Дисертації з теми "BIO/12"
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ROMANI, MARTA. "Analisi dell’interazione fra la proteina non strutturale 5A del virus dell’epatite C e le proteine cellulari." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/481.
Повний текст джерелаMERLO, PAOLA. "Post-translational modifications regulate p73 functions." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2005. http://hdl.handle.net/2108/188.
Повний текст джерелаCORINTI, SILVIA. "Ruolo dell’ossido nitrico sulle funzioni delle cellule dendritiche derivate dai monociti." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2006. http://hdl.handle.net/2108/222.
Повний текст джерелаNitric oxide (NO) has an established role in the defense against bacterial infections, and exerts multiple modulatory activities on both inflammatory and immune responses. However, the relevance of NO on dendritic cell (DC) functions has been poorly investigated. In this study, we found that addition of the NO donor S-nitrosoglutathione (GSNO) to monocyte-derived DCs matured in the presence of LPS led to a decreased capacity to activate naive allogeneic T cells but a more prominent Th1 polarization, with increased IFN- secretion and reduced IL-4 and IL-5 secretion. The presence of GSNO during maturation of DCs caused a reduced expression of surface CD86, whereas CD80, CD83 and MHC molecule expression was not affected. Moreover, GSNO induced a dose-dependent decrease of IL-10 and enhancement of TNF- release. In parallel, a marked reduction of IL-12 p40 subunit in the supernatant of mature DCs, but no significant perturbation of the bioactive IL-12 p70 production was observed. Finally, GSNO significantly reduced the release of IP-10/CXCL10 and RANTES/CCL5, but not IL-8/CXCL8 by DCs. Although GSNO can strengthen the capacity of mature DCs to induce type 1 polarization of T lymphocytes, our data suggest that it elicits distinct anti-inflammatory functions, eventually reducing T lymphocyte proliferation and recruitment.
VALERIANI, FIORENZA. "Produzione di una libreria sintetica di scFv-VH su fago T7: un metodo per l'individuazione di stabili anticorpi." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/904.
Повний текст джерелаRecombinant antibodies represent a powerful technology which can be used for different goals, such as immunocytochemical reagents or experimental clinical applications. They constitute one of the most reliable and safest applications for identifying autoimmune inflammatory diseases and cancer diseases. At present, it is possible to obtain monoclonal antibodies through genetic engineering procedures, without the use of animals or somatic cells which, thanks to these new technologies, comes to be unnecessary. This is possible through the cloning and the expression on filamentous phages of VH-VL genes, and through the isolation of immunoglobulin fragments (single chain fragment variable, scFv) from antibodies’ libraries built on filamentous phages. Furthermore, it is possible to assembly phages collections, modified through mutagenesis on hypervariable regions genes (called antibodies phages libraries), which allow to select in vitro human recombinant monoclonal antibodies in shape of scFv, specific for a wide range of antigens. Recent studies aim to use single domain VH scFv for therapeutic applications and for improving the stability and the solubility of scFv at intracellular level. In our research we try to deepen and develop antibody selections through the phage display method, by presenting a valid screening alternative to the use of filamentous phages and by taking advantage of the phage T7 lytic cycle. A new library scFv-VH on phage has been assembled on lytic phage T7 and its validity has been tested on the antigen bovine Ubiquitine, previously used for filamentous phages selections. The studies carried out demonstrate that, by employing our antibody phage library on phage T7 scFv-VH, it is possible to isolate monoclonal antibodies and achieving results comparable to the ones obtained by using the traditional methodology of selection on filamentous phages M13, but in very short time.
BAQUE, MICKAEL. "Endurance and biosignatures of the extremophilic cyanobacterium Chroococcidiopsis sp. under space and Martian simulations in the frame of the EXPOSE-R2 space mission (BOSS and BIOMEX)." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202002.
Повний текст джерелаGERBINO, VALERIA. "Functional interaction of FUS with SMN: a common pathogenic pathway in two motor neuron diseases." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2012. http://hdl.handle.net/2108/202169.
