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Dissertations / Theses on the topic 'Transactivation'

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Published: 4 June 2021
Last updated: 10 March 2023

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1

Sutherland, Jacqueline Anderson. "The transactivation functions of Fos." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309211.

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2

Park, Frances E. "NF-kB DNA binding and transactivation /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3001261.

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3

Ramakrishnan, Venkatesh. "Structural analysis of a transactivation domain cofactor complex." Doctoral thesis, [S.l. : s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976325381.

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4

Bladen, Catherine Louise. "Transcriptional transactivation properties of the human MDM2 oncoprotein." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327321.

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5

Walker, S. M. "Transactivation of human immunodeficiency virus by human cytomegalovirus." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387104.

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6

Schäfer, Beatrix. "Transactivation of the EGFR Signal in Human Cancer Cells." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-23041.

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7

Betney, Russell. "Mutational analysis of the human androgen receptor transactivation domain." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401515.

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Mutants were created within the main activation function domain to investigate the structure and function of this region. Structural studies based on limited proteolysis and fluorescence spectroscopy experiments, indicate that though the N-terminus is not as specially structured as either the LBD or DBD, there are regions of specific folding within the activation domain.  Results from in silco investigation suggest several possible regions of a helix within the AF-1 domain, and mutants designed to disrupt these regions were less folded than the wild-type protein. Protein-protein interaction studies showed that the four mutants designed to potentially disrupt function rather than structure, had reduced binding to the large subunit of TFIIF - RAP74, but had no effect on binding to the transcriptional co-activator SRC-1a. In a functional assay performed in yeast cells, these four same mutants all showed reduced activity, showing the same trend as binding to RAP74. This could be an indication that the function of the AR is dependent upon binding to the general transcription factor TFIIF. Interestingly one of the mutants that was found to show increased structure over the wild-type protein was previously shown to have a reduced interaction with RAP74. This implies that structure is important for interaction with the transcription machinery. This was confirmed by FTIR experiments which can detect changes in the proportion of secondary structure present in a protein. These data show that the proportion of a helix present in the AF-1 domain increases when it is complexed with RAP74. GST pull-down assays then demonstrated that the complex of AF-1 and RAP74 enhanced the binding of the co-activator SRC-1a. This is the first time that this cooperativity has been demonstrated with nuclear receptors and interacting proteins. Additionally, specific phosphorylation of the AF-1 domain by glycogen synthase kinase 3 also increases the level of binding with SRC-1a. These data together suggest a possible mechanism of action for the androgen receptor and its involvement in regulating transcription.
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8

Chamberlain, Nancy Louise. "Molecular analysis of transcriptional transactivation by the androgen receptor." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186951.

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The physiological effects of steroid hormones are mediated through intracellular receptors that regulate transcription of hormone response element (HRE)-containing genes. Although the androgen receptor (AR) and the glucocorticoid receptor (GR) are coexpressed in many tissues and bind identical HREs, biological actions of each hormone are distinct. Elucidating the mechanisms by which AR and GR regulate transcription of their target genes is vital to understanding cell- and receptor-specific effects of steroid hormones. These receptor-specific effects were investigated using a system in which AR and GR differ in their abilities to activate transcription from the same reporter genes. To determine if the differential activity was due to inherent differences between AR and GR functional domains, the activities of AR/GR chimeric receptors were examined. Functional differences in the N-terminal modulatory domains and, to a lesser degree, the DNA binding domains, contributed to the differential transactivation. A panel of AR derivatives was constructed to examine the function of the N-terminal domain of this receptor. The AR modulatory domain contains a tract of glutamine residues encoded by the trinucleotide CAG. Expansion of this trinucleotide repeat is correlated with the incidence and severity of the degenerative neuromuscular syndrome Kennedy's disease. To investigate the relationship of this repeat to AR function, receptors that varied in the presence, position or size of the polyglutamine tract were constructed. Elimination of the tract resulted in elevated transactivation. Progressive expansion of the repeat caused a linear decrease in transcriptional activation. These results indicate the polyglutamine tract is inhibitory to AR transactivation function. Further analysis of the AR modulatory domain revealed two regions are necessary for maximal transactivation. Secondary structure prediction and site-directed mutagenesis of one region suggest a ten residue acidic amphipathic α-helix is critical for activity. The second region may be a member of the proline-rich class of activation domains. Together, these two regions may form an interaction surface that contacts a limiting factor(s) required for activated transcription. Receptor-selective interactions with promoter- or cell-specific auxiliary factors could control the specificity of steroid-regulated gene networks.
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9

Ramsay, Nicola. "GAL4-mediated transactivation of UAS-linked transgenes in Arabidopsis thaliana." Thesis, University of Warwick, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484177.

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10

Graham, Neil Stuart. "Development of a transactivation system for use in crop plants." Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343207.

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11

Seth, Alpna. "Functional Analysis of the c-MYC Transactivation Domain: A Dissertation." eScholarship@UMMS, 1992. https://escholarship.umassmed.edu/gsbs_diss/315.

