Дисертації з теми "HMGA proteins"
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Beitzel, Brett F. "The role of HMGA proteins in retroviral integration /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3099924.
Повний текст джерелаPellarin, Ilenia. "HMGA PROTEINS IN EPITHELIAL-MESENCHYMAL TRANSITION AND TUMOUR PROGRESSION." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/10117.
Повний текст джерелаHigh Mobility Group A (HMGA1a, HMGA1b and HMGA2) proteins are architectural nuclear factors, physiological expressed during embryonic development and re-expressed at high levels following neoplastic transformation, playing essential functions in both these processes thanks to their particular plasticity and consequently multifunctionality. HMGA are involved in a wide number of cellular processes, including Epithelial-Mesenchymal transition (EMT), a biologic developmental process characterized by the conversion of epithelial cells to motile mesenchymal ones, with increased capacity of migration and invasion. EMT plays a key role during the progression of different tumours, including breast cancer and also HMGA have been linked to these processes in the acquisition of tumourigenic features. Consequently taking advantage of different breast cancer cell lines to recreate an "EMT model" we have investigated the role of HMGA proteins in EMT and breast carcinoma. We have developed a cellular model, stable for the overexpression of HMGA1 using the human breast cancer cell line MCF7. We have explored different aspects of tumourigenesis, performing transwell migration and invasion assays, demonstrating that cells with high levels of HMGA1 migrate and invade at a higher and significant level in comparison to control cells. Moreover this data was also confirmed with the development of an inducible cell line for HMGA1 overexpression. Therefore we have examined the expression status of different genes, including several specific EMT markers at mRNA level with Real Time PCR, observing a pre-malignant change towards mesenchymal status. We have investigated the response after DNA damage induced by doxorubicin drug, by colony formation assay, demonstrating that HMGA1 overexpressing cells confer a survival advantage to the cells, being able to survive and form a significant higher number of colonies in respect to control cells. Therefore to study deeper the role of HMGA in EMT, we have developed other two cellular systems, a human cellular model of EMT in MDA-MB-468 human breast carcinoma cells treated with Epidermal Growth Factor (EGF) and the well known EMT model, elicited by Transforming Growth Factor-β (TGF-β) in murine mammary epithelial NMuMG cells, in which HMGA2 is functionally determinant. We have demonstrated by Real Time PCR of EMT markers, Western Blot analyses and immunofluorescence the effective reliability of these cellular models, confirmed also by a dramatic change in morphology of treated cells, towards a mesenchymal phenotype. Concluding we have interestingly observed that overexpression of HMGA1 could confer some tumourigenic features (i.e. migration, invasion) and survival advantage to the cells in the MCF7 model after a cellular DNA damage induction; therefore we have different suggestions that HMGA are involved in EMT in other different cellular models.
Le proteine HMGA (HMGA1a, HMGA1b e HMGA2), definite come fattori architetturali della cromatina, sono fisiologicamente espresse ad alti livelli nel corso dello sviluppo embrionale diminuendo gradualmente la loro espressione nel corso del differenziamento. Sono coinvolte, oltre all'aspetto fisiologico, anche in diverse condizioni patologiche, essendo ad esempio ri-espresse ad alti livelli nel corso della trasformazione neoplastica, esercitando funzioni essenziali grazie alla loro alta plasticità, alle peculiari caratteristiche biochimiche e conseguente multifunzionalità. Le proteine HMGA utilizzano diversi meccanismi per esercitare la loro funzione nell'acquisire capacità trasformanti, inclusa la transizione epitelio-mesenchimale. Questo processo biologico, primariamente identificato come fattore chiave dello sviluppo embrionale, è risultato di essere di fondamentale importanza anche nella trasformazione tumorale. Mediante questo meccanismo una cellula epiteliale, mediante molteplici cambiamenti genetici e biochimici acquisisce caratteristiche tipiche di uno "stato mesenchimale", caratterizzato ad esempio da un'aumentata capacità invasiva e migratoria. La transizione epitelio-mesenchimale esercita un ruolo chiave nel corso della progressione di diverse tipologie tumorali, incluso il cancro al seno, a cui in particolare anche le proteine HMGA sono state associate. L'obiettivo della Tesi è quindi quello di studiare il ruolo delle proteine HMGA nella transizione epitelio-mesenchimale e in particolare nel cancro al seno. A questo scopo abbiamo sviluppato diversi modelli cellulari di transizione epitelio-mesenchimale. Il primo modello ha previsto la creazione di un sistema stabile di over-espressione della proteina HMGA1 nella linea epiteliale di tumore al seno MCF7. Abbiamo analizzato diversi aspetti della tumorigenesi mediante saggi di migrazione ed invasione in transwell, dimostrando come alti livelli della proteina HMGA1 inducano un aumento di entrambi i processi rispetto ad una condizione di controllo. Inoltre i dati di migrazione sono stati confermati in un sistema inducibile per la over-espressione di HMGA1 nella stessa linea cellulare MCF7 e da saggi condotti in condizione di deplezione di HMGA1 attraverso strategie di silenziamento, dimostrando ulteriormente come la migrazione sia un fenomeno HMGA1 dipendente. Abbiamo inoltre esaminato lo stato di espressione di diversi geni, inclusi specifici marker di transizione epitelio-mesenchimale, mediante analisi di Real Time PCR, osservando un cambiamento verso una condizione di tipo pre-maligno e di parziale transizione ad uno stato mesenchimale. Inoltre è stata verificata la risposta al danno indotto da doxorubicina mediante saggio di colony formation, dimostrando come cellule over-esprimenti HMGA1 possiedano un vantaggio in termini di sopravvivenza e di numero di colonie formate, rispetto alle cellule di controllo. Per approfondire ulteriormente il ruolo esercitato dalle HMGA nella transizione epitelio-mesenchimale, sono stati sviluppati altri due modelli cellulari, uno nella linea epiteliale umana di cancro al seno MDA-MB-468 trattata con EGF (Epidermal Growth Factor), l'altro nella linea cellulare murina mammaria di tipo epiteliale NMuMG, trattata con TGF-β (Transforming Growth Factor-β), in cui l'azione di HMGA2 è stato dimostrato avere un ruolo determinante. Mediante analisi di Real Time PCR di marker di transizione epitelio-mesenchimale, di Western Blot e di immunofluorescenza abbiamo dimostrato l'effettiva solidità di questi modelli cellulari, confermato anche dal fatto che è possibile apprezzare un consistente cambio morfologico verso un fenotipo mesenchimale e una concomitante over-espressione delle proteine HMGA. Da questi modelli è stato quindi possibile evincere come le HMGA siano coinvolte nell'acquisizione di caratteristiche di tipo tumorale anche mediante processi di transizione epitelio-mesenchimale e come questi modelli siano utili al fine di semplificare network molecolari.