Повний текст джерелаDRAGONI, MASSIMILIANO. "Fisiopatologia dell’ipotrofia muscolare nel piede torto congenito idiopatico: studio preliminare." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2016. http://hdl.handle.net/2108/203068.
Повний текст джерелаGNANI, DANIELA. "Molecular nexus between fak and ezh2 from fatty liver to hepatocellular carcinoma." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203070.
Повний текст джерелаNAFLD is one of the most common liver disease worldwide and it encompasses a wide range of liver injuries, ranging from simple steatosis (non-alcoholic fatty liver “NAFL”) to non-alcoholic steatohepatitis (“NASH”). NASH can be sometimes associated with hepatic fibrosis and may potentially progress to irreversible cirrhosis and in some cases to hepatocellular carcinoma (HCC). The number of HCC new cases with a NAFD-dependent aetiology has strongly increased during the last decade but the molecular mechanisms regulating NAFLD-related hepatocarcinogenesis remain to be explored yet. Among all the factors involved in HCC onset and progression different epigenetic mechanisms and signalling pathways, affecting cell homeostasis (e.g. cell proliferation, apoptosis, migration and invasion) may play a major role, but their action in NAFLD is still obscure and their connection with hepatocarcinogenesis is unknown. Interestingly, the focal adhesion tyrosine kinase (FAK) is often found overexpressed or hyper-phosphorylated in HCC patients suggesting a key role of this protein in the control of cancer cells behaviour. Similarly, the methyltransferase EZH2 has been recently associated with the process of hepato-carcinogenesis. Further, a recent study reported a positive correlation between FAK and EZH2 expression and their association with tumour aggressiveness in endometrial cancer. Therefore, a potential direct/indirect interplay between these proteins might affect the development of different tumours, including HCC. In this study, we point to investigate the role of FAK and EZH2 in in vitro and in vivo models of diet-induced NAFLD and of HCC. Our results demonstrated an increased expression of Tyr-397 phosphorylated FAK and of its target paxillin in vivo and in vitro NAFLD. Moreover, the silencing of FAK also promoted increased lipid accumulation via the activation of the de novo lipogenesis pathway in HepG2 cells. Interestingly, in a model of NAFLD-induced HCC, both total and pTyr397 FAK correlated with disease severity. We reported the first evidence of EZH2 connection to NAFLD observing a down-regulation of EZH2 in our in vitro and in vivo models. Furthermore, the pharmacological inhibition of EZH2 worsened liver steatosis and inflammation. Results obtained from human HCC xenografts on NOD/SCID micrevealed a crucial role of FAK in HCC development and progression. Accordingly, we found that silencing of FAK reduced cell proliferation and invasion, and induced apoptosis in HCC cells. Additionally, we demonstrated that the silencing of FAK critically affected EZH2 transcription, nuclear localization and H3K27 tri-methylation activity. Importantly, we found that p53 and E2F2/3 are key mediators of FAK-dependent effects on EZH2 expression/activity. In conclusion, we demonstrated a master role of FAK in NAFLD and HCC and provided strong evidence of its connection with EZH2, introducing a new protein network active in the control of cancer cells’ proliferation, in which p53 and E2F may act as mediators.
ADANTI, SARA. "Molecular mechanisms of carcinogenesis: identification of new targets for diagnosis and therapy." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203330.
Повний текст джерелаTranslationally Controlled Tumor Protein (TCTP) is a survival factor in tumor cells overexpressed in poorly differentiated breast cancer cells. TCTP is a specific target of Dihydroartemisinin (DHA). DHA is a metabolite of Artemisinin, the active principle of Artemisia annua L. DHA is an anti-malaria drug with antitumor properties. We studied the effect of DHA on human breast cancer cell lines (such as MDA-MB-231 and SKBR3 cells) with more aggressive phenotype. Our results show that DHA inhibits breast cancer cells growth and induces apoptosis by reducing the levels of the phosphorylated form of TCTP. We also show that DHA improves the antitumor effect of the conventional chemotherapy drugs, such as Doxorubicin and Trastuzumab. Altogether, these results suggest that phospho-TCTP is a novel therapeutic target for breast cancer cells. DHA in combination with conventional chemotherapeutics is a novel strategy to treat breast cancer
FIANCO, GIULIA. "Characterization of a novel tumorigenic role of caspace 8." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/202045.