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Many polypeptide growth factors act by binding to cell surface receptors that have intrinsic tyrosine kinase activity. Binding of these growth factors to their cognate receptors results in the initiation of mitogenic signals which then get transduced to the interior of the cell. A critical target for extracellular signals is the nucleus. A plethora of recent evidence indicates that extracellular signals can affect nuclear gene expression by modulating transcription factor activity. In this study, I have determined that the transactivation domain of c-Myc (protein product of the c-myc proto-oncogene) is a direct target of mitogen-activated signaling pathways involving protein kinases. Further, my study demonstrates that transactivation of gene expression by c-Myc is regulated as a function of the cell cycle. c-Myc is a sequence-specific DNA binding protein that forms leucine zipper complexes and can act as a transcription factor. Although, significant progress has been made in understanding the cellular properties of c-Myc, the precise molecular mechanism of c-Myc function in oncogenesis and in normal cell growth is not known. I have focused my attention on the property of c-Myc to function as a sequence-specific transcription factor. In my studies, I have employed a fusion protein strategy, where the transactivation domain of the transcription factor c-Myc is fused to the DNA binding domain and nuclear localization signal of the yeast transcription factor GAL4. This fusion protein was expressed together with a plasmid consisting of specific GAL4 binding sites cloned upstream of a minimal E1b promoter and a reporter gene. The activity of the c-Myc transactivation domain was measured as reporter gene activity in cell extracts. This experimental approach enabled me to directly monitor the activity of the c-Myc transactivation domain. Results listed in Chapter II demonstrate that the transactivation domain of c-Myc at Ser-62 is a target of regulation by mitogen-stimulated signaling pathways. Furthermore, I have determined that a mitogen activated protein kinase, p41mapk, can phosphorylate the c-Myc transactivation domain at Ser-62. Phosphorylation at this site results in a marked increase in transactivation of gene expression. A point mutation at the MAP kinase phosphorylation site (Ser-62) causes a decrease in transactivation. c-Myc expression is altered in many types of cancer cells, strongly implicating c-myc as a critical gene in cell growth control. The molecular mechanisms by which c-Myc regulates cellular proliferation are not understood. For instance, it is not clear where in the cell cycle c-Myc functions and what regulates its activity. In exponentially growing cells, the expression levels of c-Myc remain unchanged as the cells progress through the cell cycle. The function of c-Myc may therefore be regulated by a mechanism involving a post-translational modification, such as phosphorylation. Results described in chapter IV demonstrate that the level of c-Myc mediated transactivation oscillates as cells progress through the cell cycle and was greatly increased during the S to G2/M transition. Furthermore, mutation of the phosphorylation site Ser-62 in the c-Myc transactivation domain diminishes this effect, suggesting a functional role for this phosphorylation site in the cell cycle-specific regulation of c-Myc activity. Taken together, my dissertation study reveals a molecular mechanism for the regulation of nuclear gene expression in response to mitogenic stimuli.
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12

Cocklin, Simon. "Investigation into the molecular mechanism of nitrogen metabolite repression." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327280.

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13

Hassan, A. Quamrul. "Molecular complementation of mutant thyroid hormone receptors that disrupt transactivation mechanism." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 9.11 Mb., 175 p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3205433.

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14

Borcherds, Wade Michael. "Structure, Dynamics, and Evolution of the Intrinsically Disordered p53 Transactivation Domain." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4640.

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in numerous disease states, including cancers and neurodegenerative diseases. All proteins are dynamic in nature, occupying a range of conformational flexibilities. This inherent flexibility is required for their function, with ordered proteins and IDPs representing the least flexible, and most flexible, respectively. As such IDPs possess little to no stable tertiary or secondary structure, they instead form broad ensembles of heterogeneous structures, which fluctuate over multiple time scales. Although IDPs often lack stable secondary structure they can assume a more stable structure in the presence of their binding partners in a coupled folding binding reaction. The phenomenon of the dynamic behavior of IDPs is believed to confer several functional advantages but remains poorly understood. To that end the dynamic and structural properties of a family of IDPs - p53 transactivation domains (TAD) was measured and compared with the sequence divergence. Interestingly we were able to find stronger correlations between the dynamic properties and the sequence divergence than between the structure and sequence, suggesting that the dynamic properties are the primary trait being xiii conserved by evolution. These correlations were strongest within clusters of the IDPs that correlated with known protein binding sites. Additionally, we show strong correlations between the several available disorder predictors and the backbone dynamics of this family of IDPs. This indicates the potential of predicting the dynamic behavior of proteins, which may be beneficial in future drug design. The limited number of atomic models currently determined for IDPs hampers understanding of how their amino acid sequences dictate the structural ensembles they adopt. The current dearth of atomic models for IDPs makes it difficult to test the following hypotheses: 1. The structural ensembles of IDPs are dictated by local interactions. 2. The structural ensembles of IDPs will be similar above a certain sequence identity threshold. Based on the premise that sequence determines structure, structural ensembles were determined and compared for a set of homologous IDPs. Utilizing orthologues allows for the identification of important structural features and behaviors by virtue of their conservation. A new methodology of creating ensembles was implemented that broadly samples conformational space. This allowed us to find recurring local structural features within the structural ensembles even between the more distantly related homologues that were processed. This method of ensemble creation is also the first method to show convergence of secondary structural characteristics between discrete ensembles.
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15

Leeper, Thomas. "The novel ugagau hexaloop RNA structure, dipolar coupling refinement, and transactivation /." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3036840.

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16

Hart, Stefan. "Characterisation of the molecular mechanisms of EGFR signal transactivation in human cancer." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973410817.

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17

Chakraborty, Atanu. "Mechanism Of mom Gene Transactivation By Transcription Factor C Of Phage MU." Thesis, Indian Institute of Science, 2006. http://hdl.handle.net/2005/275.

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Regulation of transcription initiation is the major determining event employed by the cell to control gene expression and subsequent cellular processes. The weak promoters, with low basal transcription activities, are activated by activators. Bacteriophage Mu mom gene, which encodes a unique DNA modification function, is detrimental to cell when expressed early or in large quantities. Mu has designed a complex, well-controlled and orchestrated regulatory network for mom expression to ensure its synthesis only in late lytic cycle. The phage encoded transcription activator protein C activates the gene by promoter unwinding of the DNA and thereby recruiting of RNAP to the promoter. C protein functions as a dimer for DNA binding and transcription activation. Mutagenesis and chemical crosslinking studies revealed that the leucine zipper motif, and not the coiled coil motif in the N terminal region, is responsible for C dimerization. The DNA binding domain of C is a HTH domain which is preceded by the leucine zipper motif. The C protein is one of the few examples in the bacterial proteins containing both leucine zipper and HTH domain. Most of the transcription activators either influence initial binding of RNAP or conversion of closed to open complex formation. Very few activators act at subsequent steps of promoter-polymerase interaction. Earlier studies showed high level of transcription from a mutant mom promoter, tin7. Addition of C further increased transcription from Ptin7 indicating that C may have a role beyond polymerase recruitment. Each steps of transcription initiation have been dissected using the Ptin7 and a positive control (pc) mutant of C, R105D. The results revealed multi-step transcription activation mechanism for C protein at Pmom. C recruits RNAP at Pmom and subsequently increases the productive RNAP-promoter complex and enhances promoter clearance. To further understand the C mediated transactivation mechanism, interaction between C and RNAP was assessed. C interacts with holo and core RNAP only in presence of DNA. Positive control mutants of C, F95A and R015D, were found to be compromised in RNAP interactions. These mutants were efficient in RNAP recruitment to Pmom but do not enhance promoter clearance. Trypsin cleavage protection experiment indicated that probably C protein interacts with b¢ subunit of RNAP. Interaction between C and RNAP appears to enhance the formation of productive RNAP-promoter complex leading to promoter clearance. The connection between activator-polymerase interaction and transcription activation is well documented where the recruitment of RNAP is influenced. In case of activators acting at post recruitment steps of initiation, the role of polymerase contact is poorly understood. Our study shows that activator-polymerase interaction can lead to increased promoter clearance at Pmom by overcoming abortive initiation.
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18