XXV Ciclo
1984
Jakimovska, Frosina. "Characterization of the interaction between nucleophosmin (NPM) and highmobility group a (HMGA) proteins." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2760.
Повний текст джерелаABSTRACT HMGA proteins are members of the high mobility group (HMG) non-histone, architectural chromosomal proteins. The HMGA family consists of: A1a, A1b and A2, the first two being isoforms produced by alternative splicing. These are small proteins, about 100aa residues long, characterized by three basic stretches of AT-hooks which bind to the AT-rich sequences on the DNA minor groove. They are normally present in rapidly proliferating cells (embryo) whereas upon differentiation the levels of these proteins decrease until they are nearly absent from adult cells. Overexpression of these proteins has been correlated with various types of neoplastic transformations. The interaction network of HMGA has been an object of study for years in our laboratory and one of the most intriguing protein-protein interactions studied is the one between HMGA and nucleophosmin. Nucleophosmin (NPM, B23, numatrin or NO38) is one of the most abundant phosphoproteins, mainly localized in the nucleoli but it also shuttles between the nucleus and the cytoplasm. This versatile protein has been proven to be involved in various cellular functions and related to both proliferative and growth-suppressive roles in the cell. The first evidence of the interaction HMGA2-NPM in our lab has been obtained by in vitro assays (affinity chromatography). The step ahead was to see if this interaction occurs in vivo and if it does, to try to find ts functional significance. Thus,immunoprecipitation (IP) experiments were performed.The first one gave the proof thet interaction between HMGA2 protein and NPM (transfected and endogenous) occurs. The second IP gave the evidence that interaction occurs between HMGA1a and NPM too. This in vivo protein-protein interaction was to be given a functional significance. We tested by siRNA HMGA1a treatment if downregulation of HMGA1a expression influences the expression of the SOD2 gene (regulated by NPM). The effect of the HMGA1a silencing has proven to be very slight on the SOD2 gene (a 14% of expression reduction). EMSA experiments have been performed in order to test the effect of NPM on the DNA binding properties of the HMGA2 protein with the DNA probes E3 and HCRII. In both cases it has been observed that NPM increases the DNA binding affinity of the HMGA2 protein.
1979
Zammitti, Salvina. "Post-translational modifications of high mobility group a (HMGA) proteins in neoplastic transformation." Doctoral thesis, Università degli studi di Trieste, 2010. http://hdl.handle.net/10077/3614.
Повний текст джерелаLe proteine HMG (High Mobility Group) sono la famiglia più ampiamente e meglio caratterizata fra le proteine cromosomiche non istoniche. Esse sono raggruppate in tre sottofamiglie: HMGA, HMGB ed HMGN. Ciascuna sottofamiglia è caraterizzata da una sequenza o motivo funzionale attraverso il quale sono capaci di legarsi a specifiche strutture sul DNA o sulla cromatina. La famiglia HMGA di mammifero consiste di due geni funzionali: HMGA1 and HMGA2. Lo splicing alternativo del trascritto del gene HMGA1 dà origine alle proteine HMGA1a ed HMGA1b. La proteina HMGA2 è codificata dall’altro gene. Le proteine HMGA partecipano a specifiche interazioni proteina-DNA e proteina-proteina inducendo sia cambiamenti strutturali della cromatina che la formazione di complessi macromolecolari su regioni promotrici//enhancer di diversi geni. Pertanto esse sono descritte come fattori archietturali della trascrizione. Grazie alla loro multifunzionalità, ese partecipano a diversi processi biologici quali l’integrazione virale, l’embriogenesi e la differenziazione, l’apoptosi, la senescenza, la trasformazione neoplastica ed il riparo del DNA. La caratteristica di proteine oncofetali attribuita alle HMGA prende origine dal fatto che esse sono (i) altamente espresse durante l’embriogenesi, (ii) assenti o espresse a bassi livelli nei tessuti adulti e (iii) altamente riespresse nelle cellule trasformate. Queste proteine sono, tra le proteine nucleari, quelle più soggette a modificazioni post-traduzionali e le loro attività sono modulate da una ampia varietà di modificazioni post-traduzionali. In questo lavoro di tesi, grazie all’uso di linee cellulari di cancro mammario in cui è stata indotta la reversione del fenotipo neoplastico tramite trattamento farmacologico e successive analisi di spettrometria di massa, si è ricercata una connessione tra le modificazioni post-traduzionali delle HMGA ed il processo di trasformazione neoplastica. Inoltre, grazie ad una nuova strategia in vitro sviluppata nel nostro laboratorio per l’identificazione di partner molecolari delle proteine HMGA, si è dimostrato che la proteina HMGA1a si associa con la proteina Ku70, che è un fattore chiave coinvolto nel riparo delle rotture al doppio filamento di DNA attraverso il “non-homologous end joining”. Numerose evidenze sperimentali suggeriscono che l’inibizione del riparo del DNA da parte delle HMGA posa contribuire alle instabilità genetiche e cromosomiche comunemente ritrovate nelle celle cancerose. Perciò, si è ricercata una relazione funzionale tra le proteine HMGA e le proteine chiave nel meccanismo di riparo del DNA attraverso “non-homologous end joining”, focalizzando l’attenzione in particolare sulla proteina DNA-PK (DNA-dependent protein kinase), che ha una funzione regolatrice chiave in questo processo.