Повний текст джерелаMARSELLA, CLAUDIA. "Functional characterization of the interaction between the HIV accessory proteins VPU and VPR and the proautophagic protein AMBRA1." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202093.
Повний текст джерелаFUOCO, CLAUDIA. "Ambra1 is a novel autophagy tumour suppressor gene." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/202443.
Повний текст джерелаBON, GIULIA. "Dual targeting of HER3 and MEK may overcome HER3-dependent chemoresistance of colon cancers." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202145.
Повний текст джерелаLISI, GAIA. "Spinster is an Ambra1 interacting protein required for autophagosome maturation." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/202447.
Повний текст джерелаSASSO, FRANCESCHINA. "Role of fragile X mental retardation protein in epithelial to mesenchymal transition: insight the molecular regulation of EMT." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202123.
Повний текст джерелаGUCCINI, ILARIA. "Frataxin and the stress response." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/202279.
Повний текст джерелаDefective expression of frataxin is responsible for the degenerative disease Friedreich’s ataxia (FRDA). Frataxin is an iron-binding protein involved in the biogenesis of iron–sulfur clusters (ISC), prosthetic groups allowing essential cellular functions such as oxidative phosphorylation, enzyme catalysis and gene regulation. Frataxin is a protein required for cell survival since complete knock-out is lethal. Partial expression of the frataxin allows the development and survival of the organism, yet results in progressive degeneration of specific tissues. Although several evidence suggest that frataxin acts as an iron-chaperone within the mitochondrial compartment, it was recently demonstrated the existence of a functional extramitochondrial pool of mature frataxin in various human cell types. The aim of my work in the first part was to investigate for a physiological role of extramitochondrial frataxin in the cytoplasmic compartment searching for ISCdependent interaction. The extramitochondrial form of frataxin was demonstrated to directly interact with cytosolic aconitase/iron regulatory protein-1 (IRP1), a bifunctional protein that alternates between an enzymatic and a RNA-binding function through the “iron–sulfur switch” mechanism. Importantly, the cytosolic aconitase defect and consequent IRP1 activation occurring in FRDA cells was found to be reversed by the action of extramitochondrial frataxin. Frataxin protects tumor cells against oxidative stress and apoptosis but also acts as a tumor suppressor. The molecular bases of this apparent paradox are missing. The aim of my work in the second part was to investigate the pathways through which frataxin enhances stress resistance in tumor cells. Frataxin expression was found to be upregulated in several tumor cell lines in response to hypoxic stress, a condition often associated with tumor progression. Moreover, frataxin upregulation in response to hypoxia is dependent on HypoxiaInducible-Factors (HIFs) expression and modulates tumor suppressor p53 activation. Importantly, this work shows for the first time an in vivo increase of frataxin in human glioblastoma and colon carcinoma tumor samples. These results show that frataxin participates to the hypoxia-induced stress response in tumors, thus implying that modulation of its expression could play a critical role in tumor cell survival and/or progression.
SAGAR, VINAY. "Role of PIM1 in the activation of p53 induced by RPS19 deficiency in colon and prostate cancer cell lines." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202121.
Повний текст джерелаRIZZA, SALVATORE. "Nitrosative stress due to GSNOR deficiency induces agingrelated mitochondrial impairment and enhances vulnerability to mitochondrial complex II-targeting drugs: a potential therapeutic approach for HCC." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2012. http://hdl.handle.net/2108/202225.
Повний текст джерелаGALEOTA, EUGENIA. "Characterization and modeling of protein interaction networks dynamics." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2012. http://hdl.handle.net/2108/202167.