Gschwind, Andreas Franz. "Investigations on the Molecular Mechanisms of EGFR Signal Transactivation in Human Cancer." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-9033.

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19

Hu, Catherine. "Evaluation of ginsenosides in transactivation and transrepression of human glucocorticoid receptor alpha." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/55877.

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20

Spencer, William John. "Phorbol ester-mediated NF-kappa-B transactivation is selectively inhibited by taxol." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0007/MQ44286.pdf.

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21

Tai, C. P. Andrew. "An in vivo analysis of specificity of gene transactivation by SOX proteins." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36906438.

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22

Tai, C. P. Andrew, and 戴賜鵬. "An in vivo analysis of specificity of gene transactivation by SOX proteins." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36906438.

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23

Vincent, Karla Kristine. "Transactivation of Beta 2 Adrenergic Receptor by Bradykinin type 2 Receptor via heterodimerization." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/37117.

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Although a long standing convention maintained that G Protein Coupled Receptors (GPCRs) exist in the plasma membrane solely as monomers, substantial work over the last two decades has demonstrated that these ubiquitous receptors can and in many cases, preferentially, exist as homodimers, heterodimers, or higher order oligomers. Often, two GPCRs of the same class heterodimerize; it is less common for two GPCRs of different signaling pathways to interact. The work presented here studied the physical and functional interaction of two GPCRs from discrete classes, the Beta 2 Adrenergic Receptor (β2AR), a Gαs-coupled receptor, and Bradykinin type 2 Receptor (Bk2R), a Gαq coupled receptor. These data show that Bk2R and β2AR are physically coupled when heterologously expressed in Xenopus oocytes, and in pheochromocytoma (PC12) cells and in freshly isolated murine ventricular myocytes, two systems that endogenously express these receptors. This physical coupling led to functional consequences in heterologous and endogenous expression systems, as Bk2R was able to transactivate β2AR signaling via its direct interaction with the receptor. Furthermore, coexpression of Bk2R shifted the dose response curve of β2AR for its selective agonist rightward in Xenopus oocyte electrophysiology experiments, suggesting the presence of Bk2R negatively affected β2AR native pharmacology. Up to thirty minutes of either bradykinin (BK) or isoproterenol exposure did not change the relative amount of Bk2R/β2AR heterodimer in PC12 cells, a rat adrenal medulla tumor cell line that endogenously expresses these receptors. Despite the obvious signaling consequences, the Bk2R/β2AR heterodimer accounted for only 10% of the total β2AR protein detected and 20% of the total Bk2R protein detected. When other Bk2R-specific ligands were also tested to examine the extent of β2AR transactivation, our data showed that both Lys-des-Arg-Bradykinin, a Bk2R partial agonist and NPC 567, a Bk2R antagonist, transactivated β2AR to the same extent as BK. Taken together, our data provide a novel mode of receptor regulation and signaling via Bk2R/β2AR heterodimerization. Because a large percentage of therapeutics target GPCRs, a greater understanding of how a GPCR heterodimer functions could be beneficial for targeting new drugs and refining existing drugs. Understanding the Bk2R/β2AR heterodimer provides a new perspective on the myriad of fucntional consequences that occur when a GPCR is activated.
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24

Marg, Beatrice. "Investigation on the EGFR transactivation by G protein coupled receptors in cancer cells." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-37493.

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25

Powell, Anne Terese. "Structure and Dynamics of the p53 Transactivation Domain Binding to MDM2 and RPA70." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4207.

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The tumor suppressor protein, p53, is mutated or dysregulated in nearly all human cancers(1). The amino terminal domains are essential for transcriptional activation in stressed cells and play a vital role in cell cycle regulation, apoptosis and senescence. The transactivation (TAD) and proline rich domains in this region are dynamic and intrinsically disordered; lacking stable secondary or tertiary structure. This region contains multiple binding sites; arguably, the most significant of these is for p53's negative regulator, the E3 ligase, MDM2. An important, but less understood interaction involving the single stranded DNA binding protein, RPA70A, is hypothesized to be involved in maintaining genome integrity(2-4). Additionally, the amino terminus contains an important single nucleotide polymorphism that has demonstrated different affinity for MDM2 and is of significant biological importance in the induction of apoptosis (5). Isothermal titration calorimetry (ITC) and nuclear magnetic resonance (NMR) spectroscopy were employed to investigate how the thermodynamics and the inherent flexibility of the amino terminus of p53 play a role in complex formation with the MDM2 or RPA70 proteins. Understanding the structure, dynamics, and function of p53 is paramount in the fight against cancer.
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26

Carreau, Charlotte. "Propriétés œstrogéniques des phyto-œstrogènes dans une lignée de cancer du sein : implication des domaines de transactivation du récepteur aux œstrogènes alpha." Bordeaux 1, 2008. http://www.theses.fr/2008BOR13571.

