Dissertations / Theses: 'Genetic transcription – Regulation'

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Xie, Yunwei. "Nucleosomes, transcription and transcription regulation in Archaea." Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1127830717.

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Thesis (Ph. D.)--Ohio State University, 2005.
Title from first page of PDF file. Document formatted into pages; contains xiv, 200 p.; also includes graphics (some col.). Includes bibliographical references (p. 167-197). Available online via OhioLINK's ETD Center

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Sigvardsson, Mikael. "Regulation of immunoglobulin transcription during B-cell differentiation." Lund : Lund University, 1995. http://books.google.com/books?id=TJNqAAAAMAAJ.

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Zak, Daniel Edward. "Structured modeling of mammalian transcription networks." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 374 p, 2005. http://proquest.umi.com/pqdweb?did=954050761&sid=7&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Lee, Yiu-fai Angus. "Tissue-specific transcriptional regulation of Sox2." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B3955739X.

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Lee, Yiu-fai Angus, and 李耀輝. "Tissue-specific transcriptional regulation of Sox2." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B3955739X.

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6

Ching, Chi-yun Johannes, and 程子忻. "Transcriptional regulation of p16INK4a expression by the forkhead box transcription factor FOXM1." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29466192.

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Pang, Ting-kai Ronald. "Transcriptional regulation of the human secretin receptor gene /." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25059324.

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8

Jahangiri, Leila. "Combinatorial gene regulation by T-domain transcription factors." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610328.

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9

Cleavinger, Peter Jay. "Role of the long terminal repeat in transcriptional regulation of rous sarcoma virus gene expression." free to MU campus, to others for purchase, 1996. http://wwwlib.umi.com/cr/mo/fullcit?p9841207.

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10

Ye, Chaoyang. "Transcription regulation of adeno-associated viruses." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4709.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.
"May 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

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11

Nürnberg, Sylvia. "Transcription regulation of the megakaryocyte by MEIS1." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610001.

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12

Kwong, Ka-yee, and 鄺嘉儀. "Pituitary-specific transcription factor PIT-1 in Chinese grass carp: molecular cloning, functionalcharacterization, and regulation of its transcript expression at thepituitary level." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29474991.

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Holmqvist, Per-Henrik. "Transcription factor effects on chromatin organisation and gene regulation /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-453-8/.

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14

葉志遠 and Chi-yuen Ip. "Characterization of the 5'flanking transcriptional regulation region of the chicken growth hormone gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31226115.

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15

Leung, Kei-chun Jane. "Purification of a transcriptional regulator of the dehalogenase IVa gene of Burkholderia species MBA4." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38734709.

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Leung, Kei-chun Jane, and 梁奇珍. "Purification of a transcriptional regulator of the dehalogenase IVa gene of Burkholderia species MBA4." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38734709.

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17

Deng, Liyu, and 鄧麗瑜. "Exploration of the transcription factors that regulate the expression of the haloacid operon in Burkholderia caribensis MBA4." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208618.

