Добірка наукової літератури з теми "Alterations of transcription factors"
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Статті в журналах з теми "Alterations of transcription factors"
Tang, Jinglong, and Masaya Baba. "MiT/TFE Family Renal Cell Carcinoma." Genes 14, no. 1 (January 5, 2023): 151. http://dx.doi.org/10.3390/genes14010151.
Повний текст джерелаOrzechowska-Licari, Emilia J., Joseph F. LaComb, Aisharja Mojumdar, and Agnieszka B. Bialkowska. "SP and KLF Transcription Factors in Cancer Metabolism." International Journal of Molecular Sciences 23, no. 17 (September 1, 2022): 9956. http://dx.doi.org/10.3390/ijms23179956.
Повний текст джерелаLee, J. S., R. H. See, T. Deng, and Y. Shi. "Adenovirus E1A downregulates cJun- and JunB-mediated transcription by targeting their coactivator p300." Molecular and Cellular Biology 16, no. 8 (August 1996): 4312–26. http://dx.doi.org/10.1128/mcb.16.8.4312.
Повний текст джерелаWilson, Hannah E., David A. Stanton, Stephanie Rellick, Werner Geldenhuys, and Emidio E. Pistilli. "Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG." American Journal of Physiology-Cell Physiology 320, no. 4 (April 1, 2021): C577—C590. http://dx.doi.org/10.1152/ajpcell.00264.2020.
Повний текст джерелаPazhani, Jayanthi, Vishnu Priya Veeraraghavan, and Selvaraj Jayaraman. "Transcription factors: a potential therapeutic target in head and neck squamous cell carcinoma." Epigenomics 15, no. 2 (January 2023): 57–60. http://dx.doi.org/10.2217/epi-2023-0046.
Повний текст джерелаKoch, Marilin, Stefan Czemmel, Felix Lennartz, Sarah Beyeler, Justyna Przystal, Parameswari Govindarajan, Denis Canjuga, et al. "CSIG-15. INHIBITION OF THE bHLH TRANSCRIPTIONAL NETWORKS BY A MUTATED E47 PROTEIN LEADS TO A STRONG ANTI-GLIOMA ACTIVITY IN VITRO AND IN VIVO." Neuro-Oncology 21, Supplement_6 (November 2019): vi47. http://dx.doi.org/10.1093/neuonc/noz175.185.
Повний текст джерелаGoodson, Michael, Brian A. Jonas, and Martin A. Privalsky. "Corepressors: Custom Tailoring and Alterations While you Wait." Nuclear Receptor Signaling 3, no. 1 (January 2005): nrs.03003. http://dx.doi.org/10.1621/nrs.03003.
Повний текст джерелаZhu, Qian, Xavier Tekpli, Olga G. Troyanskaya, and Vessela N. Kristensen. "Subtype-specific transcriptional regulators in breast tumors subjected to genetic and epigenetic alterations." Bioinformatics 36, no. 4 (September 16, 2019): 994–99. http://dx.doi.org/10.1093/bioinformatics/btz709.
Повний текст джерелаChen, Shali, Biao Feng, Biju George, Rana Chakrabarti, Megan Chen, and Subrata Chakrabarti. "Transcriptional coactivator p300 regulates glucose-induced gene expression in endothelial cells." American Journal of Physiology-Endocrinology and Metabolism 298, no. 1 (January 2010): E127—E137. http://dx.doi.org/10.1152/ajpendo.00432.2009.
Повний текст джерелаZhang, Dawn X., and Christopher K. Glass. "Towards an understanding of cell-specific functions of signal-dependent transcription factors." Journal of Molecular Endocrinology 51, no. 3 (October 15, 2013): T37—T50. http://dx.doi.org/10.1530/jme-13-0216.
Повний текст джерелаДисертації з теми "Alterations of transcription factors"
Morey, Ramonell Lluís. "Chromatin alterations imposed by the oncogenic transcription factor PML-RAR." Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7138.