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Les phyto-œstrogènes (PE), molécules d’origine végétale, possèdent des homologies structurales avec les œstrogènes leur permettant de se lier aux récepteurs spécifiques aux œstrogènes (RE) et d’agir comme des molécules pro- ou anti-œstrogéniques. Les œstrogènes et les RE sont impliqués dans de nombreux processus physiologiques et physiopathologiques, notamment le cancer du sein. Il existe deux formes de RE (66 et 46 kDa) qui diffèrent par leur partie N-terminale, où est situé le domaine de transactivation AF-1. Le deuxième domaine de transactivation AF-2, ligand dépendant, est similaire dans les deux RE. L’objet de cette étude est de trouver parmi les PE testés ceux capables de moduler spécifiquement le RE (appelés SERM) dans une lignée cancéreuse mammaire, les MCF-7, afin de mieux comprendre leur impact sur le cancer du sein. Ainsi, il apparaît que les propriétés pro-œstrogéniques de certains PE sont associées à leur capacité à mobiliser le domaine AF-1 dans l’activation transcriptionnelle du RE. A l’inverse, les composés mobilisant préférentiellement le domaine AF-2 du RE induisent une faible activation transcriptionnelle et n’ont pas d’effets œstrogéniques. C’est le cas de l’entérolactone et la naringénine, SERM potentiels qui pourraient être de bons candidats dans un cadre de nutrition préventive contre le cancer du sein
Phytoestrogens (PE) are plants compounds sharing structural similarities with estrogens. These compounds, which bind to estrogen receptors (ER), may induce or inhibit estrogen action and have the potential to disrupt estrogen signalling. Estrogens and ER are involved in numerous physiological and/or pathological processes, in particular in breast cancer. The human ER (hER gene can be alternatively spliced into proteins of 66 and 46 kDa respectively, which differ on their N-terminal where is located the transactivation domain AF-1. The second transactivation domain AF-2, which is ligand-dependant, is present in both ER. To elucidate the yet unclear mechanisms of ER activation/inhibition by PE in further details and find selective estrogen receptor modulators (SERM), we performed a comprehensive analysis and potency comparison of hER transactivation by PE in a human breast cancer cell line, MCF-7. We show that estrogenic properties of some PE are linked to their capacity to induce an AF-1-dependant transactivation of hER. In contrast, the PE inducing an AF-2-dependant transactivation of hER are weak agonists and more importantly, they do not display any estrogenic properties. Such compounds, as enterolactone and naringenine, are interesting SERM, and further investigations should be performed to evaluate their potentials as candidates for a nutritional prevention of breast cancer
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27

Pollett, Jonathan Barclay. "The role of the PAR proteins, HLF and DBP, in transactivation and liver differentiation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28247.pdf.

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28

Ajumobi, Taiwo. "Beta-Blockers Act through Clathrin-Dependent Internalization and EGFR Transactivation to Promote ERK Phosphorylation." Digital Commons @ Butler University, 2014. http://digitalcommons.butler.edu/grtheses/267.

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For cardiovascular diseases such as high blood pressure, angina pectoris, and left ventricle hypertrophy; long-term activation of beta-adrenergic receptors is strongly linked to the progression of these diseases. A class of antagonistic drugs that target betaadrenergic receptors are collectively called beta-blockers. These drugs are commonly used to reduce the inotropic and chronotropic effects of beta-adrenergic receptor activation. This past decade has revealed that beta-blockers and other ligands are capable of functional selectivity at receptors. Functional selectivity describes the ability of ligands acting at 0 protein-coupled receptors (OPCRs) to preferentially activate or inhibit different signal transduction pathways. The studies on beta-adrenergic 2 receptors that explored functional selectivity showed that beta-blockers can be functionally selective by inhibiting the cAMP pathway while simultaneously activating ERK. The 0 protein coupled to beta-adrenergic receptors are the primary regulators of the cAMP, however there are a variety of pathways that can regulate ERK activity and few studies have tried to determine which pathway(s) the beta-blockers are targeting to cause this ERK activation. This is especially important for beta-adrenergic 2 receptors because they can activate ERK through multiple pathways (0 protein switching from G, to Oi/oprotein, beta-arrestin assisted or EOFR transactivation). ERK activation is linked to reversing cell damage caused by apoptosis signaling that results from G, activation by beta-adrenergic receptors. Understanding the specific pathways these beta-blockers can target for ERK activation would lead to better understanding of their therapeutic benefits. In this study we plan to elucidate the pathways several beta-blockers are targeting to activate ERK. In particular, we will investigate the role of clathrin-mediated receptor internalization and EGFR transactivation in beta-blocker-dependent ERK phosphorylation. In HEK 293 cells transfected with beta-adrenergic 2 receptors, we measured the changes in cAMP and ERK phosphorylation in response to the following beta-blockers labetalol, alprenolol, bucindolol, carvedilol, carazolol, leI 118,551 and propanolol. All of the beta-blockers studied inhibited isoproterenol-stimulated cAMP accumulation but stimulated the phosphorylation of ERK to varying degrees. Beta-blocker-mediated ERK phosphorylation was shown to be dependent on clathrin-dependent internalization and EGFR transactivation.
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29

Ozanne, Daniel M. "Isolation and characterisation of co-regulatory molecules involved in androgen receptor movement and transactivation." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327237.

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30

REIMUND, BERNARD. "Mecanismes de transactivation du promoteur e2a d'adenovirus par l'oncogene e1a et la proteine e4." Université Louis Pasteur (Strasbourg) (1971-2008), 1992. http://www.theses.fr/1992STR13057.