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Bacterial dehalogenase is a key enzyme involved in bioremediation of halogenated organic compounds. A dehalogenase, Deh4a, was isolated from the Gram-negative bacterium Burkholderia caribensis MBA4, which can utilize haloacetic acids as carbon source. The haloacid operon in MBA4 was identified and characterized. It is composed of the structural genes forDeh4a and a transporter Deh4p. Transcription of this operon is negatively regulated, but the mechanism and the relevant regulator are still poorly understood. In this study, magnetic DNA affinity chromatography and Tn5transposon mutagenesis were employed to explore the regulatory factors that affected the expression of this haloacid operon. A process that uses lysates from glycolate-grown cells, magnetic DNA affinity chromatography and LC-MS/MS has identified a TetR family transcriptional regulator, TetR8620, which binds to the promoter region of deh4a. Disruption of the TetR8620 gene in mutant Ins8620 abolished the formation of a slow migrating complex in electrophoretic mobility shift assay (EMSA) using lysates from glycolate-grown cells. Moreover, expressions of deh4a were enhanced in bothglycolate- and MCA- grown Ins8620. The addition of recombinant histidine-tagged TetR8620 to lysates of Ins8620 resumed the formation of a retardation complex, but different from that using purified His-tagged TetR8620.This suggested that TetR8620 is responsible for formation of retardation complexes, and an additional protein might be involved. To investigate other putative factors that interact with TetR8620, purified His-tagged TetR8620 was immobilized with Ni-NTA agarose and used for isolation of interacting proteins. Chemical cross-linking of the purified fraction with BS3established that TetR8620 interacts with a proteinof30 kDa. Separation of the cross-linked complex in SDS-PAGE gel also showed that a protein with similar MW was specifically pulled down. These results suggest that TetR8620 was interacting with a ~30 kDa protein. Protein identification using mass spectrometry assay proposed that this protein is probably a universal stress protein UspA encoding by peg.3485 or acetyl-glutamate kinase (EC 2.7.2.8) encoding by peg.714 in MBA4. Tn5transposon mutagenesis was also employed to explore the factors that regulate the haloacid operon ofMBA4. A derivative of MBA4, MK06, which contains a kanamycin resistant gene (kan) with a deh4apromoter was constructed. Kanamycin resistancy of this derivative was MCA inducible. Transposon mutagenesis was conducted on this derivative, and Tn-containing mutants were isolated as tetracycline resistant colonies on pyruvate plates. These colonies were further selected on their resistance tokanamycin in pyruvate plates. Gene peg.6589 encoding a putative transcriptional regulator, DehR1, was disrupted by Tn insertion. While the production of dehalogenase was still MCA-inducible, this mutant has partially relieved the repression of the haloacid operon in media containing pyruvate. Moreover, constitutive production of DehR1 in MBA4 decreased the transcript levels of deh4ain medium containing pyruvate or MCA. This study has identified two transcription factors, TetR8620 and DehR1, which regulate the expression of Deh4a negatively. TetR8620 is a DNA-binding protein that interacts with the deh4apromoter. Results from this study imply that the regulation of the haloacid operon in MBA4 is likely to be under the control of multiple factors.
published_or_final_version
Biological Sciences
Doctoral
Doctor of Philosophy

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Pang, Ting-kai Ronald, and 彭鼎佳. "Transcriptional regulation of the human secretin receptor gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243514.

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Lee, Tsz-on, and 李子安. "Transcriptional regulation of the human secretin gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30163389.

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20

Dalton, Stephen. "Transcriptional regulation of histone gene expression /." Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09PH/09phd152.pdf.

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21

Jiang, Yonghua. "Molecular cloning of AP-1 transcription factors in Chinese grass carp and their functional roles in PACAP-stimulated growth hormone geneexpression." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31245419.

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22

林大偉 and Tai-wai Lam. "Structural organization, transcriptional regulation and chromosomal localization of the human secretin gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224593.

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23

Yuan, Yuan, and 袁媛. "Transcriptional regulation of mouse secretin receptor in hypothalamic cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47752932.

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As a neuropeptide, both secretin and secretin receptor are expressed in the central nervous system (CNS). It has been revealed that the activities of secretin on hypothalamic cells of rodents are important for osmoregulation and food intake. In the present study, embryonic mouse hypothalamic cell line N42 was used to study the promoter activity of mouse secretin receptor (mSR). By 5′ deletion analysis, a promoter element was identified within ?282 to ?443, relative to the ATG codon, and it contains a GC-box (-297 to -286), a ras responsive element (RRE) (-289 to -276) and an E-box (-416 to -411). Electrophoretic mobility shift assay (EMSA) and supershift analyses showed that Sp1 interacted with the GC-box, another zinc finger As a neuropeptide, both secretin and secretin receptor are expressed in the central nervous system (CNS). It has been revealed that the activities of secretin on hypothalamic cells of rodents are important for osmoregulation and food intake. In the present study, embryonic mouse hypothalamic cell line N42 was used to study the promoter activity of mouse secretin receptor (mSR). By 5′ deletion analysis, a promoter element was identified within ?282 to ?443, relative to the ATG codon, and it contains a GC-box (-297 to -286), a ras responsive element (RRE) (-289 to -276) and an E-box (-416 to -411). Electrophoretic mobility shift assay (EMSA) and supershift analyses showed that Sp1 interacted with the GC-box, another zinc finger
published_or_final_version
Biological Sciences
Doctoral
Doctor of Philosophy