Повний текст джерелаIn mammals, as in plants, mutations in SNF2-like DNA helicases/ATPases were shown to affect not only chromatin structure but also global methylation patterns, suggesting a potential functional link between chromatin structure and epigentic marks. The SNF2-like containing NuRD complex is involved in gene transcriptional repression and chromatin remodeling. We have previously shown that the leukemogenic protein PMLRARα represses target genes through recruitment of DNMTs and Polycomb complex. In this thesis, we demonstrate a direct role of the NuRD complex in aberrant gene repression and transmission of epigenetic repressive marks in acute promyelocytic leucemia (APL). We show that PML-RARα binds and recruits NuRD to target genes, including to the tumor-suppressor gene RAR2. In turn, the NuRD complex facilitates Polycomb binding and histone methylation at lysine 27. Retinoic acid treatment reduced the promoter occupancy of the NuRD complex. Knock-down of the NuRD complex in leukemic cells not only prevented histone deacetylation and chromatin compaction, but also impaired DNA and histone methylation as well as stable silencing, thus favoring cellular differentiation. These results unveil an important role for NuRD in the establishment of altered epigenetic marks in APL, demonstrating an essential link between chromatin structure and epigenetics in leukemogenesis that could be exploited for therapeutic intervention.
Ruiz, Emmanuelle. "Coopération entre les inducteurs de l’EMT (EMT-TF/miRNA) et les altérations oncogéniques dans la tumorigenèse mammaire." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10069.
Повний текст джерелаCancer cells are able to reactivate the Epithelio-Mesenchymal Transition (EMT), an embryonic mechanism, to acquire mobility and dedifferentiation capacities. EMT leads to a genetic reprogramming with the reactivation of EMT inductors, mainly transcription factors (EMT-TF) and the inhibition of miRNA. Otherwise, oncogenic stresses are essentials to tumor progression. The aim of my thesis project was to have a better understanding about the cooperation between events of genetic reprogramming occurring during EMT and oncogenic stresses during mammary tumor transformation. First, a screening based on oncogenic cooperation in soft agar assay, between EMT-TFs and oncogenic stresses was performed. Following a bioinformatics analysis, different EMT-TFs signatures associated with an oncogenic stress were identified. Thus, for example, the expression of EMT-TF ZEB1 and GSC were associated with the deletion of tumor suppressor gene PTEN to transform immortalized mammary epithelial cells. An immunohistochemistry analysis on a set of 558 triple negative breast cancers validated in vivo the presence of a correlation between the expressions of GSC and PTEN. However, this association seems to be more complex. Indeed, the expression of GSC is negatively associated with the nuclear expression of PTEN while it’s positively associated with the cytoplasmic expression of PTEN. Finally, an analysis of public metadata on cancer samples as TCGA or METABRIC is ongoing to validate these in vitro signatures and wider to determine how EMT or EMT-TFs associated signatures correlate with classical oncogenic pathways.Secondly, an in silico analysis, from predictive algorithms of miRNA targets, was performed to select miRNA able to inhibit the expression of several EMT-TFs. Two miRNA (miR-495 and miR-590-3p) were identified targeting several members of four principal’s families of EMT-TFs (FOXC, Snail, bHLH and ZEB). In vitro tests were realized to validate these regulations identifying Slug as a target of miR-590-3p. Moreover, these miRNAs expression in mammary cell lines is negatively correlated with EMT-TFs expression and EMT markers. A treatment with TGF-, a major EMT inductor, decreases their expression, potentially meaning that these miRNA can negatively regulate EMT. In parallel, several EMT-TFs are able to repress the expression of miR-590-3p, acting directly on its promotor, thus creating feedback loops. Functional studies using stable expression vector of miR-590-3p suggest a secondary role of this miRNA in the regulation of EMT because miR-590-3p deregulates EMT secondary markers as N-Cadherin. Functions restauration studies are planned to determine how important these feedback loops in mammary tumor progression are. To open the project, expression of these identified miRNA will be correlated with EMT-TF associated signatures and with classical oncogenic pathways to determine the link between these three components in mammary tumorigenesis. My thesis works are shown that there is an interactome between EMT inductors, oncogenic stresses and miRNA during human mammary transformation
McElwee, Joshua J. "A comparative analysis of transcriptional alterations in long-lived insulin/IGF-1-like signaling mutants in Caenorhabditis elegans and Drosophila melanogaster /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/4982.
Повний текст джерелаJamrog, Laura. "Impact des altérations génétiques de PAX5 sur le développement de la lignée lymphoïde B et dans la leucémogenèse des LAL-B." Electronic Thesis or Diss., Toulouse 3, 2021. http://www.theses.fr/2021TOU30306.