XXII Ciclo
1973
ALTAMURA, SANDRO. "IDENTIFICAZIONE E CARATTERIZZAZIONE DI PARTNERS MOLECOLARI DELLE PROTEINE HMGA." Doctoral thesis, Università degli studi di Trieste, 2007. http://thesis2.sba.units.it/store/handle/item/12290.
Повний текст джерелаUesugi, Hiroko. "Prevalence and characterization of novel P-ANCA, antibodies to the high mobility group non-histone chromosomal proteins HMG1 and HMG2, in systemic rheumatic diseases." Kyoto University, 2000. http://hdl.handle.net/2433/151400.
Повний текст джерелаRagab, Anan. "Genetic and functional studies on abundant Drosophila HMGB proteins." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615068.
Повний текст джерелаZayed, Hatem. "Improvement of the sleeping beauty transposon system." [S.l. : s.n.], 2003. http://www.diss.fu-berlin.de/2003/243/index.html.
Повний текст джерелаAdair, Jennifer Eileen. "Molecular and genetic influence of HMGA1 proteins on nucleotide excision repair." Online access for everyone, 2005. http://www.dissertations.wsu.edu/Dissertations/Fall2005/j%5Fadair%5F120605.pdf.
Повний текст джерелаArnoldo, Laura. "HMGA1 proteins regulate gene expression by modulating histone H3 phosphorylation." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/10112.
Повний текст джерелаHMGA1 is an oncogene encoding for an architectural transcription factor that affects fundamental cell processes, leading to neoplastic transformation. The two main mechanisms by which HMGA1 protein is known to be involved in cancer concern the regulation of gene expression by altering DNA structure and interacting with a conspicuous number of transcription factors. Here we provide evidence of an additional level of gene expression regulation exploited by HMGA1 to exert its oncogenic activity. Starting from protein-protein interaction data showing that HMGA1 interacts with histones, we show that HMGA1 regulates gene expression by affecting the epigenetic status of cancer cells. In particular, it modulates the signalling cascade mediated by the RAS/RAF/MEKK/ERK/RSK2 pathway regulating the levels of histone H3 phosphorylation at Serine 10 and Serine 28. We demonstrate that the down-regulation of these two H3 post-translational modifications by HMGA1 silencing and by inhibitors of the RAS/RAF/MEKK/ERK pathway is linked to cell migration decrease and morphological changes resembling the mesenchymal to epithelial transition.
HMGA1 è un oncogene codificante per un fattore trascrizionale architetturale che influenza fondamentali processi cellulari, portando alla trasformazione neoplastica. I due principali meccanismi tramite cui la proteina HMGA1 è nota essere coinvolta nel cancro riguardano la regolazione dell’espressione genica tramite l’alterazione della struttura del DNA e l’interazione con un cospicuo numero di fattori di trascrizione. Qui forniamo la prova di un addizionale livello di regolazione dell’espressione genica sfruttato da HMGA1 per esercitare la sua attività oncogenica. Partendo da dati d’interazione proteina-proteina che mostrano che HMGA1 interagisce con gli istoni, mostriamo che HMGA1 regola l’espressione genica influenzando lo stato epigenetico delle cellule cancerose. In particolare, essa modula la cascata di segnalazione mediata dalla via di RAS/RAF/MEKK/ERK/RSK2 regolando i livelli di fosforilazione dell’istone H3 sulla Serina 10 e sulla Serina 28. Noi dimostriamo che la down-regolazione di queste due modificazioni post-traduzionali di H3 tramite il silenziamento di HMGA1 e l’utilizzo di inibitori della via di RAS/RAF/MEKK/ERK/RSK2 è correlata alla diminuzione della migrazione cellulare e a cambiamenti morfologici che ricordano la transizione mesenchimo-epiteliale.
XXV Ciclo
1983
Feng, Sandy. "The high mobility group proteins 14 and 17 and their interaction with nucleosomes." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253971.
Повний текст джерелаPreston, Nicola Susan. "Structure and DNA binding of HMG boxes." Thesis, University of Portsmouth, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310386.
Повний текст джерелаSimpson, Andrew. "Non-histone protein HMG-2A and chromatin structure." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359813.
Повний текст джерелаVogel, Benjamin [Verfasser], and Robert [Akademischer Betreuer] Hock. "Organisation von Chromatin durch HMGA1 Proteine / Benjamin Vogel. Betreuer: Robert Hock." Würzburg : Universitätsbibliothek der Universität Würzburg, 2012. http://d-nb.info/1025223853/34.
Повний текст джерелаPark, Semi Ph D. Massachusetts Institute of Technology. "Understanding the functions of HMGB proteins in the mechanism of action of cisplatin." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/78437.
Повний текст джерелаCataloged from PDF version of thesis. Vita.
Includes bibliographical references.