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24

Hong, Seung-Pyo School of Biochemistry &amp Molecular Genetics UNSW. "Transcriptional regulation of one-carbon metabolism genes of Saccharomyces cerevisiae." Awarded by:University of New South Wales. School of Biochemistry and Molecular Genetics, 1999. http://handle.unsw.edu.au/1959.4/22503.

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The glycine decarboxylase complex (GDC) of Succharomyces cerevisiae composed of four subunits (P, H, T and L) and plays an important role in the interconversion of serine and glycine and balancing the one-carbon unit requirements of the cell. It also enables the cell to use glycine as sole nitrogen source. This study was concerned with characterising the molecular mechanism of transcriptional regulation of the GCVgenes encoding the subunits of the GDC. The important findings of this work can be summarised as follows: i) Transcription of the GCV genes are regulated by glycine and rich nitrogen sources, which are mediated by different cis-acting elements. The LPDl gene did not show a glycine response since its transcriptional regulation is distinct from that of the other genes encoding the GDC subunits. ii) Glycine analogues or serine did not affect expression of GCV2, and therefore glycine probably needs to be metabolised to effect the glycine response of the GCV genes. iii) The repression of the GCV2 gene expression by rich nitrogen sources is mediated by a sequence between -227 and -205 of GCV2, and NCR-regulatory mutant studies showed that repression is not directly controlled by the known NCR system. iv) The glycine response of GCV2 is mediated by a motif (the glycine regulatory region; GRR; 5'-CATCN7CTTCTT-3') with CTTCTT at its core. Additional sequence immediately 5' of this motif (between -310 to -289) plays a minor role for the gene's full glycine response. v) The GRR of the GCV genes can mediate the glycine response by either activation or repression, indicating that the transcription factor(s) mediating the glycine response is/are dual-functional in nature. vi) Studies of GCV2 gene expression using different regulatory mutants showed that expression of the gene is further modulated by other transcription factors such as and Baslp which are distinct from the glycine response and possibly involved in setting up the basal expression level. vii) I n vitro studies of the GRR-protein interaction revealed THF affects the affinity of the DNA-binding protein(s) for the GRR. The importance of THF in regulation of the GCV2 gene was also shown in vivo using a foll mutant that is unable to synthesise any folates. THF or a C1-bound derivative of it acts as a ligand for the transcription factor, thus influencing transcription of the GCV genes in the appropriate physiological manner. viii) Using heparin-Sepharose chromatography fractions, four complex formations (complex I to IV) were observed with the GRR. The protein responsible for one of these was separable from the others. EMSA profiles using the GRR of the GCVI and GCV2 genes (in the presence or absence of THF) were very similar, indicating that these genes bind the same proteins and are regulated in a similar manner. ix) Mutation of the CTTCTT motif within the GRR caused significant reduction in in vitro DNA-protein complex formation, however, THF addition overcame this reduction. x) Only complex II formation was observed with a DNA fragment spanning -322 to -295, and THF affected this complex formation. xi) Footprinting analyses of complex I revealed that the binding protein protected the GRR of the GCV2 gene from DNaseI activity. This protein is an excellent candidate for the glycine response regulatory protein. Titration experiments using EMSA showed that this protein can dimerise. A preliminary genome-wide analysis of the S. cerevisiae transcriptome was carried out using miniarray membrane hybridisation. This investigated the global transcriptional changes within the cell in response to the addition of glycine into the medium. Identification of genes related to various cellular processes including onecarbon metabolism gave an insight into the regulation of the cellular metabolic flow, especially that of one-carbon metabolism. The results indicated that: xii) Glycine is transported into mitochondria to be used as substrate for the GDC which (with mitochondria1 SHMT) produces serine that is subsequently utilised for the various one-carbon metabolic pathways, such as methionine synthesis and purine synthesis. xiii) A gene of unknown function (YER183C) which showed homology to the gene for human 5,lO-CH-THF synthetase was identified from gene-array analysis to be upregulated on glycine addition, indicating the protein encoded by this gene may be involved in balancing the metabolic flow between methionine and purine synthesis when THF pools are disturbed by glycine addition. xiv) Addition of glycine to the medium also triggers the expression of other metabolic genes related to amino acid biosynthetic pathways and that of many other genes which are not directly related to one-carbon metabolism. This may be due to prolonged culturing with glycine in the medium resulting in altered expression of genes mediated by one or more secondary factors. These may reflect an adaptive response rather than a direct consequence of glycine induction. On the basis of the above data, a model for the mechanisms regulating glycine response is presented.