Повний текст джерелаThe PAX5 (Paired boX 5) gene encodes a key transcription factor crucial for B-cell differentiation. We showed that the two PAX5 isoforms are differentially regulated but have equivalent function during early B-cell differentiation. Indeed, PAX5A and PAX5B isoforms can both induce B-cell program but may have functional differences after B-cell activation. The tight control of their expression may thus reflect a way to finely tune PAX5 dosage during B-cell differentiation process. PAX5 is a well-known haploinsufficient tumor suppressor gene in human B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and is the main target of a wide diversity of somatic alterations in childhood and adult BCP-ALL, occurring in one third of sporadic cases. However, the role of PAX5 fusion proteins in BCP-ALL initiation and transformation is ill-known. We previously reported a new recurrent t(7;9)(q11;p13) chromosomal translocation in human BCP-ALL that juxtaposed PAX5 to the coding sequence of elastin (ELN). To study the function of the resulting PAX5-ELN fusion protein in BCP-ALL development, we generated a mouse model in which the PAX5-ELN transgene is expressed specifically in B cells. PAX5-ELN-expressing mice efficiently developed BCP-ALL phenotype with a penetrance of 80%. Leukemic transformation was associated with clonal Immunoglobulin gene rearrangement and recurrent secondary mutations in Ptpn11, Kras, Pax5, and Jak3 genes affecting key signaling pathways required for cell proliferation. Our functional studies demonstrated that PAX5-ELN impairs B-cell development in vitro and in vivo and induces an aberrant expansion of the pro-B cell compartment at the preleukemic stage. Our molecular and computational approaches identified PAX5-ELN-regulated candidate genes that establish the molecular bases of the preleukemic state to drive BCP-ALL initiation. In conclusion, our study provides a new in vivo model recapitulating the multistep leukemogenesis process of human BCP-ALL and strongly implicates PAX5 fusion proteins as potent oncoproteins in leukemia development. Furthermore, there is increasing evidence for an inherited genetic basis of susceptibility to childhood BCP-ALL. In this context, four unrelated families with childhood BCP-ALL expressing heterozygous PAX5 germline point mutations were recently reported: the recurrent mutation PAX5 G183S affecting the octapeptide domain of PAX5 has been described in three families while PAX5 R38H affecting its DNA-binding paired domain has been identified in another one. We strengthen the hypothesis of inherited character of familial BCP-ALL with the description of three novel familial BCP-ALL cases in related patients that express the germline PAX5 R38H mutation. To uncover the intrinsic effect of PAX5 R38H mutant in B-cell development, we performed in vitro, and in vivo functional assays combined with a gene expression analysis, based on a retroviral complementation approach. Our results indicated that PAX5 R38H mutant acts as a strong hypomorphic variant that fails to drive B-cell differentiation and does not exert a dominant-negative effect on wild-type PAX5. Syngeneic transplantation of PAX5 R38H-expressing cells demonstrated maintenance of engraftment capacity and led to development of BCP-ALL phenotype in mice. Our transcriptomic analysis of these PAX5 R38H-expressing cells showed that PAX5 R38H drastically alters the pattern of expression of PAX5 target genes but also revealed a distinct molecular signature specific to PAX5 R38H. Together with previous unrelated family study, our observations allow to establish the recurrence of the germline PAX5 R38H mutation associated with BCP-ALL. Our data also highlight the importance of transcriptional dysregulation in leukemogenesis of familial BCP-ALL, particularly of genes involved in B-cell differentiation
Redondo, Monte Enric [Verfasser], and Philipp [Akademischer Betreuer] Greif. "Investigation of transcription factor alterations in core binding factor leukemia : implications in clonal expansion, cell metabolism and lineage fate decisions / Enric Redondo Monte ; Betreuer: Philipp Greif." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/122568269X/34.
Повний текст джерелаBorralleras, Fumaña Cristina 1988. "Correlation between cognitive phenotype, neural morphology and molecular alterations in mouse models of Williams-Beuren syndrome : new therapeutic approaches." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/388032.
Повний текст джерелаLa síndrome de Williams-Beuren (SWB) és una malaltia rara del neurodesenvolupament causada per una deleció heterozigota d’entre 26 i 28 gens contigus a la regió 7q11.23. Fins ara, una gran part de l’atenció s’ha centrat en el seu característic perfil neurocognitiu. Tot i que s’han fet progressos molt importants pel que fa a la caracterització clínica o a les correlacions genotip-fenotip, seria de gran interès aprofundir en les característiques neuropatològiques de la SWB. En aquesta tesi, hem utilitzat un model de ratolí del SWB amb una deleció heterozigota que mimetitza la deleció més comuna d’aquests pacients. Hem caracteritzat el fenotip cognitiu i comportamental d’aquests ratolins i hem identificat alteracions moleculars i neuroanatòmiques rellevants per a la malaltia. Per altra banda, hem dut a terme dues estratègies terapèutiques: una teràpia gènica i un tractament farmacològic. Els resultats obtinguts remarquen la utilitat d’aquest model animal per a l’estudi dels mecanismes subjacents a la malaltia així com també per a avaluar noves aproximacions terapèutiques.
