Littérature scientifique sur le sujet « ZNF318 »
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Articles de revues sur le sujet "ZNF318"
Nizhnichenko, Vladimir A., Alexey V. Boyko, Talia T. Ginanova et Igor Yu Dolmatov. « Muscle Regeneration in Holothurians without the Upregulation of Muscle Genes ». International Journal of Molecular Sciences 23, no 24 (16 décembre 2022) : 16037. http://dx.doi.org/10.3390/ijms232416037.
Texte intégralMitchell, Emily, Michael Spencer Chapman, Nicholas Williams, Kevin J. Dawson, Nicole Mende, Emily Calderbank, Hyunchul Jung et al. « Clonal Dynamics of Normal Haematopoiesis with Human Ageing ». Blood 138, Supplement 1 (5 novembre 2021) : 598. http://dx.doi.org/10.1182/blood-2021-150152.
Texte intégralSobocińska, Joanna, Joanna Nowakowska, Sara Molenda, Anna Olechnowicz, Kacper Guglas, Joanna Kozłowska-Masłoń, Urszula Kazimierczak et al. « Zinc Finger Proteins in Head and Neck Squamous Cell Carcinomas : ZNF540 May Serve as a Biomarker ». Current Oncology 29, no 12 (16 décembre 2022) : 9896–915. http://dx.doi.org/10.3390/curroncol29120779.
Texte intégralDougherty, Michael P., Lynn P. Chorich et Lawrence Clarke Layman. « Evaluation of Mayer-Rokitansky-Kuster-Hauser (MRKH) Patient Families by Whole Genome Sequencing ». Journal of the Endocrine Society 5, Supplement_1 (1 mai 2021) : A501—A502. http://dx.doi.org/10.1210/jendso/bvab048.1025.
Texte intégralIshikawa, S., M. Kai, Y. Takei, K. Okui, T. Takahashi, M. Suzuki, M. Ogawa et Y. Nakamura. « Isolation and mapping of a human zinc finger gene (ZNF188) homologous to ZNF187, a serum-response-element binding protein ». Cytogenetic and Genome Research 77, no 3-4 (1997) : 185–89. http://dx.doi.org/10.1159/000134572.
Texte intégralYan, Feng-Juan, Yong-Jian Wang, Shi-Ran Yan, Jun Lu et Yuan-Lin Zheng. « ZNF300 stimulates fatty acid oxidation and alleviates hepatosteatosis through regulating PPARα ». Biochemical Journal 476, no 2 (31 janvier 2019) : 385–404. http://dx.doi.org/10.1042/bcj20180517.
Texte intégralPieraccioli, Marco, Sara Nicolai, Consuelo Pitolli, Massimiliano Agostini, Alexey Antonov, Michal Malewicz, Richard A. Knight, Giuseppe Raschellà et Gerry Melino. « ZNF281 inhibits neuronal differentiation and is a prognostic marker for neuroblastoma ». Proceedings of the National Academy of Sciences 115, no 28 (25 juin 2018) : 7356–61. http://dx.doi.org/10.1073/pnas.1801435115.
Texte intégralDeng, Yu-Qin, Gang-Yong Kong, Song Li, Fen Li et Si-Lu Wen. « Upregulation of lnc-ZNF281 Inhibits the Progression of Glioma via the AKT/GSK-3β/β-Catenin Signaling Pathway ». Journal of Immunology Research 2021 (11 mai 2021) : 1–9. http://dx.doi.org/10.1155/2021/5573071.
Texte intégralFahmé, Pia, Farah Ramadan, Diep Tien Le, Kieu-Oanh Nguyen Thi, Sandra E. Ghayad, Nader Hussein, Chantal Diaz, Martine Croset, Philippe Clézardin et Pascale A. Cohen. « The Intricate Interplay between the ZNF217 Oncogene and Epigenetic Processes Shapes Tumor Progression ». Cancers 14, no 24 (8 décembre 2022) : 6043. http://dx.doi.org/10.3390/cancers14246043.