High mobility group box (HMGB) proteins are DNA-binding proteins that regulate many important DNA-related processes. They are known to recognize the major lesion present in cisplatin-modified DNA, and have been assumed to increase cisplatin cytotoxicity by "shielding" the damaged site from the cellular repair apparatus. This thesis will describe the work in the area of molecular biology and biochemistry to improve our understanding of the functions of HMGB proteins in the mechanism of action of cisplatin. In Chapter 1, the molecular biology of cisplatin and HMGB proteins is described based on previously reported in vivo and in vitro experiments. The interaction of HMGB proteins and platinated DNA is reviewed based on several structural studies of platinum-DNA adducts of cisplatin, HMG box motif, and the binding complex of the two. Several cell-based studies supporting a repair-shielding hypothesis, suggesting an inhibitory function of HMGB proteins in the repair of cisplatin damage will be introduced with a focus on HMGB1, the most vigorously investigated HMGB protein. Additionally, other HMGB 1-mediated processes that may be related to cisplatin-triggered cell death will be discussed. Lastly, the correlation between testis-specific HMGB proteins and the cisplatin hypersensitivity of testicular germ cell tumors will be discussed. Although some HMGB proteins including HMGB 1 inhibit the repair of platinated damage on DNA in vitro, experiments conducted in live cells reveal conflicting correlation between the expression level of HMGB1 and cisplatin cytotoxicity. Chapter 2 describes studies in cultured human cancer cells aimed at examining the intracellular repair of platinum-modified DNA and the influence of HMGB1 on the repair processes. The expression of HMGB1 is artificially down-regulated by RNAi. HeLa and A549 cell lines present different trends in cisplatin cytotoxicity upon HMGB1 knockdown. Intracellular repair of cisplatin is lower in knockdown cells regardless of the parental cell line. This result stands in opposition to what is expected from the repair-shielding hypothesis. In addition, the repair of different cisplatin adducts was investigated in fibroblast cells deficient in one of the nucleotide excision repair proteins in order to understand the repair mechanisms of each adduct. Chapter 3 presents an in vitro study investigating the redox-dependence of the binding interaction of HMGB1 to the cisplatin-1,2-d(GpG) intrastrand cross-link. Two cysteine residues in HMGB1 domain A form a reversible disulfide bond under mildly oxidizing conditions. Both HMGB 1 domain A and full-length HMGB 1 presented significantly weaker binding to a DNA probe containing a 1,2-d(GpG) intrastrand cross-link when in their oxidized state compared to their fully-reduced form. Mutagenesis studies on the cysteine residues revealed that this redoxdependence originates from disulfide bond formation. Footprinting analysis of a platinated DNA probe bound to oxidized or reduced domain A showed that the asymmetric binding mode of domain A to platinated DNA is not significantly altered by oxidation. These results suggest that the cellular redox environment can influence the interaction of HMGB 1 with the platinated DNA. In Chapter 4, the binding properties and repair inhibitory function of HMGB4 to cisplatin-modified DNA are described. Based on its testis-restricted expression profile and sequence similarity with HMGB 1, we propose that HMGB4 functions as a cisplatin cytotoxicity enhancer in TGCT. To verify this hypothesis, HMGB4 and its binding domains were generated recombinantly and interactions with cisplatin-modified DNA were investigated in vitro. The binding properties of HMGB4 are quite similar to those of HMGB 1 except for a few differences: i) full-length HMGB4 has stronger binding affinity than full-length HMGB1, because of a lack of a C-terminal acidic tail. ii) binding of HMGB4 domain A is much more symmetric with respect to the platinated lesion than that of HMGB 1 domain A. Furthermore, HMGB4 presented stronger repair inhibition capacity than HMGB1 at an equimolar concentration. These results support the hypothesis that HMGB4 enhances cisplatin cytotoxicity in TGCT. Chapter 5 will be the conclusion chapter of this thesis. Works in this thesis will be summarized with what we can learn from those results. In additions, future directions in the study of HMGB proteins will be suggested. Appendices A and B describe the incomplete work on HMGB4 in live cells. Appendix A delineates the expression profile of human HMGB4 established by western blot analysis. Human HMGB4 presented a testis-preferred expression. In Appendix B, attempts to establish a HMGB4 knockdown testicular cancer cell line are described.
by Semi Park.
Ph.D.in Inorganic chemistry
Bharath, M. M. Srinivas. "Towards The Understanding Of The Structural Biology Of Histone H1." Thesis, Indian Institute of Science, 2000. http://hdl.handle.net/2005/167.
Повний текст джерелаLucey, Michelle M. "The expression of the High Mobility Group N (HMGN) family of proteins during development of the mouse eye." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 120 p, 2008. http://proquest.umi.com/pqdweb?did=1597629771&sid=19&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Повний текст джерелаMohan, Gokula. "Chromatin-binding HMGN proteins and the neuronal differentiation of enbryonal carcinoma cells in vitro." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3316/.
Повний текст джерелаShearer, Alexander Glennon. "HMG-CoA reductase : protein regulation by a quality control pathway /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3144341.
Повний текст джерелаBonne-Andrea, Catherine. "Contribution à l'étude des propriétés et du rôle biologique de la protéine non-histone HMG1." Paris 6, 1986. http://www.theses.fr/1986PA066451.
Повний текст джерелаElashry, Abd-elNasser. "Two C. elegans high mobility group genes, hmg-12 and hmg-1.1, function in neural postembryonic development and cell survival." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972602518.
Повний текст джерелаNatarajan, Suchitra. "Roles of high mobility group AT-hook protein 2 (HMGA2) in human cancers." Elsevier, 2013. http://hdl.handle.net/1993/31092.
Повний текст джерелаFebruary 2016
McA'Nulty, Megan Moore. "Cisplatin in yeast--repair of DNA adducts and binding of HMG domain proteins." Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/32176.
Повний текст джерелаDenbow, Cynthia J. "Membrane Domain of Plant 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase: Targeting, Topology, and Function." Diss., Virginia Tech, 1997. http://hdl.handle.net/10919/30472.
Повний текст джерелаPh. D.
Roemer, Sarah Clark. "Structural and functional analysis of progesterone receptor-DNA interaction /." Connect to full text via ProQuest. IP filtered, 2005.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 165-185). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Ronfani, Lorenza. "Cloning and knock-out of the mouse gene coding for the high mobility group 2 protein (HMG2)." Thesis, Open University, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342940.