Chanapai, Seni. "Photocontrol of artificial transcription factors." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58014/.
Повний текст джерелаPinacho, Garcia Raquel. "SP Transcription factors in psychotic disorders." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/327025.
Повний текст джерелаMüller, Susanne. "Transcription factors regulating the Btk promoter /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2717-0.
Повний текст джерелаPaik, Elizabeth Jae-Eun. "Caudal Transcription Factors in Hematopoietic Development." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10254.
Повний текст джерелаКниги з теми "Alterations of transcription factors"
Ravid, Katya, and Jonathan D. Licht, eds. Transcription Factors. New York, USA: John Wiley & Sons, Inc., 2000. http://dx.doi.org/10.1002/0471223883.
Повний текст джерелаGossen, Manfred, Jörg Kaufmann, and Steven J. Triezenberg, eds. Transcription Factors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6.
Повний текст джерелаHiggins, Paul J., ed. Transcription Factors. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-738-9.
Повний текст джерела1947-, Locker Joseph, ed. Transcription factors. Oxford: BIOS, 2001.
Знайти повний текст джерелаYamaguchi, Nobutoshi, ed. Plant Transcription Factors. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8657-6.
Повний текст джерелаLink, Wolfgang, ed. FOXO Transcription Factors. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8900-3.
Повний текст джерелаYuan, Ling, and Sharyn E. Perry, eds. Plant Transcription Factors. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-154-3.
Повний текст джерелаMaiese, Kenneth, ed. Forkhead Transcription Factors. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1599-3.
Повний текст джерелаLatchman, David S. Eukaryotic transcription factors. 5th ed. Amsterdam: Elsevier/Academic Press, 2008.
Знайти повний текст джерелаEukaryotic transcription factors. 4th ed. Oxford: Academic, 2004.
Знайти повний текст джерелаЧастини книг з теми "Alterations of transcription factors"
Carlberg, Carsten, and Ferdinand Molnár. "Transcription Factors." In Mechanisms of Gene Regulation, 57–73. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7741-4_4.
Повний текст джерелаArampatzis, Adamantios, Lida Mademli, Thomas Reilly, Mike I. Lambert, Laurent Bosquet, Jean-Paul Richalet, Thierry Busso, et al. "Transcription Factors." In Encyclopedia of Exercise Medicine in Health and Disease, 867. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3139.
Повний текст джерелаGooch, Jan W. "Transcription Factors." In Encyclopedic Dictionary of Polymers, 929. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14992.
Повний текст джерелаCarlberg, Carsten, and Ferdinand Molnár. "Transcription Factors." In Mechanisms of Gene Regulation, 55–70. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7905-1_4.
Повний текст джерелаHerrera, F. J., D. D. Shooltz, and S. J. Triezenberg. "Mechanisms of Transcriptional Activation in Eukaryotes." In Transcription Factors, 3–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_1.
Повний текст джерелаSheen, J. H., and R. B. Dickson. "c-Myc in Cellular Transformation and Cancer." In Transcription Factors, 309–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_10.
Повний текст джерелаLasar, A., R. Marienfeld, T. Wirth, and B. Baumann. "NF-κB: Critical Regulator of Inflammation and the Immune Response." In Transcription Factors, 325–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_11.
Повний текст джерелаKumar, V., and D. P. Sarkar. "Hepatitis B Virus X Protein: Structure-Function Relationships and Role in Viral Pathogenesis." In Transcription Factors, 377–407. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_12.
Повний текст джерелаPascussi, J. M., Z. Dvorák, S. Gerbal-Chaloin, E. Assenat, L. Drocourt, P. Maurel, and M. J. Vilarem. "Regulation of Xenobiotic Detoxification by PXR, CAR, GR, VDR and SHP Receptors: Consequences in Physiology." In Transcription Factors, 409–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_13.
Повний текст джерелаMorishita, R., N. Tomita, Y. Kaneda, and T. Ogihara. "Potential of Transcription Factor Decoy Oligonucleotides as Therapeutic Approach." In Transcription Factors, 439–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_14.