Texte intégralKubanov, A. A., A. A. Kubanova, A. E. Karamova et A. A. Mineyeva. « Prevalence of genetic risk factors of psoriasis among the population of the Russian Federation ». Vestnik dermatologii i venerologii 90, no 6 (24 décembre 2014) : 69–76. http://dx.doi.org/10.25208/0042-4609-2014-90-6-69-76.
Texte intégralThèses sur le sujet "ZNF318"
Ke, Qi. « Negative Regulation of Host Innate Immune Signaling and Response Pathways by Viral and Host Regulatory Factors ». University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1470185159.
Texte intégralStrachan, Joanna. « Expression and interactions of the ubiquitin receptor ZNF216 ». Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12707/.
Texte intégralHahn, Stefanie. « Characterization of ZNF281 and its role in colorectal carcinogenesis ». Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-177446.
Texte intégralNguyen, Thanh Nhan. « Deeper insights into the deleterious roles of ZNF217 in tumorigenesis and the identification of a novel and functional interplay between ZNF217 and ERalpha in breast cancer ». Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10331.
Texte intégralZNF217 is a candidate oncogene encoding for a Krüppel-like transcription factor. This study aims at exploring deeper insights on deleterious roles of ZNF217 and the prognostic significance of ZNF217 expression in breast cancers. We found that: (i) high levels of ZNF217 expression (at both mRNA and protein levels) are associated with poor prognosis in breast cancer patients, more particularly in ER+/Luminal/Luminal A breast cancers; (ii) ZNF217 induces epithelial-mesenchymal transition (EMT) in human mammary epithelial cells via the TGF-beta-activated Smad signaling pathway; (iii) in vitro ZNF217 stimulates several aggressive phenotypes in breast cancer cells, including anchorage-independent growth, cell migration and invasion; (iv) ZNF217 stimulates tumor growth and promotes the development of metastases in vivo; (v) ZNF217 binds with ERalpha and enhances 17beta- estradiol (E2)-induced ERalpha transactivation by increasing the recruitment of ERalpha to estrogen-responsive elements (EREs); (vi) ZNF217 increases mammosphere formation in ER– or ER+ breast cancer cell lines; (vii) ZNF217 confers resistance to endocrine therapy (tamoxifen) in ER+ breast cancer cells, and (viii) high levels of ZNF217 expression are associated with shorter relapse-free survival (RFS) in breast cancer patients treated with endocrine therapy only. Our findings suggest that ZNF217 expression represents a novel and powerful prognostic biomarker in ER+/Luminal/Luminal A breast cancers, allowing the re-stratification of these “good prognosis” breast cancers, which are currently not further classified by any other biomarkers available. In conclusion, ZNF217 could be a potential therapeutic target for a personalized treatment strategy in patients overexpressing ZNF217, in particular in ER+/ZNF217+ patients
Mallin, Lucy Janet. « Understanding the relationship between IRF-1 and the transcriptional repressor ZNF350 ». Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15893.
Texte intégralBellanger, Aurélie. « ZNF217, un rôle majeur dans le cancer du sein : un nouvel instigateur du développement de métastases ostéolytiques : isoforme ZNF217-ΔE4 : implication en cancérogénèse mammaire et valeur pronostique ». Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1007.
Texte intégralZNF217 is an oncogene encoding for a Krüppel-like transcription factor. Our aims were to explore the roles of the ZNF217 oncogene in the development of breast cancer metastases to the bone and to decipher the prognostic value and the functions of a new ZNF217 isoform. Our work identified that high ZNF217 mRNA expression levels within the primitive breast tumor could represent an indicator for future recurrence to the bone. Further in vitro experiment demonstrated that ZNF217 is a new activator of the BMP pathway and that the inhibition of this pathway could inhibit the metastatic properties of ZNF217-positive breast cancer cells in vitro (migration, invasion, chemotaxis to bone cells). In vivo in mice, ZNF217-positive breast cancer cells developed osteolytic metastases very faster. In our second axis, we have proven the existence of the ZNF217-?E4 isoform and we found that this isoform possesses a prognostic significance associated with a poor prognosis in ER-a+ breast cancer. Furthermore, cells overexpressing ZNF217-?E4 developed a more aggressive phenotype than cells overexpressing ZNF217-WT (proliferation, paclitaxel resistance). Interestingly, ZNF217-?E4 seems to play a regulatory role regarding ZNF217-WT expression. In conclusion, ZNF217 and/or the BMP pathway could represent potential therapeutical targets in the management of ZNF217 positive breast cancer
PIERACCIOLI, MARCO. « Functional role of the zinc finger factor ZNF281 in DNA damage response ». Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2015. http://hdl.handle.net/2108/203092.