Повний текст джерелаPAGLIARINI, VITTORIA. "Apoptotic cell death modulation by ER stress and autophagy." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/202461.
Повний текст джерелаROSSI, SIMONA. "C9orf72 repeat expansion alters post-transcriptional gene regulation in a cellular model of amyotrophic lateral sclerosis." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202111.
Повний текст джерелаCAROLLO, VALERIA. "Terapie antitumorali per bersagli molecolari specifici: heat shock protein 90 Hsp90." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/203197.
Повний текст джерелаCECCARELLI, ARIANNA. "Characterization of TRAF2 aggregation state and its interaction with model membranes." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203011.
Повний текст джерелаThe TNF receptor-associated factor 2 (TRAF2) is a member of the Tumor Necrosis Factor (TNF) receptor associated factor (TRAF) protein family which associate with, and mediate the signal transduction from members of the TNF receptor superfamily. Upon TNF receptor activation, TRAF2 is recruited at the receptor site resulting in the activation of downstream signaling cascades that, depending on the kind of stimulus, can lead to apoptosis or to cell survival. We have characterized both the protein secondary and tertiary structure as a function of temperature using conventional UV spectroscopy in cuvette (namely Circular Dicroism, steady-state and dynamic fluorescence) while the quaternary structure and aggregation state have been investigated by light scattering experiments. The stability and the protein unfolding/refolding transition have been also studied in detail using high hydrostatic pressure, chemical denaturing agents (guanidine) and temperature. We found that in solution, at room temperature, the protein exhibits an oligomeric structure compatible with that found in the crystal, which has been demonstrated to be a trimer of identical subunits. We also demonstrated that the TRAF2 quaternary structure stability is strongly dependent on the presence of 3 α-helices segments that are stuck together in the native, folded protein molecule. We also carried on a study to monitor the interaction of TRAF2 with model membranes (GUV) since it has been suggested that lipid rafts play a crucial role in the TRAF2 function. We were able to evaluate the diffusion rate of the protein within different kind of membranes, both synthetic and extracted from real tissues, using Fluorescence Correlation Spectroscopy (FCS) techniques. We also used Laurdan Generalized Polarization and Spectral Phasor Analysis to study how TRAF2 affects the membrane fluidity. Our results demonstrated that TRAF2 exert a mechanical effect on the lipid bilayer since its addition to GUVs induces the formation of intraluminar vesicles.
BRUNI, EMANUELE. "Multiple apoptotic pathways elicited by etoposide." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202149.
Повний текст джерелаREFOLO, GIULIA. "Characterization of HCV NS5A cellular interactors: role of MOB1B and LRPPRC in viral replication and assembly." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2012. http://hdl.handle.net/2108/202215.
Повний текст джерелаSFERRA, ANTONELLA. "RNF220: a novel ubiquitin E3 ligase associated to autosomal recessive leukodystrophy with ataxia and deafness AR-LAD: is involved in nuclear lamina integrity control." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2012. http://hdl.handle.net/2108/202231.
Повний текст джерелаFREZZA, VALENTINA. "Role of TG3 in the protection of epidermis from UVB photodamage." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2015. http://hdl.handle.net/2108/202954.
