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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
191

The Role of p21 <sup>CIP1/WAF1</sup> and CDK2/Cyclin E in Regulating Centrosome Duplication

Horn, Henning Friedrich 25 January 2006 (has links)
No description available.
192

LOSS OF HDMX LEADS TO ALTERATIONS IN GENE EXPRESSION AND INHIBITION OF CELL GROWTH IN TUMOR CELLS WITH WILD-TYPE p53

Heminger, Katherine Ann 12 June 2007 (has links)
No description available.
193

In Search For New p53 Regulated Genes

Mpagi, Meldrick Daniel 21 November 2008 (has links)
No description available.
194

Investigating the Molecular Mechanism of Novel Quinuclidinone Derivatives in Lung Cancer Cells with Different p53 Status

Soans, Eroica 22 September 2010 (has links)
No description available.
195

Identification of the Functional Significance of a Novel Genetic Modifier of p53 – Ovca1

Du, Shuhua 25 July 2011 (has links)
No description available.
196

Suppression of malignant rhabdoid tumors through Chb-M′-mediated RUNX1 inhibition / Chb-M′を介したRUNX1阻害は悪性ラブドイド腫瘍の増殖を抑制する

Daifu, Tomoo 23 March 2022 (has links)
京都大学 / 新制・論文博士 / 博士(医学) / 乙第13480号 / 論医博第2255号 / 新制||医||1059(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 小川 誠司, 教授 羽賀 博典, 教授 伊藤 貴浩 / 学位規則第4条第2項該当 / Doctor of Medical Science / Kyoto University / DFAM
197

Mathematical Models of Some Signaling Pathways Regulating Cell Survival and Death

Zhang, Tongli 25 November 2008 (has links)
In a multi-cellular organism, cells constantly receive signals on their internal condition and surrounding environment. In response to various signals, cells proliferate, move around or even undergo suicide. The signal-response is controlled by complex molecular machinery, understanding of which is an important goal of basic molecular biological research. Such understanding is also valuable for clinical application, since lethal diseases like cancer show maladaptive responses to growth-regulating signals. Because the multiple feedbacks in the molecular regulatory machinery obscure cause-effect relations, it is hard to understand these control systems by intuition alone. Here we translate the molecular interactions into differential equations and recapture the cellular physiological properties with the help of numerical simulations and non-linear dynamical tools. The models address the physiological features of programmed cell death, the cell fate decision by p53 and the dynamics of the NF-?B control system. These models identify key molecular interactions responsible for the observed physiological properties, and they generate experimentally testable predictions to validate the assumptions made in the models. / Ph. D.
198

Modelling the hair follicle dermal papilla using spheroid cell cultures.

Schallreuter, Karin U., Salem, Mohamed M.A. 07 1900 (has links)
No / Vitiligo occurs in Northern Europe in one of 200 people. The disease can cause significant psychological stress for the affected individual. These patients generate and accumulate massive amounts of H2O2- and peroxynitrite in the epidermal compartment. Consequently many proteins are oxidized or nitrated, leading in turn to partial or complete loss of functionality. Moreover, presence of DNA damage in the skin as well as in plasma has been shown, while apoptosis is not enhanced. Induction of DNA repair is associated with up-regulated functioning p53 protein. Considering possible genetic predisposition and /or spontaneous mutations, autoimmune reactions in the disease are put forward in the context of oxidative stress. In addition a review of recent and novel treatment modalities including the role of oxidative stress reduction and combined climatotherapy at the Dead Sea in a group are discussed.
199

Designing anticancer copper(II) complexes by optimizing 2-pyridine-thiosemicarbazone ligands

Deng, J., Yu, P., Zhang, Z., Wang, J., Cai, J., Wu, Na (Anna), Sun, H., Liang, H., Yang, F. 26 May 2020 (has links)
Yes / To develop potential next-generation metal anticancer agents, we designed and synthesised five Cu(II) 2-pyridine-thiosemicarbazone complexes by modifying the hydrogen atom at the N-4 position of ligands, and then investigated their structure-activity relationships and anticancer mechanisms. Modification of the N-4 position with different groups caused significant differences in cellular uptake and produced superior antitumor activity. Cu complexes arrested the cell cycle at S phase, leading to down-regulation of levels of cyclin and cyclin-dependent kinases and up-regulation of expression of cyclin-dependent kinase inhibitors. Cu complexes exerted chemotherapeutic effects via activating p53 and inducing production of reactive oxygen species to regulate expression of the B-cell lymphoma-2 family of proteins, causing a change in the mitochondrial membrane potential and release of cytochrome c to form a dimer with apoptosis protease activating factor-1, resulting in activation of caspase-9/3 to induce apoptosis. In addition, Cu complexes inhibited telomerase by down-regulating the c-myc regulator gene and expression of the human telomerase reverse transcriptase. / Natural ScienceFoundation of China (31460232, 21431001, 21561017, 21462004),the Natural Science Foundation of Guangxi (2017GXNSFEA198002,AD17129007), IRT_16R15, Guangxi“Bagui”scholar program to HBSun, and High-Level Innovation Team and Distinguished Scholarprogram of Guangxi universities to F Yang.
200

The Effects of Tarsh Overexpression on Lung Carcinomas

Kim, Young 26 April 2013 (has links)
Lung cancer arises from epithelial cells that line the air passages of the lungs. It is the second most common malignancy in the United States; trends suggest that over 228,000 new patients will be diagnosed with lung cancer in 2013. Due to the fact that lung cancer is highly aggressive, it has proven difficult to control. The 5-year survival rate has been shown to be only 15.9%, despite the advances made in terms of diagnosis and treatment. Therefore, we are faced with the problem of finding more effective methods that allow for an earlier diagnosis and the improved treatment of lung cancer. This study attempts to address these issues by investigating Tarsh, a novel molecule that is involved in the regulation of cellular senescence. Previous studies have shown that Tarsh is expressed in normal lung cells, but is significantly downregulated in lung tumors. These studies also determined that Tarsh is likely dependent upon the expression of p53, a tumor suppressor gene. The current study investigated these results, in addition to the biological effects of ectopically increasing Tarsh and/or knocking down p53 expression in two lung cancer cell lines: A549 and H1299 cell lines. It was determined that increasing the expression of Tarsh decreased the rate of proliferation in both cell lines. Additionally, it was shown that the knockdown of p53 increased proliferation in A549 cells. In regards to the migration rate of these cell lines, the overexpression of Tarsh decreased migration in A549 cells, but had no effect on H1299 cells. However, the role of p53 in migration is still unclear. The results of this study suggest that the knockdown of p53 decreases cell migration in A549 cells. This contradicts the fact that H1299 cells do not express p53, yet was found to have the highest migration rate. It is evident that a further investigation is needed to make more concrete conclusions. Nevertheless, the suppressive features of Tarsh on cell proliferation, and possibly migration, make it a promising target of research for lung cancer therapy.

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