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Dialécticas do poder : a representação do individualismo em Robinson CrusoeCunha, Gualter January 1986 (has links)
No description available.
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The effect of Oncoprotein 18 ubiquitination on tubulin polymerizationTsai, Pei-chia 27 October 2010 (has links)
Oncoprotein18 (Op18) is a 19 kDa cytosolic phosphoprotein critical for cell growth and differentiation. Unphosphorylated Op18 associates with £\£]-tubulin heterodimer to form 2 tubulin-1 stathmin T2S complex and promotes microtubule catastrophe in interphase. Numerous cellular signals activate downstream protein kinases result in the phosphorylation of Ser16, Ser25, Ser38 and Ser 63 residues in Op18 that lowers its affinity for tubulin thereby increases the stability of microtubule and facilitates the formation of spindle during mitosis. Here, we found in addition to phosphorylation, Op18 could also be ubiquitin modified in vivo. An expression plasmid encodes for mutant EGFP-Op18-M5K protein whose potential lysine residues K42, K53, K75, K104, and K119 were mutated to arginines was generated to investigate the effect of ubiquitin modification of Op18 on the tubulin polymerization. Our results revealed a decrease of ubiquitin modification of mutant EGFP-Op18-M5K in comparison with that of wildtype EGFP-Op18. The expression of mutant but not the wildtype Op18 resulted in a significant increase of polymerized tubulin in mitotic cell implying that they might exhibit differential tubulin binding affinity. Moreover, the result of western blotting showed that the mutant Op18 detected in the mitotic cell corresponds to the phosphorylated version of Op18. In summary, these results imply the ubiquitination of Op18 might interfere with its phosphorylation and decrease its tubulin binding potential, thereby facilitates the polymerization of tubulin in mitotic cells. The in vitro tubulin polymerization assay will be performed to further confirm the above finding.
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Studio del controllo trascrizionale del gene VM32E in Drosophila: analisi genetica delle vie di segnalazione coinvolteBernardi, Fabio <1977> 02 April 2007 (has links)
No description available.
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Utilizzo della rapamicina come farmaco immunosoppressore in pazienti sottoposti a trapianto di fegato per epatocarcinomaCescon, Matteo <1969> 26 September 2007 (has links)
No description available.
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Ricerca della tolleranza clinica e recidiva di Epatite C nel trapianto di fegato: effetti a lungo termine dell'induzione con anticorpi policlonali anti-timocitide Ruvo, Nicola <1966> 26 September 2007 (has links)
No description available.
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Immunosoppressione farmacologica e recidiva neoplastica in pazienti sottoposti a trapianto di fegato per epatocarcinomaSalone, Mariacristina <1968> 26 September 2007 (has links)
No description available.
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Ruolo della rapamicina nei pazienti sottoposti a trapianto di fegato che hanno sviluppato complicanze secondarie all'uso di farmaci inibitori della calcineurinaVarotti, Giovanni <1972> 26 September 2007 (has links)
No description available.
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Avventure urbanistiche e architettoniche dell'Eni di Enrico Mattei (1953-1962): tra progetto e strategia aziendaleDeschermeier, Dorothea <1976> 30 May 2007 (has links)
No description available.
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Wing shape evolution: a role for cell competition in shaping the proximal distal axis of Drosophila wingZiosi, Marcello <1978> 13 May 2008 (has links)
No description available.
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Analisi funzionale dei recettori per le neurotrofine p75NTR e Trka in neuroblastomaPapa, Antonella <1978> 03 April 2008 (has links)
The biological complexity of NGF action is achieved by binding two distinct Neurotrophin
receptors, TrkA and p75NTR. While several reports have provided lines of evidence on the
interaction between TrkA and p75NTR at the plasma membrane, much fewer data are
available on the consequence of such an interaction in terms of intracellular signaling. In
this study, we have focused on how p75NTR may affect TrkA downstream signaling with
respect to neuronal differentiation. Here, we have shown that cooperation between p75NTR
and TrkA results in an increased NGF-mediated TrkA autophosphorylation, leads to a
sustained activation of ERK1/2 and accelerates neurite outgrowth. Interestingly, neurite
outgrowth is concomitant with a selective enhancement of the AP-1 activity and the
transcriptional activation of genes such as GAP-43 and p21(CIP/WAF), known to be
involved in the differentiation process. Collectively, our results unveil a functional link
between the specific expression profile of neurotrophin receptors in neuronal cells and the
NGF-mediated regulation of the differentiation process possibly through a persistent ERKs
activation and the selective control of the AP-1 activity. In our studies we discuss the
functional role of the neurotrophin receptor p75NTR and TrkA in a ligand-dependent signal
transduction.
It is known that p75NTR is also involved in the mediation of cell death ligand dependent.
Here we show for the first time that the membrane receptor p75NTR, upon binding to b-
Amyloid (Ab) peptide, is able to transduce a cytotoxic signal through a mechanism very
similar to the one adopted by Tumor Necrosis Factor Receptor 1 (TNFR1), when activated
by TNFa. We define that in neuroblastoma cell line Ab cytotoxicity signals through a
pathway depending on p75NTR death domain (DD), mostly through some specific
conserved residues. We identified that TRADD is the first interactor recruiting to the
membrane and activates JNK and NF-kB transcription factors. Since Ab is defined as the
most important aetiologic element associated with the Alzheimer’s Disease (AD),
characterization of the mechanism involved in the mediation of the neurodegeneration can
suggest also new therapeutic approaches.
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