Повний текст джерелаTransglutaminase (TG3) is a soluble protein that belongs to an important family of Ca2+-dependent enzymes responsible for protein cross-linking. Transglutaminases stabilize protein assemblies by catalysing the formation of intra- or intermolecular Nε(γglutamyl)lysine bonds between adjacent polypeptides. TGs family includes nine members, among them three (TG1, TG3 and TG5) expressed in the skin during keratinocyte differentiation. This process is an exclusive model of terminal differentiation and programmed cell death, also known as cornification. During cornification, TG3 undergoes to proteolytic activation resulting in high cross-linking activity enzyme. It cooperates with TG1 for the assembly and the reinforcement of the stratum corneum, by catalysing the cross-linking of several structural proteins, including loricrin, small proline-rich proteins, and trichohyalin. In our study, we characterized a novel TG3-deficient mouse. TG3-depleted mice have normal gross morphology, but we identified an altered expression of the late differentiation markers in the TG3KO epidermis. Since CEs isolated from TG3KO epidermis are more susceptible to sonication than WT, we hypothesized that TG3KO mice could be more sensitive to apoptosis induced by UVB than WT mice, due to the decreased UVBfiltering capacity of the stratum corneum. We found that the skin of TG3-deficient mice is high sensitive to the formation of cyclobutane pyrimidine dimers after UVB irradiation of new-born mice skin, leading to increased level of UVB-induced cell death. This data have been confirmed by a stronger activation of the caspase 3 and a higher amount of TUNEL-positive cells in irradiated TG3KO skin. Our results indicate that TG3 strongly contributes to the protective function of the stratum corneum from UVB, by reinforcing CEs adding specific crosslinks. This novel finding could explain the reason for including TG3 among candidate tumour suppressor genes in human head and neck cancers.
RICCIO, ANNA. "Role of HSF1 in proteasome regulation during proteotoxic stress." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/202105.
Повний текст джерелаMAGLIONI, SILVIA. "Prevention of neuronal degeneration in human mitochondria-associated diseases (HMAD): C. elegans as a model organism for high-content screenings." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/202075.
Повний текст джерелаDE, BENEDETTO MARIA LISA. "Study of the involvement of glutaredoxin 1 in copper homeostasis in neuroblastoma cells." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2012. http://hdl.handle.net/2108/202151.
Повний текст джерелаCELARDO, IVANA FRANCESCA. "Biological effects of cerium oxide nanoparticles on leucocyte cell lines." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/202261.
Повний текст джерелаAntioxidant therapy is the novel frontier to prevent and treat an impressive series of severe human diseases, and the search for adequate antioxidant drugs is fervent. Cerium oxide nanoparticles (nanoceria) are redox-active owing to the co-existence of Ce3+ and Ce4+ oxidation states and to the fact that Ce3+ defects, and the compensating oxygen vacancies, are more abundant at the surface. Nanoceria exert outstanding antioxidant effects in vivo acting as well tolerated anti-age and anti-inflammatory agents, potentially being innovative therapeutic tools. However, the biological antioxidant mechanisms are still unclear. Here, the analysis on two leukocyte cell lines undergoing apoptosis via redox-dependent or independent mechanisms, allowed demonstrating a direct cause-effect relationship between the cell anti-radical and pro-survival effects of nanoceria. Sm doping, which decreases Ce+3 and increases oxygen vacancy contents, blunts these effects, demonstrating that Ce+3/Ce+4 redox reactions are responsible for the outstanding in vivo properties of nanoceria.
GRAZIANI, ILARIA. "Role of mitophagy in kaempferol-induced neuroprotection in in vitro models of Parkinson’s Disease." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/202285.
