Less Strain of Synechocystis sp. PCC 6803 for Analysis of Mutations in the Photosystem II Proteins D2 and CP43". W Photosynthesis: from Light to Biosphere, 483–86. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0173-5_111.
Pełny tekst źródłaStreszczenia konferencji na temat "PTC mutation"
Sawa, T. "Radial network reconfiguration method in distribution system using mutation Particle Swarm Optimization". W 2009 IEEE Bucharest PowerTech (POWERTECH). IEEE, 2009. http://dx.doi.org/10.1109/ptc.2009.5281827.
Pełny tekst źródłaDanysh, Brian P., Maria E. Cabanillas i Marie-Claude Hofmann. "Abstract 2933: Long-term BRAF(V600E) inhibition results in a spontaneous KRAS(G12D) mutation and increased epithelial to mesenchymal transition (EMT) in papillary thyroid cancer cells (PTC)". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2933.
Pełny tekst źródłaWu, Xiaoxue, Wei Zheng, Zhao Shi, Zehai Wang, Lixin Cao i Dejun Mu. "Concurrency Bug-Oriented Mutation Operators Design for Java". W 2018 IEEE International Conference on Progress in Informatics and Computing (PIC). IEEE, 2018. http://dx.doi.org/10.1109/pic.2018.8706335.
Pełny tekst źródłaMuhovic, D., B. Smolovic, A. Hodzic i B. Peterlin. "CAROLI'S DISEASE (CD) CAUSED BY VERY RARE GENETIC MUTATION, MISDIAGNOSED WITH ERCP AND MRCP AS PRIMARY SCLEROSING CHOLANGITIS (PSC)". W ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681852.
Pełny tekst źródłaLeeman-Neill, Rebecca J., Alina V. Brenner, Mark P. Little, Andre C. Bouville, Tetyana I. Bogdanova, Maureen Hatch, Kiyohiko Mabuchi, Mykola D. Tronko i Yuri E. Nikiforov. "Abstract 2544: Associations between RET/PTC rearrangements, BRAF and RAS mutations and radiation dose, age at exposure, and latency in post-Chernobyl thyroid cancer". W 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.am2012-2544.
Pełny tekst źródłaSeynaeve, C., P. Vencken, M. Hooning, M. Menke-Pluymers, A. Heemskerk-Gerritsen, Doorn L. Van, M. Collee i in. "P4-11-04: Risk of Primary (PBC) and Contralateral Breast Cancer (CBC) after Ovarian Cancer (OC) in BRCA1 and BRCA2 Mutation Carriers; Implications for Surveillance and Risk Reducing Mastectomy." W Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-11-04.
Pełny tekst źródłaLu, Shun, Jian Fang, Lejie Cao, Xingya Li, Qisen Guo, Jianying Zhou, Ying Cheng i in. "Abstract CT031: Preliminary efficacy and safety results of savolitinib treating patients with pulmonary sarcomatoid carcinoma (PSC) and other types of non-small cell lung cancer (NSCLC) harboringMETexon 14 skipping mutations". W 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-ct031.
Pełny tekst źródłaLu, Shun, Jian Fang, Lejie Cao, Xingya Li, Qisen Guo, Jianying Zhou, Ying Cheng i in. "Abstract CT031: Preliminary efficacy and safety results of savolitinib treating patients with pulmonary sarcomatoid carcinoma (PSC) and other types of non-small cell lung cancer (NSCLC) harboringMETexon 14 skipping mutations". W 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-ct031.
Pełny tekst źródłaRaporty organizacyjne na temat "PTC mutation"
Sessa, Guido, i Gregory Martin. role of FLS3 and BSK830 in pattern-triggered immunity in tomato. United States Department of Agriculture, styczeń 2016. http://dx.doi.org/10.32747/2016.7604270.bard.
Pełny tekst źródłaOhad, Itzhak, i Himadri Pakrasi. Role of Cytochrome B559 in Photoinhibition. United States Department of Agriculture, grudzień 1995. http://dx.doi.org/10.32747/1995.7613031.bard.
Pełny tekst źródłaGrumet, Rebecca, i Benjamin Raccah. Identification of Potyviral Domains Controlling Systemic Infection, Host Range and Aphid Transmission. United States Department of Agriculture, lipiec 2000. http://dx.doi.org/10.32747/2000.7695842.bard.
Pełny tekst źródłaMcClure, Michael A., Yitzhak Spiegel, David M. Bird, R. Salomon i R. H. C. Curtis. Functional Analysis of Root-Knot Nematode Surface Coat Proteins to Develop Rational Targets for Plantibodies. United States Department of Agriculture, październik 2001. http://dx.doi.org/10.32747/2001.7575284.bard.
Pełny tekst źródłaAvni, Adi, i Gitta L. Coaker. Proteomic investigation of a tomato receptor like protein recognizing fungal pathogens. United States Department of Agriculture, styczeń 2015. http://dx.doi.org/10.32747/2015.7600030.bard.
Pełny tekst źródłaOhad, Nir, i Robert Fischer. Regulation of Fertilization-Independent Endosperm Development by Polycomb Proteins. United States Department of Agriculture, styczeń 2004. http://dx.doi.org/10.32747/2004.7695869.bard.
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