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Le gene e2a d'adenovirus, exprime durant la phase precoce de l'infection, sous le controle des proteines virales e1a et e4, est un excellent systeme-modele pour l'etude des mecanismes impliques dans la regulation de l'expression des genes transcrits par l'arn polymerase b (ou ii). L'analyse detaillee de la structure de ce promoteur a notamment revele l'existence de deux sites e2f, d'un site atf et de plusieurs sites c alpha, essentiels a la fois pour l'activite basale et la transactivation du gene par les proteines e1a et e4. Nous avons determine la contribution respective de chacun de ces elements dans le controle de l'activite du promoteur e2a et tente de caracteriser les mecanismes mis en uvre. Ainsi, nos resultats permettent de conclure que l'activation du promoteur par e1a implique des interactions directes entre cette proteine et le facteur atf, ainsi qu'une modulation eventuelle des liaisons des facteurs e2f et c alpha sur des sites communs. L'activation par e4 resulte d'une interaction de cette proteine avec le facteur e2f qui entraine la fixation cooperative de 2 molecules e2f sur le promoteur. D'autre part, l'etude de la regulation du promoteur e2a par les proteines e1a et e4 dans des cellules d'embryocarcinomes de souris, avant et apres differentiation, nous a permis d'approcher certains aspects de la differentiation cellulaire. Ainsi, nous avons pu etablir une relation entre l'activite du promoteur e2a et la presence de la proteine du retinoblastome qui module l'activite du facteur e2f et la presence de la proteine du retinoblastome qui module l'activite du facteur e2f en se complexant a celui-ci
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31

JOHN, MATTHIAS. "Analyse biochimique des domaines de dimerisation et de transactivation des proteines jun et fos." Université Louis Pasteur (Strasbourg) (1971-2008), 1996. http://www.theses.fr/1996STR13123.

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Le facteur de transcription ap-1 est compose d'homodimeres ou d'heterodimeres des proteines jun et fos qui possedent trois domaines majeurs: un domaine de dimerisation, le leucine zipper (zip), le domaine basique (b) pour la reconnaissance du site tre et un domaine de transactivation. En utilisant des peptides synthetiques, nous avons etudie l'importance de deux pairs de residus de charge oppose pour l'efficacite d'heterodimerisation des leucine zippers de jun et fos. Une etude biochimique et physico-chimique des domaines bzip entier de jun et fos fixe sur l'adn a montre qu'un site tre en solution subit un changement de conformation compatible avec une structure intermediaire entre les conformations b et a. Le facteur de transcription c-jun contient un domaine de transactivation appartenant a la famille des activateurs de transcription acide. Afin d'analyser la structure secondaire de ce domaine, j'ai synthetise un peptide correspondant aux acides amines 61 a 98 de c-jun et un deuxieme peptide avec deux phosphoserines en positions 63 et 73. En presence de trifluoroethanol, les peptides adoptent une conformation alpha-helicoidale
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32

Guilbert, Matthieu. "Impact de la transactivation des récepteurs membranaires par le (pro)NGF dans les cancers." Thesis, Lille 1, 2015. http://www.theses.fr/2015LIL10097/document.

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Le laboratoire INSERM U908 a montré que le Nerve Growth Factor (NGF) et son précurseur, le proNGF, sont impliqués dans l’agressivité des tumeurs mammaires via des effets sur la croissance, l’angiogenèse ou encore la migration/invasion. Pour autant, aucunes thérapies ciblées n’a à ce jour été approuvée suite à des essais cliniques de traitements visant à inhiber les effets du (pro)NGF et de leurs récepteurs dans les cancers. Ces résultats indiquent que la phosphorylation de TrkA est nécessaire mais pas suffisante pour expliquer le(s) mécanisme(s) par lequel(s) le NGF ou son précurseur participe(nt) au développement tumoral. L’obtention de lignées tumorales résistantes au lestaurtinib est un phénomène rapide, nous avons donc émis l’hypothèse que la signalisation de TrkA indépendante de sa phosphorylation existe de façon « innée » dans les cellules tumorales. Par l’analyse protéomique, nous avons ainsi découvert que le NGF induit le recrutement de CD44 et d’une cascade de signalisation p115RhoGEF/RhoA/ROCK1 (Aubert L*, Guilbert M* et al, Oncotarget, 2015 ; *co-premier auteur). Nous avons ainsi montré que le NGF via le complexe TrkA/CD44 induit la migration et l’invasion des cellules cancéreuses de sein in vivo, et augmente la tumorigénicité in vivo. Quant au proNGF, j’ai pu observer qu’il induit l’internalisation de l’EGFR par la phosphorylation du résidu Y1068. Il en résulte une diminution des effets prolifératif et pro-invasif de l’EGF dans les cellules tumorales. Ces résultats fondamentaux sont tout à fait intéressants même s’ils nécessitent leurs consolidations et doivent permettre de démontrer le caractère pronostic de la détection de TrkA et ses corécepteurs dans le cancer. Ainsi nos études permettront le développement de thérapie ciblée par des firmes pharmaceutiques
The INSERM U908 unit has showed that Nerve Growth factor (NGF) and its precursor (ProNGF) are implicated in tumor agressivness via their effects on growth, angiogenesis or migration/invasion and metastasis. Nevertheless, (pro)NGF and their receptors targeted therapies failed to demonstrate efficiency and clinical trial are disappointing. These results indicate that TrkA phosphorylation is not sufficient to explain molecular mechanisms of (pro)NGF effects on tumors. Indeed, we obtained lestaurtinib resistant cell lines within 3 weeks of treatment which indicated that resistant mechanisms are innate. So, by functional proteomics analyses, we described that NGF induced the formation of TrkA/CD44 complex and then the recruitment of p115RhoGEF/RhoA/ROCK1 signalling cascade (Aubert L*, Guilbert M* et al, Oncotarget, 2015 ; *equally contributed to this work). We showed that CD44 mediated effects participate to invasive effects of NGF in vitro, and in vivo, we demontrated that CD44 increases NGF induced tumoriginicity. In a second part, I observed that the proNGF regulated EGFR turn over through its phosphorylation on Y1068. This effect on EGFR decreased proliferative and pro-invasive effects of EGF in cancer cells. These fundamental results are interesting and need to be consolidated to ensure development of prognosis or targeted therapies
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33

Pearson, James L. "Analysis of transactivation of the capsid gene promoter of MVM by the NS1 protein." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9962554.

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34

Bureau, Marina. "Etude de la protéine P6 du virus de la mosaïque du chou-fleur (CaMV) : localisation cellulaire et identification de partenaires d'interaction." Paris 6, 2004. http://www.theses.fr/2004PA066032.