Texte intégralThe survival of organisms depends on the accurate transmission of genetic information from one cell to its daughters. Such faithful transmission requires not only extreme accuracy in replication of DNA and precision in chromosome distribution, but also the ability to survive spontaneous and induced DNA damage while minimizing the number of heritable mutations. Therefore, cells are constantly under threat from the cytotoxic and mutagenic effects of DNA damaging agents. To respond to these threats, eukaryotes have evolved the DNA damage response (DDR). The DDR is a complex array of different mechanisms that have the ability to sense DNA damage and transduce this information to the cell in order to modulate cellular responses to DNA damage. Cells possess several enzymatic tools capable of remodeling and repairing DNA; however, their activities must be tightly regulated in a temporal, spatial, and DNA lesion-appropriate fashion to optimize repair and prevent unnecessary and potentially deleterious alterations in the structure of DNA during normal cellular processes. During the past several years, considerable progress has been made in elucidating the components and the processes of the eukaryotic DDR. A central issue in this field, which remains to be understood in greater detail, is the identification of the controllers of the expression of DDR proteins. Interestingly, in recent years an increasing number of studies have revealed that several TFs regulate DNA repair directly and can function as integral components of the repair machinery itself in a transcription independent fashion. In fact, DNA damage-inducing insults (irradiation, chemotherapy drugs) promote translocation of some TFs directly to DNA lesions, where they actively facilitate DNA repair. ZNF281 is a zinc finger transcription factor involved in the control of cellular stemness and Epithelial Mesenchymal Transition (EMT). In this study we analyze the roles of ZNF281 during DDR. We report that ZNF281 expression increased after genotoxic stress caused by DNA damaging drugs (Etoposide, Doxorubicin, Camptothecin) in cancer cell lines, normal keratinocytes and in mouse skin in vivo. Comet assays demonstrated that DNA repair was delayed in cells silenced for the expression of ZNF281 and treated with Etoposide. Furthermore, RT profiler array analysis demonstrated that the expression of ten DDR genes was down-regulated in cells treated with Etoposide and silenced for ZNF281. In line with these findings, XRCC2 and XRCC4, two genes that take part in Homologous Recombination (HR) and Non Homologous End Joining (NHEJ) respectively, were transcriptionally activated by ZNF281 through a DNA binding-dependent mechanism as demonstrated by luciferase assays and Chromatin crosslinking ImmunoPrecipitation (ChIP) experiments. In addition, ZNF281 works as a c-Myc co-factor to stimulate the expression of nucleolin and cyclin B1; instead c-Myc, which also binds to the promoters of XRCC2 and XRCC4, was unable to promote their transcription or to modify ZNF281 activity. Bioinformatic analysis of 1971 breast cancer patients disclosed a significant correlation between the expression of ZNF281 and XRCC2. Moreover proteomic analysis and Proximity Ligation Assay (PLA) demonstrated that ZNF281 interacts with DNA-PK, an important protein of DDR, suggesting a transcription-independent role of ZNF281 in DDR. Our data highlight, for the first time, the involvement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the expression of genes that act in different repair mechanisms and through interaction with with corecomponents of DNA repair pathways.
Ogo, Ogo Agbor. « Cellular responses to zinc involving the transcription factor ZNF658 and its target genes ». Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2752.
Texte intégralHahn, Stefanie [Verfasser], et Heiko [Akademischer Betreuer] Hermeking. « Characterization of ZNF281 and its role in colorectal carcinogenesis / Stefanie Hahn. Betreuer : Heiko Hermeking ». München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1065610114/34.