Повний текст джерелаParkinson Disease (PD) is a neurodegenerative disorder characterized by degenerative loss of neurons in the nigrostriatal dopaminergic pathway. So far, although several studies concerning PD have been performed, its aetiology remain still unclear. Familiar or hereditary forms account only for the 5 - 10% of the PD cases, while the remaining 95%, defined idiopathic or sporadic, rely on environmental factors without any certain genetic involvement. Therefore, PD can be considered a complex multifactorial pathology, where genetic background should be considered a predisposing factor towards environmental insults such as pesticides and chemicals. By now oxidative stress and mitochondrial injury have been extensively indicated to be involved in PD neuronal demise and are tightly related each other. Moreover the unsuccessful removal of damaged proteins and/or organelles, probably due to the impairment of either the ubiquitin-proteasome system or autophagy, is a further event associated with PD aetio-pathogenesis. In particular, autophagy has been observed to be deregulated in PD brains and in line with this evidence, it has been recently demonstrated that rapamycin, a well-known autophagic inducer, protects from PD toxins and that suppression of basal autophagy causes neurodegeneration in mice. Several therapeutical approaches to slow down PD symptoms have been developed but none of them is currently able to prevent neuronal degeneration. In the last few years the attention of many researchers has been focused on natural-occurring compounds, such as polyphenols, because their use has been suggested to be a promising therapeutic/preventing strategy in oxidative-related diseases. In fact, in addition to their primary antioxidant activity, they could display a wide variety of other biological functions and these properties could be helpful in a complex and multifactorial pathology such as PD. On the basis of this knowledge, this PhD thesis is aimed to elucidate the processes underlying neuroprotection of a natural occurring compound kaempferol in in vitro models of PD. We demonstrate that kaempferol protects SH-SH5Y cells and primary cortical neurons from rotenone toxicity, as a reduction of caspases cleavage and apoptotic nuclei are observed. Reactive oxygen species levels and mitochondrial carbonyls decrease significantly. Mitochondrial network, transmembrane potential and oxygen consumption are also deeply preserved. We demonstrate that the main event responsible for the kaempferol-mediated antiapoptotic and antioxidant effects is the enhancement of mitochondrial turnover by autophagy. Indeed, fluorescence and electron microscopy analyses show an increase of the mitochondrial fission rate and mitochondria-containing autophagosomes. Moreover, the autophagosome-bound microtubule-associated protein light chain-3 increases during kaempferol treatment and chemical/genetic inhibitors of autophagy abolish kaempferol protective effects. Kaempferol induced-autophagy affords protection also toward other mitochondrial toxins (1-methyl-4-phenylpiridinium, paraquat) used to reproduce the typical features of PD, but is inefficient against apoptotic stimuli not directly affecting mitochondria (H2O2, 6-hydroxydopamine, staurosporine). Striatal glutamatergic response of rat brain slices is also preserved by kaempferol, suggesting a more general protection of kaempferol in PD. Overall, this data provide further evidence for kaempferol to be identified as an autophagic enancher with potential therapeutic capacity.
REGINA, CARLA. "Setdb1: a novel interactor of ΔNp63α, involved in breast tumorigenesis". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203104.
Повний текст джерелаΔNp63α has been widely studied in breast cancer, and recent studies indicate that it is involved in both breast tumorigenesis and self-renewal potential of breast cancer stem cells. Although the p63 transcriptional profile has been extensively characterized, our knowledge about p63 binding partners, potentially involved in the regulation of breast tumor progression, is limited. Here, we performed the yeast-twohybrid approach to identify p63α interactors involved in breast tumorigenesis. We found that Setdb1, a histone lysine methyltransferase, interacts with ΔNp63α and that this interaction contributes to p63 protein stability. Setdb1 is often amplified in primary breast tumours and its depletion confers growth disadvantage to breast cancer cells. Also, we identified a list of thirty genes repressed by ΔNp63 in a Setdb1dependent manner and the expression of four of them is positively correlated to survival of breast cancer patients. These results suggest that p63 and Setdb1 may have diagnostic and prognostic potential via the repression of common target genes.
CESARINI, VALERIANA. "Regulation of neuroectodermal cancers invasive behavior: role of PDE5 in Glioblastoma Multiforme and of Sox2 in Melanoma." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203040.
Повний текст джерелаSANARICO, ANNA GIULIA. "The e3 ubiquitin ligase wwp1 sustains growth of acute myeloid leukemia." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203124.