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35

Fischer, Katharina. "The mineralocorticoid receptor amino terminal transactivation domain investigation of structural plasticity and protein-protein interactions /." Thesis, Available from the University of Aberdeen Library & Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24694.

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Thesis (Ph.D.)--Aberdeen University, 2008.
Title from web page (viewed on Feb. 23, 2009). With: Natural disordered sequences in the amino terminal domain of nuclear receptors : lessons from the androgen and glucocorticoid receptors / Iain J. McEwan ... et al. Nuclear Receptor Signalling. 2007: 5. Includes bibliographical references.
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36

Dhasarathy, Archana. "Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene." Texas A&M University, 2004. http://hdl.handle.net/1969.1/3272.

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In higher eukaryotes, DNA is packaged with histones and other proteins into chromatin. While this is important in the control of unwanted gene expression, chromatin also serves as a barrier to many vital functions in the cell. Therefore, cells have evolved many different types of chromatin remodeling enzymes to contend with this inhibitory structure and enable gene expression and other functions. The Saccharomyces cerevisiae PHO5 gene is triggered in response to phosphate starvation. In this study, I evaluate the chromatin remodeling requirements of this gene with respect to the multisubunit complexes SWI/SNF and SAGA. I show, for the first time, physical recruitment of SWI/SNF to the PHO5 promoter. I also demonstrate the role of promoter occupancy in influencing requirements for chromatin remodeling enzymes. Further, I describe various interactions between these two complexes at the PHO5 promoter. This study presents evidence for the first instance of excess recruitment of an ATP-dependent remodeler potentially compensating for the lack of a histone acetyltransferase.
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37

Dewar, Brian J. Graves Lee M. "PPAR[gamma]-independent mechanisms of Src kinase activation and EGFR transactivation in response to thiazolidinediones." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1222.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Mar. 26, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Toxicology." Discipline: Toxicology; Department/School: Medicine. On title page, [gamma] appears as Greek character.
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38

Wan, Shanshan. "DEK oncoprotein is a novel regulator of NF-κB transactivation and DNA damage-induced apoptosis." University of Toledo / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1248881814.

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39

Gobinet, Jérôme. "Mécanismes de régulation de la transactivation dépendante du récepteur des androgènes par des inhibiteurs transcriptionnels." Montpellier 1, 2002. http://www.theses.fr/2002MON1T012.

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LE RECEPTEUR DES ANDROGENES EST UN FACTEUR DE TRANSCRIPTION MEMBRE DE LA SUPERFAMILLE DES RECEPTEURS NUCLEAIRES (NRs). ALORS QU'UN GRAND NOMBRE DE FACTEURS ACTIVATEURS DU AR ONT ETE ISOLES, LE MECANISME PAR LEQUEL LE AR EST REPRIME AU SEIN DE LA CELLULE EST ENCORE PEU COMPRIS. JUSQU'A PRESENT, UN NOMBRE RESTREINT DE PROTEINES INHIBITRICES, COMPRENANT TR4, AES, HBO1, DAX, Smrt ET NCoR, ONT ETE DECRITES POUR LEUR CAPACITE A REGULER NEGATIVEMENT L'ACTIVITE DU AR. NOUS NOUS SOMMES INTERESSES AUX PROTEINES CAPABLES DE RELAYER L'INHIBITION DE L'ACTIVITE DU AR. NOUS AVONS DEMONTRE QUE LA PROTEINE SHP (SHORT HETERODIMER PARTNER) EST UN NOUVEL INHIBITEUR TRANSCRIPTIONNEL DU AR. CETTE PROTEINE A ETE, A L'ORIGINE, ISOLEE POUR SON INTERACTION AVEC D'AUTRES NRs. NOUS AVONS, DANS UNE PREMIERE ETUDE, CARACTERISE LES DOMAINES DU AR IMPLIQUES DANS L'INTERACTION AVEC SHP. EN PARALLELE, NOUS AVONS MONTRE QUE LE MOTIF LXXIL CENTRAL PRESENT SUR SHP EST ESSENTIEL POUR L'INTERACTION AVEC LE DOMAINE DE LIAISON DU LIGAND DU RECEPTEUR. POURSUIVANT NOTRE TRAVAIL, NOUS AVONS DEMONTRE QUE SHP RECRUTE DES PROTEINES INHIBITRICES A ACTIVITE HISTONE DESACETYLASE (HDAC) ET QUE CES DERNIERES SONT IMPLIQUEES DANS LE MECANISME DE REPRESSION DU AR. L'INHIBITION D'AUTRES NRs TEL LE RECEPTEUR DES OESTROGENES (ER) PAR SHP SEMBLE ETRE RELAYEE PAR UN MECANISME COMMUN IMPLIQUANT LES HDACs. LA REGULATION DE LA TRANSCRIPTION EST MULTIFACTORIELLE. AUSSI, PARALLELEMENT A CETTE ETUDE, NOUS AVONS DEBUTE L'ANALYSE DE L'IMPLICATION DE LA PROTEINE RIP140 DANS LA REGULATION DE LA TRANSCRIPTION DU AR. CETTE PROTEINE ISOLEE POUR SON INTERACTION AVEC LE ER A DEJA ETE DECRITE POUR SA CAPACITE A INTERAGIR AVEC DE MULTIPLES NRs ET A INHIBER LEUR ACTIVITE. NOUS AVONS MONTRE QUE RIP140 EST UN INHIBITEUR DE L'ACTIVITE DEPENDANTE DU AR N'AFFECTANT QUE SON ACTIVITE DEPENDANTE DE LA PARTIE LBD. DE PLUS, RIP140 INTERAGIT AVEC AR GRACE A SES PARTIES CENTRALE ET CARBOXY-TERMINALE IN VITRO. L'ENSEMBLE DE NOS TRAVAUX NOUS ONT PERMIS DE METTRE EN EVIDENCE DE NOUVEAUX MODES DE REGULATION DE L'ACTIVITE DU AR.
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40

Reid, James Arthur. "Structural and functional analysis of the amino-terminal transactivation domain of the human androgen receptor." Thesis, University of Aberdeen, 2001. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU149342.