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25

Zaugg, Judith Barbara. "A computational study of promoter structure and transcriptional regulation in yeast on a genomic scale." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609838.

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26

Motallebipour, Mehdi. "Genetic and Genomic Analysis of Transcriptional Regulation in Human Cells." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9407.

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There are around 20.000 genes in the human genome all of which could potentially be expressed. However, it is obvious that not all of them can be active at the same time. Thus, there is a need for coordination achieved through the regulation of transcription. Transcriptional regulation is a crucial multi-component process involving genetic and epigenetic factors, which determine when and how genes are expressed. The aim of this thesis was to study two of these components, the transcription factors and the DNA sequence elements with which they interact. In papers I and II, we tried to characterize the regulatory role of repeated elements in the regulatory sequences of nitric oxide synthase 2 gene. We found that this type of repeat is able to adopt non B-DNA conformations in vitro and that it binds nuclear factors, in addition to RNA polymerase II. Therefore it is probable that these types of repeats can participate in the regulation of genes. In papers III-V, we intended to analyze the genome-wide binding sites for six transcription factors involved in fatty acid and cholesterol metabolism and the sites of an epigenetic mark in a human liver cell line. For this, we applied the chromatin immunoprecipitation (ChIP) method together with detection on microarrays (ChIP-chip) or by detection with the new generation massively parallel sequencers (ChIP-seq). We found that all of these transcription factors are involved in other liver-specific processes than metabolism, for example cell proliferation. We were also able to define two sets of transcription factors depending on the position of their binding relative to gene promoters. Finally, we demonstrated that the patterns of the epigenetic mark reflect the structure and transcriptional activity of the promoters. In conclusion, this thesis presents experiments, which moves our view from genetics to genomics, from in vitro to in vivo, and from low resolution to high resolution analysis of transcriptional regulation.

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Sasmono, R. Tedjo. "Transcriptional regulation of c-fms gene expression /." [St. Lucia, Qld.], 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17479.pdf.

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Schwalie, Petra Catalina. "Genome-wide analyses of transcriptional regulation across multiple tissues and species." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610749.

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Laurencikiene, Jurga. "Regulation of germline transcription in the immunoglobulin heavy chain locus /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-989-7/.

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30

Lorson, Christian. "An analysis of transcriptional regulation of the MVM capsid gene promoter." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841319.

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31

Champigny, Marc J. Igdoura Suleiman. "Transcriptional regulation of neu1 expression: Implications for lysosomal storage disease /." *McMaster only, 2005.

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32

Ronsmans, Aria. "Mechanisms of nitrogen catabolite repression-sensitive gene regulation by the GATA transcription factors in Saccharomyces cerevisiae." Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209169.

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The process of specific gene transcription by RNA polymerase II (Pol II) is initiated by the

binding of specific transcription factors to DNA. A global understanding of the mechanisms of gene

transcriptional regulation of Saccharomyces cerevisiae goes through the description of the targets and

the behavior of those transcription factors.

The GATA factors are specific transcription factors intervening in the regulation of Nitrogen

Catabolite Repression (NCR)-sensitive genes, a mechanism encompassing the transcriptional

regulations leading to the preferential use of good nitrogen sources of the growth medium of yeast in

the presence of less good nitrogen sources. Those 4 GATA factors involved in NCR comprise 2

activators (Gat1 and Gln3) and 2 repressors (Gzf3 and Dal80).