Повний текст джерелаAcute Myeloid Leukaemia (AML) is a genetically heterogeneous aggressive disorder resulting from accumulation of multiple karyotipic, genetic or epigenetic changes that lead to impaired differentiation (class II mutations, targeting transcriptional factors such as PML-RARα) and increase self-renewal ability (class I mutations, usually targeting tyrosine kinases like FLT3-ITD, tumour suppressors like p53, and oncogenes like N-Ras) of hematopoietic progenitors. The whole spectrum of abnormalities underlying AML pathogenesis has not been fully elucidated. Further characterization of potentially druggable and prognostic relevant molecules might improve riskassessment and therapeutic strategies for AML patients. The E3 ubiquitin ligase WWP1 is a potential oncogene found deregulated in solid human cancers and its overexpression has been associated with increased solid cancer cell proliferation and survival. The oncogenic activity of WWP1 is empathized by the observation that a number of its protein targets are molecules relevant for the regulation of cell proliferation, differentiation and apoptosis. Hence it is likely that pro-survival and growth promoting actions exerted by WWP1 in solid epithelial tumours arise from the regulation of relevant signalling pathways, and these mechanisms could be shared also in leukaemias. With the aim to investigate the role of WWP1 in the pathogenesis of myeloid leukaemogenesis, we have evaluated the expression profile of WWP1 in a cohort of patients with de novo AML, and found increased levels of WWP1 mRNA in the leukemic samples as compared to healthy donor controls. Noteworthy, inactivation of WWP1 in AML cell lines led to cell cycle arrest, decreased cell viability, and promoted differentiation of leukaemia cells, indicating WWP1 to be functionally relevant in AMLs. The use of the NB4 cell lines as an AML model-system, brought the attention on PML-RARα fusion protein regulation upon WWP1 knockdown. We found oncogene down-regulation at protein levels, with subsequent reactivation of the RARα target genes involved in granulocytic differentiation (e.g. C/EBPε). As a result, we observed induction of morphological and functional differentiating features upon WWP1-silencing in the NB4 cells as compared to the control group. The induction of autophagy as therapeutic mechanism of PML-RARα clearance in clinic brought us to investigate the possible involvement of the ligase in autophagy. We indeed found that depletion of WWP1 increased the autophagic flux of AML cells, thus contributing to the differentiation phenotype. Moreover, the non-apoptotic cell death observed in our system, highlighted a role for autophagy for the clearance of AML blasts. The cyclindependent kinase inhibitor p27 resulted our candidate as downstream target of WWP1: it is overexpressed at protein level when WWP1 is silenced in all the AML cell lines tested, and its is involved in G0/G1 cell cycle arrest, contributing to the growth arrest induction observed in NB4 cell line. Moreover, in vivo experiments showed that the survival of the mice transplanted with sh-WWP1 transduced NB4 cells was higher as compared to mice which received sh-Scr transduced NB4 cells, thus recapitulating the growth inhibition phenotype of AML cells seen in vitro. Together, these mechanisms point to unveil WWP1 biological effect in leukaemia sustainment, thus pointing at possible molecular targets for new therapeutic molecules.
BENINI, MONICA. "Identification of the frataxin-specific E3 ligase as a potential therapeutic target for Friedreich’s Ataxia." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2015. http://hdl.handle.net/2108/203003.
Повний текст джерелаMoayedi, Atousa <1991>. "Antibacterial effects of Nitric Oxide releasing Silica Nano particles." Master's Degree Thesis, Università Ca' Foscari Venezia, 2021. http://hdl.handle.net/10579/20250.
Повний текст джерелаSANTIMONE, Iolanda. "Association between amount of injured heart and Novel molecular/bio markers in myocardial infarction." Doctoral thesis, Università degli studi di Ferrara, 2016. http://hdl.handle.net/11392/2403398.