Повний текст джерелаТези доповідей конференцій з теми "Alterations of transcription factors"
Zhang, Ji, and Morton H. Friedman. "The Adaptive Response of Endothelial Transcription to Increased Shear Stress In Vitro." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19318.
Повний текст джерелаCollins, Corolyn J., Richard B. Levene, Christina P. Ravera, Marker J. Dombalagian, David M. Livingston, and Dennis C. Lynch. "MOLECULAR CLONING OF THE HUMAN GENE FOR VON WILLEBRAND FACTOR AND IDENTIFICATION OF THE TRANSCRIPTION INITIATION SITE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642830.
Повний текст джерелаAbdel-Sayed, Philippe, Arne Vogel, and Dominique P. Pioletti. "Dissipation Can Act as a Mechanobiological Signal in Cartilage Differentiation." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-62268.
Повний текст джерелаGaykalova, Daria A., Chad A. Glazer, Rajita Vatapalli, Sheetal Bhan, Chunbo Shao, Patrick K. Ha, and Joseph A. Califano. "Abstract 2042: Cancer-specific transcription factor BORIS has different effects on expression of its target genes via chromatin structure alterations." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2042.
Повний текст джерелаHussain, Showket, Neha Singh, Irfana Salam, Mohammad A. Bhat, Nandita Kakkar, Mohammad M. Mir, Mushtaq A. Siddiqi, et al. "Abstract 2722: Transcription factor NF-kB in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2722.
Повний текст джерелаPonomarenko, J., T. Merkulova, G. Orlova, E. Gorshkova, O. Fokin, and M. Ponomarenko. "Mining genome variation to associate disease with transcription factor binding site alteration." In Proceedings 2nd Annual IEEE International Symposium on Bioinformatics and Bioengineering (BIBE 2001). IEEE, 2001. http://dx.doi.org/10.1109/bibe.2001.974424.
Повний текст джерела"Neuronal transcription factors in lifespan control." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-405.
Повний текст джерелаIsmail, Ayman M., and Hussam B. Khalail. "Urban design factors associated with coastal alterations." In 2010 International Conference on Environmental Engineering and Applications (ICEEA). IEEE, 2010. http://dx.doi.org/10.1109/iceea.2010.5596087.
Повний текст джерелаTsai, Zing Tsung-Yeh, Grace Tzu-Wei Huang, and Huai-Kuang Tsai. "Simultaneous Identification for Synergistic Transcription Factors and their Transcription Factor Binding Sites." In 2011 International Conference on Complex, Intelligent and Software Intensive Systems (CISIS). IEEE, 2011. http://dx.doi.org/10.1109/cisis.2011.90.
Повний текст джерелаVerdine, Gregory L. "Abstract IA1-2: Drugging oncogenic transcription factors." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-ia1-2.
Повний текст джерелаЗвіти організацій з теми "Alterations of transcription factors"
Arazi, Tzahi, Vivian Irish, and Asaph Aharoni. Micro RNA Targeted Transcription Factors for Fruit Quality Improvement. United States Department of Agriculture, July 2008. http://dx.doi.org/10.32747/2008.7592651.bard.
Повний текст джерелаMichelotti, Julia M. Identification of Mammary Specific Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada303179.
Повний текст джерелаSederoff, Ronald, Ross Whetten, David O'Malley, and Malcolm Campbell. Transcription Factors in Xylem Development. Final report. Office of Scientific and Technical Information (OSTI), July 1999. http://dx.doi.org/10.2172/760586.
Повний текст джерелаIyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436905.
Повний текст джерелаIyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada485280.
Повний текст джерелаLyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada455791.
Повний текст джерелаLyer, Vishwanath R. Genome-Wide Chromosomal Targets of Oncogenic Transcription Factors. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470576.
Повний текст джерелаGrotewold, Erich. Engineering phenolics metabolism in the grasses using transcription factors. Office of Scientific and Technical Information (OSTI), July 2013. http://dx.doi.org/10.2172/1088660.
Повний текст джерелаSchaber, John D. Expression and Activation of STAT Transcription Factors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 1998. http://dx.doi.org/10.21236/ad1012061.
Повний текст джерелаCharles J. Daniels. The Role of Multiple Transcription Factors In Archaeal Gene Expression. Office of Scientific and Technical Information (OSTI), September 2008. http://dx.doi.org/10.2172/937513.
Повний текст джерела