Generally speaking, the promoters of genes have always been described like the main place for

the integration of the transcription regulation signals relayed by the general and specific transcription

factors and the chromatin remodeling factors. Furthermore, the GATA factors have been described as

integrating the external signals of nitrogen availability thanks to their specific DNA binding to

consensus GATA sequences in the promoter of NCR-sensitive genes. The results presented here

introduce many nuances to the model, notably implying new proteins but also new regions in the

regulation process of the NCR-sensitive gene regulation. Indeed, the first goal of this work is to

discover and understand the mechanisms of NCR-sensitive gene regulation that will explain the

variations in their expression levels in the presence of various nitrogen sources and their dependency

towards the GATA factors.

Strikingly, it appeared that GATA factor positioning was not limited to the promoter, but

occurred also in the transcribed region. It seems that the transcription factors may have been driven

by the general transcription machinery (Pol II). The binding of a chromatin remodeling complex, RSC,

has also been demonstrated in the coding region of NCR-sensitive genes. Moreover, the binding of the

histone acetyltransferase complex, SAGA, recruited by the GATA activators, was highlighted along

NCR-sensitive genes. The SAGA complex was also implied in their transcriptional regulation.

Finally, a ChIP-sequencing experiment revealed an unsuspected number and diversification of

targets of the GATA factors in yeast, which were not limited to NCR-sensitive genes.

Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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Pinto, Desterro Maria Joana. "Role of SUMO-1 modification in transcriptional activation." Thesis, University of St Andrews, 1999. http://hdl.handle.net/10023/2724.

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In unstimulated cells, the transcription factor NF-κB is held in the cytoplasm in an inactive state by IκB inhibitor proteins. Activation of NF--KB is mediated by signal induced degradation of IκBα via the ubiquitin proteasome-dependent pathway. Targeting the proteins for ubiquitin-mediated proteolysis is an irrevocable decision, and as such, the process needs to be highly specific and tightly regulated. This task is achieved by conjugation and deconjugation enzymes that act in a dynamic and coordinated mechanism. In a yeast two hybrid screen designed to identify proteins involved in IκBα signalling Ubch9 was found to interact with the N-terminal regulatory region of IκBα. Although Ubch9 is an enzyme homologous to E2 ubiquitin conjugating enzymes we have shown that is unable to form a thioester with ubiquitin but it is capable to form a thioester with the small ubiquitin-like protein SUMO- 1. To fully characterise the SUMO-1 modification reaction we have purified the proteins and cloned the genes encoding the SUMO-1 activating enzyme (SAEl/SAE2) and shown that it is homologous to enzymes involved in the activation of ubiquitin, Smt3p, the yeast SUMO-1 homologue, and Rublp/Nedd8, another ubiquitin-like protein. SUMO-1 is conjugated to target proteins by a pathway that is distinct from, but analogous to, ubiquitin conjugation. SUMO-1 was efficiently conjugated, both in vivo and in vitro, to IκBα on lysine 21, which is also utilised for ubiquitin modification. Thus, by blocking ubiquitination SUMO-1 modification acts antagonistically to generate a pool of IκBα resistant to proteasome-mediated degradation which consequently inhibits NF-κB dependent transcription activation. In view of several lines of similarity between NF-kB and p53, the involvement of SUMO-1 modification in the metabolism of the tumour supressor p53 was investigated. We have shown that p53 is modified by SUMO-1 at a single site, lysine 386 in the C-terminus of p53. Although p53 is regulated by ubiquitination, SUMO-1 and ubiquitin modification do not compete for the same lysine in p53. However, overexpression of SUMO-1 activates the transcriptional activity of wild type p53, but not K386R p53 where the SUMO-1 acceptor site has been mutated. A consensus sequence was obtained by comparison of the sequences surrounding the SUMO-1 acceptor lysine in proteins that have been shown to be modified by SUMO-1 and revealed a possible recognition site for SUMO-1 conjugation machinery. Tagging of proteins with SUMO-1 regulates transcriptional activation, either by interfering with subcellular location or with the ubiquitination pathway. The pathway may represent a novel target for drug development.