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The androgen receptor (AR) belongs to the steroid/nuclear receptor family of ligand-activated transcription factors. Most of these receptors activate transcription through two distinct regions known as activation functions (AF). The first, AF-1, is located within the variable amino-terminal domain (NTD) and the second, AF-2, within the ligand binding domain (LBD). However, the AR is unusual amongst the steroid receptor family in that an independent AF-2 function has not been demonstrated. Transactivation by the AR is therefore dependent primarily upon AF-1. Previous work in our laboratory has shown that an amino-terminal fragment of the AR (amino acids 142 to 485) is able to interact specifically with RAP74, the large subunit of general transcription factor TFIIF. Using a series of deletion constructs, two distinct AR binding sites have been identified with RAP74, one at the amino-terminus and one at the carboxyl-terminus of the protein. Functional analyses of these interactions suggest that the interaction between the AR and the carboxyl-terminus of RAP74 is the most significant with respect to transcriptional activation by the receptor. Mutational analysis of the AR-NTD identified a six amino acid motif, PSTLSL, as being involved in RAP74 binding. In addition to RAP74, an interaction has been identified between the p160 coactivator protein SRC-1a and amino acids 142-485 of the AR. Interestingly, another high related p160 coactivator protein, TIF2, showed little or no binding to this region of the receptor. Structural analysis, using circular dichroism and fluorescence spectroscopy and sensitivity to protease digestion, indicates that the AR-NTD exists in an extended conformation in aqueous solution but retains a propensity to fold into a more ordered structure in the presence of the hydrophobic solvent trifluoroethanolor the osmolyte trimethylamine-N-oxide. Significantly, RAP74 also confers protection to trypsin digestion, consistent with folding of the AR-NTD (aa 142 to 485) upon interaction with a target factor.
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41

Johnson, Thomas M. "p53 transactivation domain mutant knock-in mice provide novel insight into p53 tumor suppressor function /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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42

Wan, Shanshan. "DEK oncoprotein is a novel regulator of NF-kB transactivation and DNA damage-induced apoptosis /." Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1248881814.

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Dissertation (Ph.D.)--University of Toledo, 2009.
Typescript. "Submitted as a partial fulfillment of the requirements for the Doctor of Philosophy degree in Biology." Bibliography: leaves 135-146.
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43

Schneider, Matthias [Verfasser], and Georg [Akademischer Betreuer] Krohne. "Characterisation of Metalloprotease-mediated EGFR Signal Transactivation after GPCR Stimulation / Matthias Schneider. Betreuer: Georg Krohne." Würzburg : Universitätsbibliothek der Universität Würzburg, 2011. http://d-nb.info/1014892147/34.

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44

Zhao, Jing. "Protein Kinases can differentially regulate transactivation activities of hLRH-1 through the modulation of cofactors interactions." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1271686070.

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45

Lavery, Derek Norman. "The amino-terminal transactivation domain of the human androgen receptor : protein-protein interactions and structural characteristics." Thesis, University of Aberdeen, 2007. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU490182.

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An important target protein for the AR-AF1 domain is Transcription Factor IIF (TFIIF). At initiation of transcription, TFIIF recruits additional basal transcription factors, stabilises the transcriptional complex and increases elongation efficiency. Using chromatin immunoprecipitation, it was observed that the AR occupied distinct regions of the prostate-specificantigen enhancer but did not migrate with the elongating transcriptional complex. The major subunit of TFAAF, RAP74, has previously been shown to interact with AR-AF1 by our laboratory and it was observed that AR-AF1 can interact with both terminal regions of RAP74. Now, by selectively disrupting helices that structure the globular RAP74 C-terminal domain it appears that AR-AF1 binds to a groove within this region and specific hydrophobic amino acids are important in this generation. The kinetics of RAP74/AR-AF1 interactions have not been determined using surface plasmon resonance. Interestingly, AR-AF1 interacts differently with N- and C-terminal regions of RAP74 and the overall affinities are in the nanomolar range. The structural properties of AR-AF1 were examined using both fluorescence spectroscopy and gel filtration chromatography. It was found that the transactivation domain is structurally flexible and exists in a conformation that is not random coil or globular suggesting that it may be a molten globule. AR-AF1 interacted weakly with 8-anilinonaphthalene-1-sulfonic acid, a hydrophobic probe used to characterise the molten globule folding state. Gel filtration chromatography indicates that AR-AF1 is ∼65 kDa and has a hydrodynamic radius of ∼36 Co much larger than predictions suggest. Surprisingly, by plotting these properties on "folding curves", AR-AF1 is positioned alongside molten globules.
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46

Scian, Mariano J. "MODULATION OF GENE EXPRESSION BY TUMOR-DERIVED MUTANT p53. ROLE OF TRANSACTIVATION IN GAIN-OF-FUNCTION." VCU Scholars Compass, 2005. https://scholarscompass.vcu.edu/etd/5518.