Повний текст джерелаSparkes, Andrew Charles. "The isolation and characterisation of Sry-related HMG box gene from Droposhila melanogaster." Thesis, University of Portsmouth, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310391.
Повний текст джерелаGupta, R. "Isolation, characterisation and expression of genes encoding plant high mobility group HMG-I/Y proteins." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599793.
Повний текст джерелаMenezes, Amanda Caroline Cardoso Corrêa Carlos. "Efeito do hidrolisado proteico do grão de amaranto (Amaranthus cruentes L. BRS Alegria) processado na solubilização micelar do colesterol e na ação da HMGR." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-16102017-094758/.
Повний текст джерелаIntroduction: Obesity and dyslipidemia are major contributors of cardiovascular diseases. The consumption of vegetables, especially their protein, acts protectively on the magnitude of these injuries. There is evidence that amaranth protein has a cholesterol-lowering effect by the action of peptides originating from its incomplete digestion. Objective: To assess the effect, in vitro, of the hydrolyzed protein of amaranth, submitted to different processes, on the reduction of the micellar solubilization of cholesterol and on the inhibition of HMGR enzyme activity. Methods: The raw and processed flours were analyzed for their content of amino acids. The isolated protein from amaranth grain flour toasted, extruded and raw, were subjected to enzymatic hydrolysis. Subsequently, it was prepared a solution of bile salts and cholesterol to assess the ability of the hydrolyzed protein to decrease the micellar solubilization of cholesterol. It was used the ultra-filtered peptides (MW up to 3 kDa) at concentration of 3 mg/mL equivalent albumin; and for higher molecular weights, it was used 10 mg/mL. In order to verify the mechanism of inhibition of the cholesterol endogenous synthesis, only it was used the hydrolyzed ultra-filtered peptides with MW < 3 KDa. In the assays of HMGR inhibition, several concentrations of peptides were used (0.1, 0.5 and 1 mg/mL) to compare the inhibition to pravastatin (a known inhibitor). Results: The amino acid composition showed to be adequate when compared to the recommendation of essential amino acids for children 2-5 years. Hydrophobic amino acids compose 30 per cent in total amino acids. When evaluating the effect of the hydrolyzate micellar solubilization of cholesterol has been observed that significant difference (p <0.004) from the processing. The peptides from raw flour hydrolyzed protein (IPHc) with a molecular weight greater than 3 kDa reduced micellar solubilization of cholesterol by 44.09 ± 1.5 per cent , while those from the roasted flour (IPHt) and extruded flour (IPHe) reduced by 31.24 ± 5.9 per cent and 24.97 ± 4.1 per cent . Peptides with a molecular weight up to 3 kDa showed little difference (p < 0.03) due to processing. The reduction of the observed micellar solubility of IPHc and IPHe were similar: 37.21 ± 0.4 per cent and 35.45 ± 1.65 per cent , respectively. The IPHt showed the smallest decrease of 22.47 ± 4.6 per cent . The peptides from amaranth flour were also able to inhibit the activity of the enzyme HMGR in various concentrations. The control of normal enzyme activity showed 0.65 ± 0.05 mol of NAPH oxidized min/mg equivalent of albumin. The IPHc at concentrations of 0.1 and 0.5 mg/mL had an effect similar to that of pravastatin, different from control (p < 0.05), yielding: 0.24 ± 0.03 and 0.29 ± 0.13 mol of the NAPH oxidized min/mg equivalent of albumin. On the other hand, IPHt showed a similar effect to higher concentration of pravastatin in the raw, and in 1 mg/mL produced from 0.20 ± 0.09 mol of oxidized NAPH min/mg equivalent of albumin. The IPHe showed the inhibitory effect on the enzyme concentration as lower as 0.1 mg/mL, but less pronounced than pravastatin. Conclusions: The peptides from hydrolysis of amaranth grain has evidence of hypocholesterolemic activity. They are able to act both in exogenously and endogenous pathways, inhibiting the absorption of cholesterol and its synthesis. The thermal processing reduces this capacity, but still shows significant results. Among the processing, extrusion deserves less attention than other one, although their results may have been influenced by the amount of the isolated protein components, such as lipids and phenolic compounds.
Winston, Eugenia Michele. "The Utilization of the Hmg2 Inducible Promoter to Genetically Engineer Parasite Resistance in Tobacco." Diss., Virginia Tech, 2003. http://hdl.handle.net/10919/27200.
Повний текст джерелаPh. D.
Shinn, Annie Heekyung. "Evaluating the effects of HMG -CoA reductase inhibitors on C -reactive protein, butyrylcholinesterase, and lipids." Scholarly Commons, 2004. https://scholarlycommons.pacific.edu/uop_etds/2675.
Повний текст джерелаSchlüter, Claudia. "Untersuchungen zur Bedeutung ausgewählter HMG-Proteine bei der Differenzierung und Proliferation von Endothel- und glatten Muskelzellen." kostenfrei, 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975431765.
Повний текст джерелаCanaple, Laurence. "Structure et fonction du gene dspi codant pour une proteine a boites hmg chez drosophila melanogaster." Orléans, 1997. http://www.theses.fr/1997ORLE2031.
Повний текст джерелаWeihrauch, Marc-Andreas Günter. "Butyrat moduliert die Expression der Nicht-Histon-Proteine HMGA1, HMGN1 und HMGN2 in humanen Adenokarzinomzellen des Kolons und des Magens." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971750556.
Повний текст джерелаOHYAMA, YUMIKO. "Etude par resonance magnetique nucleaire 2d et 3d de la structure tridimensionnelle de la boite a de la proteine hmg1." Paris 6, 1996. http://www.theses.fr/1996PA066309.
Повний текст джерелаSuraty, Thaís Rezende. "Efeito da proteína de amaranto (Amaranthus cruentus L. BRS Alegria) na atividade enzimática hepática da HMG-CoA redutase e seu papel no metabolismo lipídico em hamsters." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/89/89131/tde-29062015-170422/.