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Wong, Chui-shan, and 黃翠珊. "Transcriptional regulation of receptor tyrosine kinases AXL and MER inthe testis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45015120.

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Wong, Hiu-ting. "A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085726.

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Xia, Ninuo. "Non-coding RNA's role in epigenetic gene regulation." Diss., UC access only, 2009. http://proquest.umi.com/pqdweb?index=109&did=1871884811&SrchMode=1&sid=1&Fmt=7&retrieveGroup=0&VType=PQD&VInst=PROD&RQT=309&VName=PQD&TS=1270486124&clientId=48051.

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Thesis (Ph. D.)--University of California, Riverside, 2009.
Includes abstract. Includes bibliographical references (leaves 105-122). Issued in print and online. Available via ProQuest Digital Dissertations.

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Zhu, Jiang. "HOXB5 cooperates with TTF1 in the transcription regulation of human RET promoter." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278607.

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Cresawn, Steven Gaines. "Genetic inquiry into vaccinia virus intermediate and late gene regulation." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010102.

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Thesis (Ph.D.)--University of Florida, 2005.
Typescript. Title from title page of source document. Document formatted into pages; contains 150 pages. Includes Vita. Includes bibliographical references.

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Wong, Kam Wai. "Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20WONGK.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2002.
Includes bibliographical references (leaves 95-108). Also available in electronic version. Access restricted to campus users.

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Wong, Hiu-ting, and 王曉婷. "A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085726.

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41

朱江 and Jiang Zhu. "RET transcriptional regulation by HOXB5 in Hirschsprung's disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/193397.

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Hirschsprung’s disease (HSCR) is the major enteric nervous system anomaly affecting newborns with high incidence in Asians. HSCR is a congenital complex genetic disorder characterized by a lack of enteric ganglia along a variable length of the intestine. The receptor tyrosine kinase gene (RET) is the major HSCR gene and cis-elements in the promoter and intron of RET gene are crucial for RET expression. Abnormal RET expression leading to insufficient RET activity causes defective development of the enteric nervous system and is implicated in the pathogenesis of the Hirschsprung’s disease. The human homeobox B5, HOXB5, has an important role in the development of enteric neural crest cells, and perturbation of HOXB5 signaling causes reduced RET expression and HSCR phenotypes in mice. To investigate the roles of HOXB5 in the regulation of RET expression and in the aetiology of HSCR, I sought to(i) elucidate the underlying mechanisms that HOXB5 mediates RET expression, and (ii) to examine the interactions between HOXB5 and other transcription factors including SOX10 and NKX2-1 that have been implicated in RET expression and HSCR. In this study, I demonstrated that HOXB5 binds to the RET promoter and regulates RET expression. HOXB5 and NKX2-1 forma protein complex and mediate RET expression in a synergistic manner. In contrast, HOXB5 cooperates in an additive manner with SOX10in trans-activation from RET promoter. ChIP assay further revealed that HOXB5 and NKX2-1 interact with the same chromatin region proximate to the transcription start site of RET, suggesting that these two factors may interact with each other and regulate the transcription of RET. In silico analysis, EMSA and ChIP analysis showed that HOXB5 also binds to an enhancer element (MCS+9.7)in the intron 1 of RET gene, and HSCR-associated SNPs have been identified in this enhancer element. To further access the HOXB5 trans-activity onMCS+9.7, RET mini-gene was constructed by ligating the RET promoter to the 5’and MCS+9.7 to the 3’of a luciferase gene. Luciferase assay indicated that MCS+9.7 enhances the HOXB5 trans-activation from the RET promoter. In addition, previously identified HSCR-associated SNPs inintron 1 markedly reduce the HOXB5 trans-activation from the RET mini-gene. Moreover, the result of IP-LC-MS/MS indicated that HOXB5 could form protein-protein complexes with nuclear proteins involved in the transcription initiation of genes with TATA-less promoter. This evidence suggested that HOXB5 may cooperate with other activators or co-factors in the remodeling of chromatin conformation, local histone modification and recruitment of essential transcription factors for RNA Polymerase II based transcription from TATA-less promoter, such as RET. My data indicated that HOXB5 in coordination with other transcription factors mediates RET expression. Therefore, defects in cis-or trans-regulation of RET by HOXB5 could lead to a reduction of RET expression and contribute to the manifestation of the HSCR phenotype.
published_or_final_version
Surgery
Doctoral
Doctor of Philosophy

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42

Spåhr, Henrik. "The transcription machinery in Schizosaccharomyces pombe and its regulation /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-863-7/.