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It was hypothesized that the C-terminal sequences for mutant p53 would be required for oligomerization. and oligomerization may be critical for gain-of-function. An N-terminal deletion mutant of p53 that deletes amino acids 1-293 was used as a tool to perform hetero-oligomerization studies. This mutant retains the entire oligomerization domain but dispenses off the transactivation domain and a large portion of the sequence- specific DNA-binding domain. Co-transfection experiments show that p53 del. 1-293 forms hetero-oligomeric complexes with p53-D281G. Also. co-expression of p53 del. 1- 293 with p53-D281G inhibited p53-D28lG-mediated transactivation of the EGFR and MDRl promoters suggesting that hetero-oligomerization inactivates transcriptional functions of mutant p53. The interaction of p53 deli 1-293 and p53-D281G reduced transactivation potential of p53-D281G in stably transfected 10(3) murine cells. Therefore, the data presented supports the idea that proper oligomeric forms of mutant p53 are required for its transactivation function. Expression of mutant p53-D2810 also resulted in increased growth rate (H1299 cells), decreased chemosensitivity (H1299 and 21PT cells) and increased plating efficiency (Saos-2 cells). Expression of a transactivation deficient mutant p53 did not induce gain-of-function properties (increased growth rate and decreased chemosensitivity). Unlike the other gain-of-function properties tested, soft agar plating efficiency in Saos-2 cells was not significantly affected by the expression of a transactivation deficient mutant p53, suggesting that transactivation may not be the only factor affecting this gain-of-function property In order to identify the genes responsible for the observed phenotypes, global gene expression analyses were carried out using p53-null H1299 cell stably transfected to express mutant p53 (-Rl75H, -R273H and -D281G). A thorough and stringent analysis revealed 150 genes up-regulated by the expression of mutant p53. Up-regulation of a number of these genes was confirmed by QPCR and transient transcriptional promoter analyses; expression of the transactivation deficient mutant p53-D2810 (L22Q/W23S) did not result in up-regulation of the tested genes further supporting the idea that transactivation of genes is directly related to gain-of-function phenotypes. Using the ASNS gene as a model, this transactivation by mutant p53 was concentration dependent and that the increased transcription did indeed result in increased protein levels.
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47

Niro, Sandra. "La 7β-hydroxy-épiandrostérone dans des modèles in vitro de cancer du sein : effets anti-estrogéniques et rôle des récepteurs des estrogènes." Phd thesis, Conservatoire national des arts et metiers - CNAM, 2012. http://tel.archives-ouvertes.fr/tel-00727277.

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La 7β-hydroxy-épiandrostérone, stéroïde endogène dérivant de la DHEA, présente des propriétés anti-inflammatoires. En effet, elle module la voie des prostaglandines (PGs) en inhibant la production de la PGE2 pro-inflammatoires et en augmentant la production de la 15-Deoxy-∆12,14-PGJ2 cyto-protectrice in vivo et in vitro. Les faibles doses de 7β-hydroxy-épiandrostérone (1nM, 10nM, 100nM) pour lesquelles ces effets sont observés, suggèrent une liaison à un récepteur spécifique. L'inflammation et la production des PGs jouent un rôle important dans le développement et la prolifération des tumeurs mammaires estrogéno-dépendantes. Le 17β-estradiol (E2), en se fixant sur les récepteurs des estrogènes (REs), induit la production de PGE2 et la prolifération cellulaire dans ces cellules tumorales. De ce fait, notre objectif était de tester les effets de la 7β-hydroxy-épiandrostérone sur la prolifération (comptage avec exclusion au bleu trypan), le cycle cellulaire et l'apoptose (cytométrie de flux) dans les lignées cellulaires de cancer du sein MCF-7 (REα+, REβ+, GPR30+) et MDA-MB-231 (REα-, REβ+, GPR30+) et d'identifier une(des) cible(s) potentielle(s) dans ces cellules (transactivation) et dans des cellules négatives pour les REs nucléaires SKBr3 (GPR30+) (études de prolifération). Cette étude a montré que la 7β-hydroxy-épiandrostérone exerce des effets anti-estrogéniques dans les cellules MCF-7 et MDA-MB-231 associés à une inhibition de la prolifération et un arrêt du cycle cellulaire. Les études de transactivation et de prolifération avec les agonistes spécifiques des REs ont montré une interaction avec le REβ. De plus, les résultats des études de proliférations sur les trois lignées cellulaires suggèrent que la 7β-hydroxy-épiandrostérone pourrait également interagir avec le GPR30. Ces résultats indiquent que ce stéroïde androgène agit comme un anti-estrogène. De plus, c'est la première fois qu'un stéroïde androgène à faible dose montre une action anti-proliférative dans des lignées de cancers du sein. Des études ultérieures restent à réaliser afin de mieux comprendre ces effets observés.
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48

Majumdar, Sonali. "Structural and functional divergence of the transcription factor Pit-1, analysis of the pou and transactivation domains." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0008/NQ28006.pdf.

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49

GUYADER, MIREILLE. "Hiv-2 : un nouveau retrovirus humain associe au sida. organisation genomique, transactivation et etude d'un gene specifique." Paris 7, 1989. http://www.theses.fr/1989PA077268.

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L'analyse de la sequence nucleotidique du genome du virus hiv-2 (human immunodeficiency virus type 2) associe au sida en afrique de l'ouest, a permis de montrer que ce virus presente une organisation genomique similaire a celle du virus hiv-1, indiquant leur origine comme dans l'evolution. Cependant, les divergences significatives observees au niveau nucleotidique et proteique entre hiv-1 et hiv-2 (45% seulement d'homologie globale) indiquent que ces deux virus representent deux elements distincts d'une meme famille, le virus hiv-2 etant beaucoup plus proche d'un virus simien apparente, le virus sivmac. D'autre part, nous avons montre que le phenomene de transactivation de l'expression virale n'etait pas specifique du virus hiv-1 mais est aussi observe pour le virus hiv-2. Comme dans hiv-1, seul le premier exon codant du gene tat du virus hiv-2 est necessaire pour sa fonction. Nous avons egalement defini les sequences necessaires a l'activite de la proteine transactivatrice du virus hiv-2, au niveau du ltr viral, et montre que les proteines tat des virus hiv-1 et hiv-2 presentent des specificite differentes, bien qu'elles semblent utiliser un mecanisme similaire pour leur action. Enfin, notre etude d'un gene specifique des virus hiv-2 et siv, le gene vpx, a permis de caracteriser le produit de ce gene dans les cellules infectees. Cette proteine de 16 kd, dans le cas du virus hiv-2, n'est pas necessaire a l'infectivite des particules dans les lignees lymphocytaires ou monocytaires. Par contre, des mutations dans le gene vpx reduisent considerablement la capacite des particules produites a infecter les lymphocytes du sang peripherique
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50

Measures, Elaine Maria. "Hypoxia-inducible factor (HIF)transactivation in a chronic hypoxia model : HIF disruption as an anti-cancer strategy." Thesis, University of Manchester, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548996.

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