Повний текст джерелаToday, myocardial infarction and the consequent loss of fully functional myocardium is the major aetiology for heart failure. Despite aggressive primary therapy, prognosis remains serious in patients with large infarction and severe left ventricular dysfunction. Thus, it would be highly desirable to influence healing of the cardiac wound to maintain structure and function of the heart. Factor XIII (FXIII) is activated by thrombin in the final step of the clotting cascade coagulation and it has a prominent role in cross-linking soluble fibrin to a stable insoluble clot. Experimental evidence in mouse models suggests that Factor XIII might play a key role in myocardial healing after infarction. To quantify the real contribution of FXIII in this process, and to explore its possible prognostic role, we monitored the FXIII-A subunit levels in 350 acute MI patients during the first six days (d0-d5) plus a control at 30-60 days (d30). A one-year follow-up was performed for all the patients. Here, we compare FXIII levels to those of standard cardiac markers to predict the damage due to the infarction and the clinical outcome, but also to evaluate the therapeutic potential of this molecule. The main result of our translational research was to attribute a poor prognosis for patients with higher consumption of FXIII in the early days post-MI when compared with the subgroup of patients in whom FXIII consumption (rated as residual levels of the same) was negligible. This interesting observation is independent of the amount of Troponin_T and CK-MB, thus attributing to FXIII a role as an independent prognostic factor in heart attacks. Furthermore, common FXIII gene variants (Val34Leu, Pro564Leu, Tyr204Phe, Val650Ile, Glu651Gln) significantly influence molecular activity. So, in addition, we have analyzed all mentioned variants involved in the healing process of the heart muscle and in determining the extention of the damage, factors that are with directly related to heart failure and, consequently, to survival. Different FXIII-A dynamics and levels could be utilized as early prognostic indicators during acute MI, toghether with traditional markers of ischemia routinely performed, in patients with suspected or overt heart failure to personalize treatment. Furthermore, they could be an alternative method for biomarker studies aimed to more practical assesment of progression.
Squellerio, I. "The L-arginine/nitric oxide metabolic pathway in coronary artery disease : role of cardiovascular risk factors." Doctoral thesis, Università degli Studi di Milano, 2008. http://hdl.handle.net/2434/59853.
Повний текст джерелаRamasamy, S. "THE EVOLUTION OF CHEMORECEPTION IN THE INVASIVE PEST DROSOPHILA SUZUKII AND OTHER ARTHROPODS." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/503297.
Повний текст джерелаAl, Chawaf Basem [Verfasser]. "Healing of human extraction sockets augmented with Bio-Oss collagen after 6 and 12 weeks / Basem Al Chawaf." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1026264073/34.
Повний текст джерелаDI, GIACOMO GIUSEPPINA. "Role of Transglutaminase 2 in immunogenic and ER-stress induced cell death in cancer." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/202267.
Повний текст джерелаSilva, Tobar María Francisca. "Efectos de la condición socioeconómica en la prevalencia de caries para una pobación de niños de 12 y 13 años en la Comuna de Concepción, Región de Bio-Bio." Tesis, Universidad de Chile, 2015. http://repositorio.uchile.cl/handle/2250/141188.
Повний текст джерелаPICCIRILLI, ALESSANDRA. "Biochemical and molecular characterization of GES and NDM engineered variants: interactions with β-lactams and inhibitors". Doctoral thesis, Università degli Studi dell'Aquila, 2019. http://hdl.handle.net/11697/148003.
Повний текст джерелаCRACCHIOLO, SALVATORE. "Is suramin truly a good inhibitor of the bacterial RecA protein? Inhibition and activation, two sides of the same coin." Doctoral thesis, Università degli Studi dell'Aquila, 2021. http://hdl.handle.net/11697/169597.
Повний текст джерелаBONFILI, LAURA. "Modulation of intracellular proteolytic pathways in neoplastic and neurodegenerative diseases." Doctoral thesis, Università degli Studi di Camerino, 2014. http://hdl.handle.net/11581/401774.
Повний текст джерелаStorni, Elisa <1970>. "Applicazione di metodi molecolari nella diagnosi di alcune infezioni batteriche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/36/1/tesi_Storni.pdf.
Повний текст джерелаStorni, Elisa <1970>. "Applicazione di metodi molecolari nella diagnosi di alcune infezioni batteriche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/36/.
Повний текст джерелаCottignoli, Stefano <1979>. "Expression and cellular localization of Copper transporter 2 (Ctr2) in Mus musculus." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2009. http://amsdottorato.unibo.it/1883/1/Cottignoli_Stefano_tesi.pdf.
Повний текст джерелаCottignoli, Stefano <1979>. "Expression and cellular localization of Copper transporter 2 (Ctr2) in Mus musculus." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2009. http://amsdottorato.unibo.it/1883/.
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