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43

Mou, Yi. "Molecular analysis of the roles of NRSF in TUBB3 transcription control." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B3742869X.

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44

Ip, Chi-yuen. "Characterization of the 5'flanking transcriptional regulation region of the chicken growth hormone gene /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23735855.

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45

Warshamana, Gnana Sakuntala. "Interactions of T7 RNA polymerase with its promoters : Part I: T7 promoter contacts essential for promoter activity in vivo ; Part II: Isolation and characterization of a mutant T7 RNA polymerase with altered promoter specificity." Diss., Georgia Institute of Technology, 1992. http://hdl.handle.net/1853/26303.

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46

Girdwood, David William Haxton. "Transcriptional regulation mediated through the conjugation and deconjugation of the small ubiquitin-like modifiers SUMO-1, SUMO-2, and SUMO-3." Thesis, University of St Andrews, 2004. http://hdl.handle.net/10023/2729.

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SUMO-1/2/3 are members of the ubiquitin-like family of protein modifiers. These proteins are covalently attached to numerous proteins in a directed and controlled manner. SUMO conjugation primarily occurs to proteins containing an exposed SUMO conjugation motif, (I, V, L, F)KxE, where x represents any amino acid. SUMO conjugation is controlled by key enzymes, a SUMO activating enzyme, SAE1/2 and a SUMO conjugating enzyme, Ubc9, which is responsible for substrate recognition, and the efficiency of this pathway can be increased by one of many SUMO ligase enzymes. This modification alters the substrate's characteristics and results in a change of state, such as stability, localisation, or activity. p300, a transcriptional co-activator, contains an evolutionary conserved tandem SUMO modification motif, located in a transcriptional repression domain. p300 was efficiently conjugated, both in vitro and in vivo, by SUMO-1/2/3, within this repression domain to both SUMO conjugation motifs. The SUMO conjugation to p300 correlated with p300 ability to repress transcription, requiring both SUMO conjugation motifs for full transcription repression activity. This repression activity was mediated through SUMO recruitment of histone deacetylase 6. Repression could be alleviated through co-expression of a SUMO-specific protease thereby suggesting a potential regulatory mechanism for transcription control of SUMO modified substrates. Despite utilising the same conjugation machinery, there remained the potential for distinct roles for the SUMO isoforms. SUMO -2/3, which form a distinct group from SUMO-1, were shown to preferentially mediate the transcription repression abilities of a number of known SUMO modifiable substrates: p300, Elk-1, and SP3. Further differences were observed in the ability of SUMO-1 and SUMO-2/3 to influence the nuclear organisation of p80 coilin.

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47

Yatherajam, Gayatri. "Regulation of transcription by factors interacting with the TATA binding protein." Access citation, abstract and download form; downloadable file 7.32 Mb, 2004. http://wwwlib.umi.com/dissertations/fullcit/3131704.

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48

Chan, Yee-man, and 陳綺雯. "Transcriptional regulation in the EcoRI-F immunity region of the Bacillus subtilis phage [phi] 105." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29474528.

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49

Xie, Qunhui. "Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20XIE.

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50

Xiong, Yalin. "Downstream NTP effects on human RNA polymerase II transcription elongation." Diss., Connect to online resource - MSU authorized users, 2008.

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Thesis (Ph.D.)--Michigan State University. Dept. of Biochemistry and Molecular Biology, 2008.
Title from PDF t.p. (viewed on Apr. 2, 2009) Includes bibliographical references. Also issued in print.

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Dissertations / Theses on the topic 'Genetic transcription – Regulation'

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