Texte intégralJordanovski, Darko [Verfasser], Thorsten [Akademischer Betreuer] Hoppe et Herbert [Akademischer Betreuer] Pfister. « Posttranslationale Kontrolle des zellulären Transkriptionsfaktors PBF/ZNF395 / Darko Jordanovski. Gutachter : Thorsten Hoppe ; Herbert Pfister ». Köln : Universitäts- und Stadtbibliothek Köln, 2012. http://d-nb.info/1038224853/34.
Texte intégralChapitres de livres sur le sujet "ZNF318"
Jordanovski, Darko, Christine Herwartz et Gertrud Steger. « ZNF395 (HDBP2 /PBF) is a Target Gene of Hif-1α ». Dans Huntington's Disease - Core Concepts and Current Advances. InTech, 2012. http://dx.doi.org/10.5772/30659.
Texte intégralActes de conférences sur le sujet "ZNF318"
Pérez Huacuja Urista, J. M., M. Maldonado, J. Calyeca, R. Ramirez, C. Becerril, M. Selman et A. Pardo. « Role of ZNF365 in Pulmonary Fibrosis ». Dans American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5238.
Texte intégralPérez Huacuja Urista, J. M., M. Maldonado, F. Toscano-Marquez, R. Ramírez, C. Becerril, Y. Romero, M. Selman et A. Pardo. « ZNF365 Downregulation Induces Senescence in Lung Fibroblasts and Epithelial Cells ». Dans American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1951.
Texte intégralMessana, Matthew J., Chao Yang et Laurie E. Littlepage. « Abstract 4252 : Regulation of the oncogene ZNF217 by localization in breast cancer ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4252.
Texte intégralMessana, Matthew J., et Laurie E. Littlepage. « Abstract 1979 : Regulation of the oncogene ZNF217 by localization in breast cancer ». Dans 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.am2015-1979.
Texte intégralFurukawa, Daisuke, Tsuyoshi Chijiwa, Masahiro Matsuyama, Masaya Mukai, Ei-ichi Matsuo, Osamu Nishimura, Kenji Kawai et al. « Abstract 1543 : Clinical significance of ZNF185 intracellular localization in pancreatic ductal carcinoma ». Dans 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.am2016-1543.
Texte intégralNolte, Elke, Jaroslaw Szczyrba, Martin Hart, Celina Döll, Sven Wach, Helge Taubert, Bastian Keck et al. « Abstract 3090 : miR-24 influences proliferation of prostate cancer cellsin vitrovia targeting ZNF217. » Dans 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.am2013-3090.
Texte intégralSuarez, Christopher, Sunil S. Badve et Laurie E. Littlepage. « Abstract B47 : The role of ZNF217 in the development of breast cancer chemoresistance ». Dans Abstracts : AACR Precision Medicine Series : Drug Sensitivity and Resistance : Improving Cancer Therapy ; June 18-21, 2014 ; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-b47.
Texte intégralBrown, Kevin M., Jun Fang, Jinping Jia, Zhaoming Wang, Matthew Makowski, Tongwu Zhang, Jason Hoskins et al. « Abstract 4610 : Functional characterization of a multicancer risk locus on chr5p15.33 reveals regulation ofTERTby ZNF148 ». Dans 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.am2015-4610.
Texte intégralFacchine, Beth, Junmin Wu, Megan Fabry, Matt Messana, William Kaliney et Laurie Littlepage. « Abstract 3341 : Inhibiting the destruction of the oncogene ZNF217 promotes breast cancer metastasis to lung ». Dans 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.am2018-3341.
Texte intégralMartínez, Alejandra Rodríguez, Elisa M. Vuorinen, Anastasia Shcherban, Nina K. Rajala, Matti Nykter et Anne Kallioniemi. « Abstract 3353 : ZNF414 as a functionally relevant transcription factor in pancreatic and breast cancer cells ». Dans 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.am2018-3353.
Texte intégralRapports d'organisations sur le sujet "ZNF318"
Gregg, Jeffrey P., et Sheryl R. Krig. The ZNF217 Breast Cancer Oncogene Amplified at 20q13 : A Potential Marker for Invasiveness. Fort Belvoir, VA : Defense Technical Information Center, mars 2012. http://dx.doi.org/10.21236/ada564327.
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