Повний текст джерелаIntroduction: Nowadays, Non-Communicable Chronic Diseases (NCCD) are a major challenge in health public. It is evident the role of diet in the control of cholesterol and incidence of cardiovascular disease. In this sense, amaranth arouses great interest due to its hypocholesterolemic property. Studies suggest that amaranth\'s hypocholesterolemic effect is associated with the inhibition of the enzyme HMG-CoA reductase, known as the key process to the endogenous cholesterol synthesis. Objective: Evaluate the hepatic enzymatic activity of HMG-CoA reductase in hamsters fed with amaranth protein. Methodology: Amaranth protein was isolated according to the conventional isoelectric precipitation methodology. Thirty hamsters were divided in 5 groups and were fed diets with different protein source. Experimental groups (I and lcol) had a diet containing 20% of protein amaranth and control groups(C and Cool) received a diet with 20% of casein. Moreover, groups \"col\" had also a diet with 0.1% cholesterol and 13.5% coconut oil in their composition. The lipid metabolism was accompanied through monitoring of plasma concentrations of total cholesterol, triglycerides, HDL and non-HDL fraction in animals. Excretion of cholesterol and bile acids were quantified in the feces of animals and the degree of hepatic steatosis was determined by histological analysis of the liver\'s right lobe. The HMGR enzyme activity in the liver was measured by the CS 1090 Kit from Sigma-Aldrich adjusted in accordance with Cong et al, 2012. The analysis is based on spectrometry with absorbance of 340nm at 37 ° C, which represents the oxidation of NADPH by HMG-CoA reductase in the presence of HMG-CoA substrate. Conclusions: Amaranth protein can be considered as an ally in reducing of injuries generated by dyslipidemia, since it significantly reduced levels of plasma cholesterol and hepatic fat. Furthermore, it was demonstrated its effect on reducing activity of HMG-CoA reductase enzyme in hypercholesterolemic animals, which were fed with amaranth protein. Therefore, once verified the hypocholesterolemic effect of amaranth and its possible action mechanism through HMG-CoA reductase enzyme, stimuli on the production of amaranth are expected as an alternative to diversify the diet and agriculture.
Milner, Michael James. "Isolation and characterisation of genes encoding HMG domain proteins from Coprinus cinereus and an analysis of their role in mating." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365718.
Повний текст джерелаRittenhouse, Kimberley Rochelle. "Bullwinkle, an HMG box protein, is required for proper development during oogenesis, embryogenesis and metamorphosis in Drosophila melanogaster /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/10267.
Повний текст джерелаBounaix, Morand du Puch Christophe. "Analyse des interactions ADN lésé / protéines : Optimisations méthodologiques et applications aux dommages de l’ADN engendrés par les dérivés du platine." Grenoble, 2010. https://theses.hal.science/tel-00549987.
Повний текст джерелаDNA lesions contribute to the alteration of DNA structure, thereby inhibiting essential cellular processes. Such alterations may be beneficial for chemotherapies, for example in the case of platinum anticancer agents. They generate bulky adducts that, if not repaired, ultimately cause apoptosis. A better understanding of the biological response to such molecules can be obtained through the study of proteins that directly interact with the damages. These proteins constitute the DNA lesions interactome. This thesis presents the development of tools aiming at increasing the list of platinum adduct-associated proteins. Firstly, we designed a ligand fishing system made of damaged plasmids immobilized onto magnetic beads. Three platinum drugs were selected for our study: cisplatin, oxaliplatin and satraplatin. Following exposure of the trap to nuclear extracts from HeLa cancer cells and identification of retained proteins by proteomics, we obtained already known candidates (HMGB1, hUBF, FACT complex) but also 29 new members of the platinated-DNA interactome. Among them, we noted the presence of PNUTS, TOX4 and WDR82, which associate to form the recently-discovered PTW/PP complex. Their capture was then confirmed with a second model, namely breast cancer cell line MDA MB 231, and the biological consequences of such an interaction now need to be elucidated. Secondly, we adapted a SPRi biochip to the study of platinum-damaged DNA/proteins interactions. Affinity of HMGB1 and newly characterized TOX4 for adducts generated by our three platinum drugs could be validated thanks to the biochip. Finally, we used our tools, as well as analytical chemistry and biochemistry methods, to evaluate the role of DDB2 (a factor involved in the recognition of UV-induced lesions) in the repair of cisplatin adducts. Our experiments using MDA MB 231 cells differentially expressing DDB2 showed that this protein is not responsible for the repair of platinum damages. Instead, it appears to act as a positive mediator of their cytotoxicity. In the near future, the abovementioned microsystems will be adapted to the study of the interactome of other DNA lesions
Arce, Cerezo Altamira. "Study of the role of the overexpression of the high mobility group-AT-hook-1 (HMGA1) protein in the adipose tissue and its implications in the development of obesity and insulin resistance." Doctoral thesis, Universitat Autònoma de Barcelona, 2013. http://hdl.handle.net/10803/126522.
