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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.
1

Study on the role of osmotic stress, oxidative stress and poly(ADP-ribose) polymerase in the pathogenesis of diabetic cataract

Chan, Wai-ho. January 2005 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.
2

In vitro binding of base excision repair glycosylases to poly(adp-ribose)

Nichols, Joseph A., January 2008 (has links) (PDF)
Thesis (M.S. in genetics and cell biology)--Washington State University, August 2008. / Includes bibliographical references (p. 39-43).
3

Interaction of Poly(ADP-ribose) and Specific Binding Proteins as a Function of Chain Length

Fahrer, Jörg. January 2007 (has links)
Konstanz, Univ., Diss., 2007.
4

Studies on a novel poly(ADP-ribosyl)ation polymerase PARP-10 and its functional interaction with c-Myc

Yu, Mei. Unknown Date (has links) (PDF)
Techn. Hochsch., Diss., 2005--Aachen.
5

Study on the role of osmotic stress, oxidative stress and poly(ADP-ribose) polymerase in the pathogenesis of diabetic cataract

Chan, Wai-ho., 陳韋豪. January 2005 (has links)
published_or_final_version / abstract / Physiology / Doctoral / Doctor of Philosophy
6

PARP inhibitor ABT-888 as potentiating agent for topoisomerase inhibitor SN-38

Sohail, Honeah, January 2009 (has links)
Thesis (M.S.)--Rutgers University, 2009. / "Graduate Program in Microbiology and Molecular Genetics." Includes bibliographical references (p. 49-53).
7

The down-regulation of Ku70, DNA-PKcs, and Parp-1 in mammalian cell lines

Wickersham, Stephanie January 2012 (has links)
DNA double strand breaks (DSBs) are primarily repaired in eukaryotic cells by two different mechanisms – non-homologous end joining (NHEJ) or homologous recombination (HR). In mammalian somatic cells the balance between the two highly favours NHEJ. Gene targeting is a technique that exploits HR repair to alter a defined gene locus. While it holds potential to be implemented as a treatment option for several diseases, the outlook for using it in a clinical setting has been obstructed by a low gene targeting efficiency. This has been coupled to the low frequency of HR in mammalian cells. With the intention of shifting the repair balance, antibodies against DSB repair proteins will be introduced into mammalian cells. It is predicted that by targeting key repair proteins with antibodies, a compensatory increase in the frequency of HR can be fostered, ultimately resulting in improved gene targeting. / xv, 168 leaves : ill. ; 29 cm
8

Human Poly(ADP-Ribose) Polymerase-1-Expressing Embryonic Stem Cells and Mice Generation and Phenotypic Characterization /

Mangerich, Aswin. January 2008 (has links)
Konstanz, Univ., Diss., 2008.
9

Tumor necrosis factor-induced necroptosis is regulated by nicotinamide adenine dinucleotide in a sirtuin-dependent manner

Preyat, Nicolas 28 June 2013 (has links)
Nicotinamide adenine dinucleotide (NAD+) represents a long-known key molecule in cellular metabolism. It was initially identified for its ability to convey electrons and protons between redox partners in multiple bioenergetic and biosynthetic reactions. In addition, NAD+ also serves as a substrate for NAD+-consuming enzymes such as sirtuins and poly ADP-ribose polymerases (PARPs). These latter enzymes catalyze dynamic post-translational modifications that control virtually every signaling pathway orchestrating cell fate. The aim of this work was to analyze the role of NAD+ in the context of programmed cell death mechanisms.<p>Our findings indicate that NAD+ is protective against DNA damage-induced cell death and FAS-induced apoptosis, while, unexpectedly, it promotes TNF-induced necroptosis, a regulated form of necrosis. Indeed raising NAD+ cellular levels sensitized culture cells to necroptosis, while NAD+ depletion protected cells from this form of cell death. Furthermore, specific silencing of NAD+-dependent sirtuins was also found to be protective against TNF-induced necroptosis. Consistently, a pharmacological pan-sirtuin inhibitor called cambinol protected cells from necroptosis. Then, as necroptosis represents a back-up mechanism that may have evolved in response to viral pathogens expressing anti-apoptotic proteins, we demonstrated in an in vitro model mimicking viral infection that pharmacological sirtuin inhibition protected cells from poly I:C-induced necroptotic cell death. In vivo, we demonstrated that cambinol partially protected kidney from necrosis after ischemia/reperfusion. We have also shown that enhancing liver NAD+ concentration via isonicotinamide increases the susceptibility of mice to systemic inflammatory response syndrome (SIRS). Moreover, our preliminary data show that isonicotinamide substantially improves the ability of cyclophosphamide to trigger the rejection of the murine mastocytoma P815 tumor cell line.<p>Collectively, our observations point to a role for NAD+ in the control of necroptosis in a sirtuin-dependent manner. These observations may bear relevance to the better understanding of the pathophysiological consequences of excessive production of the pro-inflammatory cytokine TNF and the control of viral infections and tumor progression/immunotherapy. & / Doctorat en Sciences / info:eu-repo/semantics/nonPublished
10

PARP12, a novel interferon stimulated gene potentially involved in the control of protein translation and innate immunity

Welsby, Iain 16 April 2012 (has links)
Poly(ADP-ribose) polymerases belong to a family of proteins with 17 members in human beings. PARP1, the founding member of the family is a protein that synthesizes linear or branched polymers of ADP-ribose on itself or on target proteins. Different members of this family, that do not all possess ADP-ribosyl polymerase activity, are involved in the regulation of various cellular mechanisms. Some members of the family are particularly involved in the positive or negative control of the immune response. PARP1 is a key player in the regulation of inflammation, through its positive control of cell death and of proinflammatory cytokine production. On the other hand, the tankyrases (PARP5a and PARP5b) and PARP14 seem to regulate inflammatory responses in a negative fashion. PARP12 is a poorly characterized member of the family, whose expression is greatly increase following stimulation with type-I interferons, cytokines mainly involved in antiviral defences.<p>PARP12 is a protein that possesses three main domains: A putative RNA binding N-terminal domain composed of tandem CCCH zinc-fingers, a central WWE domain and a C-terminal PARP catalytic domain. In this work, we have shown that the expression of PARP12 is strictly-dependent on type-I interferons, that it possesses ADP-ribosyl transferase activity and that in can regulate the translation of messenger RNA into proteins. PARP12 can be found in stress granules, sites of storage of untranslated mRNAs, and is capable of directly inhibiting the translation of a reporter mRNA when tethered to it, in a manner dependent on its catalytic activity. Furthermore overexpression of wild-type PARP12, in contrast to overexpression of a mutant with no detectable catalytic activity (PARP12-G575W), leads to a general arrest of most cellular translation.<p>On the other hand, we have shown that PARP12 can activate the transcription of genes under the control of an NFκB-dependent promoter, especially when its zinc-fingers are deleted or mutated (PARP12ΔZnF). PARP12ΔZnF is located in structures that can enclose TRIF, RIP1, NEMO, p62/SQSTM1 and ubiquitin. These proteins have all possess an important role in the activation of NFκB signalling cascades. Moreover, we have shown that endogenous PARP12 is situated in ALIS (Aggresome-Like Induced Structures) in LPS-stimulated macrophages. These structures have a possible role in the presentation of antigens on class I major histocompatibility complexes, implying that PARP12 may be involved in the regulation of antigen presentation. <p> / Doctorat en Sciences / info:eu-repo/semantics/nonPublished

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