Повний текст джерелаObesity is a complex metabolic disorder that has reached epidemic proportions in both developed and developing countries. Moreover, obesity is a major risk factor that enhances the risk of developing other diseases such as insulin resistance, type 2 diabetes and cardiovascular diseases. These pathologies represent a great threat to global human health. Knowledge of the causes and mechanisms that trigger the development of these diseases is of vital importance for its prevention and treatment. However, the mechanisms through which obesity originates, develops and predisposes to other metabolic complications are not fully understood. Adipocyte and obesity development have been largely study through many cellular models. In addition, several rodent and non-rodent models have been generated for the better understanding of obesity phisiopathogenesis. As High Mobility –AT-hook- Group-1 (HMGA1) proteins have been implicated on adipogenesis in vitro, we sought to examine the metabolic effects of HMGA1 overexpression in adipose tissue in vivo. To this aim, we generated a line of transgenic mice specifically overexpressing HMGA1 in adipose tissue. Overexpression of HMGA1 in adipose tissue reduced adiposity in aP2-HMGA1 transgenic mice. In addition, these animals were normoglycaemic and normoinsulinemic. Furthermore, transgenic mice presented higher metabolic rate. Although reduced adiposity and reduced adipocyte mean area, no major differences in the adipocytes from epididymal white adipose tissue (epWAT) were detected. However, an active remodelling process was detected in this depot. In contrast, aP2-HMGA1 transgenic animals showed reduced adipose tissue mass and serious morphological alterations in brown adipose tissue (BAT). These changes implicated downregulation of genes and proteins involved in specific brown adipocyte differentiation programme, mitochondrial biogenesis and function and lipid metabolism, leading to impaired thermogenic capacity of BAT. Gene expression analysis of epWAT and BAT from transgenic mice showed dysregulation of gene pathways involved in cell cycle, fatty acid and insulin metabolism, and adipogenesis. When fed a high fat diet (HFD), transgenic mice gained less weight and showed lower adiposity than wild type littermates. Moreover, transgenic mice showed decreased epWAT weight and decreased mean adipocyte area. Consistent with the lack of fat accumulation, lipid related metabolites and adipokine secretion were reduced in transgenic mice in comparison to wild type mice. In contrast to wild-type obese and insulin resistant mice, transgenic mice remained protected against dietinduced obesity, insulin resistance and glucose intolerance. In addition, transgenic mice presented high macrophage infiltration in epWAT. Transgenic mice showed an increase in the percentage of total macrophages, although no shift from M2 anti-inflammatory to M1 proinflammatory macrophage population was observed. This was parallel to a reduction in the levels of pro-inflammatory cytokines, such as IL-6, MCP-1 and TNF-a, which were elevated in epWAT of HFD-fed wild-type mice. Taken together, these results indicate that specific HMGA1 overexpression in the adipose tissue impaired terminal differentiation of adipocytes. These effects protected transgenic mice from high fat diet-induced obesity, insulin resistance and glucose intolerance. Thus, this study suggests that HMGA1 proteins may be active players in adipogenesis and adipose tissue development, although the exact mechanism of action still remains unclear.
BEAUJEAN, NATHALIE. "Structure de la chromatine et activite transcriptionnelle dans les embryons de souris normaux ou apres transferts de noyaux : role de la proteine hmg-i." Paris 6, 2001. http://www.theses.fr/2001PA066013.
Повний текст джерелаBoucher, Philippe. "Régulation nutritionnelle de l'expression des principaux gènes qui contrôlent le métabolisme et la toxicité de l'alcool et du cholestérol alimentaire : CYP2E1, LDL récepteurs, HMG CoA réductase et LRP." Lyon 1, 1999. http://www.theses.fr/1999LYO1T160.
Повний текст джерелаSlunga, Lisbeth. "Serum lipoprotein(a) in relation to ischemic heart disease and associated risk factors." Doctoral thesis, Umeå universitet, Klinisk kemi, 1993. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101298.
Повний текст джерелаDiss. (sammanfattning) Umeå : Umeå universitet, 1993, härtill 5 uppsatser.
digitalisering@umu
Sterenczak, Katharina Anna [Verfasser], Jörn [Akademischer Betreuer] Bullerdiek, and Ingo [Akademischer Betreuer] Nolte. "Structural and quantitative characterisation of canine RAGE gene transcripts and evaluation of canine HMG genes and proteins for the establishment of therapeutic strategies / Katharina Anna Sterenczak. Gutachter: Jörn Bullerdiek ; Ingo Nolte. Betreuer: Jörn Bullerdiek." Bremen : Staats- und Universitätsbibliothek Bremen, 2011. http://d-nb.info/1071898140/34.
Повний текст джерелаSchmahl, Michelle Jordan. "Metabolic Profiling of Urine, Fecal, and Serum Samples and Pancreatic Tumors and Evaluation of HMGA1 Expression Levels in Pancreatic Intraepithelial Neoplasia Cells in the Ptf1a-Cre; LSL-KrasG12D Transgenic Mouse Model of Pancreatic Cancer." Miami University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=miami1523977530802748.
Повний текст джерелаHourcade-Potelleret, Florence. "De la dose à l'effet clinique : utilisation de la modélisation dans les différentes étapes du processus de prédiction du critère clinique : Exemple avec un nouveau médicament en prévention secondaire de la morbidité-mortalité cardiovasculaire." Phd thesis, Université Jean Monnet - Saint-Etienne, 2012. http://tel.archives-ouvertes.fr/tel-00979667.
Повний текст джерелаBunce, Michael Anthony. "Chromatin architecture and transcription of the HIV-1 promoter : the role of HMGA." Phd thesis, 2002. http://hdl.handle.net/1885/148641.
Повний текст джерелаVogel, Benjamin. "Organisation von Chromatin durch HMGA1 Proteine." Doctoral thesis, 2011. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-65295.
Повний текст джерелаHMGA1 proteins are small basic non-histone proteins characterized by three DNA binding domains, the AT-hooks, which bind to the minor groove of DNA. As differentially expressed architectural chromatin proteins, they perform important functions in the regulation of DNA dependent processes and in development. Aberrant expression leads to developmental defects and cancer. In this thesis the influence of HMGA1 proteins on chromatin organization is investigated. Initially C2C12 myogenic precursor cells were studied, which can be differentiated to myotubes. Previously it had been shown that down-regulation of HMGA1 proteins is crucial for the initiation of myogenic differentiation. Constant over-expression of HMGA1a-eGFP prevents myogenic differentiation by influencing the expression of myogenic genes and by the establishment of a stable chromatin structure. Here it was shown that the differential HMGA1 expression does not only influence the expression of myogenic specific genes but also affects total chromatin composition. This was shown by reduced and aberrant expression of chromatin proteins such as histone H1, HMGB1, HMGN1 and HP1 proteins. Recently it was demonstrated that HMGA1 together with ORC proteins function in origin definition in eukaryotic cells. ORC proteins were also identified as components of heterochromatin and direct interaction partners of HP1α. Here, it was shown by co-immunoprecipitation, pull-down assays, siRNA and displacement experiments that HMGA1 proteins can interact with ORC proteins directly and that they can cooperate with HP1α in heterochromatin. It could be shown that HP1α indeed does not directly interact with HMGA1 but together with ORC proteins is relevant for heterochromatin maintenance. Thus HMGA1 proteins turned out to be important stabilizers of heterochromatin. Until recently it was thought that HMGA1 proteins bind DNA collinearly. In principle the three independent DNA binding AT-hooks of HMGA1 also suggest a concomitant binding to neighboring DNA strands, which could lead to a three dimensional stabilization of DNA. This assumption was affirmed by the occurrence of chromatin aggregates in HMGA1a-eGFP overexpressing cells, which was analyzed by confocal and high resolution (dSTORM) microscopy. By using a newly developed DNA cross-linking assay, which allows the analysis of a DNA crosslinking capability of a protein, it was proven that HMGA1 proteins can bind two individual DNA fibers simultaneously. Furthermore a novel domain in HMGA1 proteins was discovered which is significantly involved in the DNA cross-linking. Electron microscopic analyses confirmed that HMGA1 proteins can specifically generate crossings and loops in DNA molecules. These results support the assumption that HMGA1 proteins can create a DNA scaffold that has influence on cell typical chromatin organization and possibly also affects DNA dependent processes. To what extent HMGA1 induced DNA cross-linking plays a role in vivo, for example in the organization of chromocenters of C2C12 cells or in cancer cells, where HMGA1 proteins are over-expressed, will need to be elucidated in further experiments In summary, this work shows, that HMGA1 proteins influence chromatin structure and composition by affecting the expression of chromatin proteins, by interacting with other architectural chromatin proteins or by producing a higher organization of chromatin on its own
Schütz, Monika. "Dynamik und Funktion der HMG-Proteine." Doctoral thesis, 2005. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-15627.
Повний текст джерелаHMG proteins are architectural chromatin proteins that regulate different DNA dependent processes such as replication, transcription and DNA repair. To understand how HMG proteins manage to fulfill their multiple functions they were investigated in vivo with the help of EGFP and DsRed2 fusion proteins. Using photobleaching techniques their dynamic properties were characterized in detail. Furthermore, the expression pattern of HMGN proteins in tumor cell lines was investigated for the first time. As presented in this thesis, it was found that HMGN2 proteins exhibited an elevated expression level in some tumor cells (HT-29, FTC-133, MCF-7, RPMI 8226, 697, Ishikawa, LNCap) correlating with the tumor differentiation status. In contrast a reduced expression of HMGN1 found in Mammacarcinoma and Non-Hodgkin-Lymphoma correlated with tumor aggressiveness. Therefore the analyses of HMGN expression may be a suitable diagnostic marker at least in the tumors investigated. FRAP analyses with cells expressing EGFP fusion proteins revealed that HMGN1, HMGN2, HMGA1a, HMGA1b and HMGB1 move very rapidly through the cell nucleus and only bind transiently to chromatin. It was demonstrated that the decision where HMG proteins bind in vivo is essentially mediated by their specific DNA binding motifs. However, the individual residence times in eu- or heterochromatin and chromosomes are regulated by protein modifications (phosphorylation, acetylation). This has been demonstrated using point mutated and truncated HMGA fusion proteins and by the application of specific drugs as well. FRAP analyses also indicated that the splice variants HMGA1a and HMGA1b exhibit different kinetic properties. This supports the view that both variants have different functions. The kinetic parameters characteristic for each HMG protein lead to a model of a dynamic chromatin network in which all HMG proteins are able to regulate DNA dependent processes via multiple interactions with other proteins as components of a cocktail of dynamic chromatin proteins. In this model, individual residence times of all HMG proteins which are regulated by secondary modifications would determine how long other chromatin modulating proteins could reside on chromatin. Therefore the dynamic parameters of the HMG proteins directly affect the capability of other proteins to modulate chromatin structure, e.g. by modifications of core histones. This explains the multiple functions of HMG proteins in chromatin packaging and function. The kinetic parameters of some rapidly moving members of the HMG protein family, such as HMGB1, are beyond the time resolution capacities of most confocal microscopes. However, novel setups of modern confocal microscopes are now capable to determine the dynamic parameters of HMGB proteins and allow investigations of drug induced effects on HMGB dynamics. Control experiments revealed that other fluorophors such as DsRed2 modulate the dynamic parameters of HMG fusion proteins. Due to an increased residence time of HMG DsRed2 fusion proteins it is possible to monitor even very transient interactions. Moreover, it could be observed that this increased residence time may interfere with binding of other proteins (i.e. proteins which occupy the same binding sites) leading to a reorganization of chromatin. Thus, fusion proteins with DsRed fluorophores may be used as helpful tools to investigate protein functions. However, results should always be considered against the background of DsRed modulated kinetics and thus they should be interpreted very carefully. Taken together the results presented in this thesis provide novel information about the dynamic behaviour of HMG proteins which is crucial to understand how chromatin is modulated during differentiation processes or development of neoplasia. Their transient interactions with DNA or other proteins and the fact that overexpression correlates with tumor progression might be relevant for the development of novel strategies for tumor treatment
An, Woojin. "Interaction of linker proteins, H1 and HMG1, with nucleosome reconstituted on positioning sequences." Thesis, 1998. http://hdl.handle.net/1957/33954.
Повний текст джерела