We reported previously that, in addition to direct effects, somatostatin (SST) affects tumor growth inhibiting the tumoral neoangiogenesis, via an interference with NO synthesis. Here, we analyzed the effects of SST on nitric oxide (NO) production induced by different agonists [basic fibroblast growth factor (bFGF), insulin, cholecystokinin...
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2005 (v1)PublicationUploaded on: May 11, 2023
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2012 (v1)Publication
In several neurodegenerative diseases, such as Parkinson, Alzheimer's, Huntington, and prion diseases, the deposition of aggregated misfolded proteins is believed to be responsible for the neurotoxicity that characterizes these diseases. Prion protein (PrP), the protein responsible of prion diseases, has been deeply studied for the peculiar...
Uploaded on: April 14, 2023 -
2007 (v1)Publication
To date the most relevant role for the amyloid precursor protein (APP) and for the presenilins (PSs) on Alzheimer's disease (AD) genesis is linked to the amyloid hypothesis, which considers an aberrant formation of amyloid-P pepticles the cause of neurodegeneration. In this view, APP is merely a substrate, cleaved by the -gamma-secretase...
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2010 (v1)Publication
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Uploaded on: March 27, 2023 -
2002 (v1)Publication
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Uploaded on: April 14, 2023 -
2012 (v1)Publication
Transmissible spongiform encephalopathies (TSE), or prion diseases, are a group of fatal neurodegenerative disorders of animals and humans. Human diseases include Creutzfeldt-Jakob (CJD) and Gerstmann-Straussler-Scheinker (GSSD) diseases, fatal familial insomnia, and Kuru. Human and animal TSEs share a common histopathology with a pathognomonic...
Uploaded on: April 14, 2023 -
2008 (v1)Publication
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Uploaded on: March 31, 2023 -
2017 (v1)Publication
Glia over-stimulation associates with amyloid deposition contributing to the progression of central nervous system neurodegenerative disorders. Here we analyze the molecular mechanisms mediating microglia-dependent neurotoxicity induced by prion protein (PrP)90–231, an amyloidogenic polypeptide corresponding to the protease-resistant portion of...
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2013 (v1)Publication
Prion diseases recognize, as a unique molecular trait, the misfolding of CNS-enriched prion protein (PrP(C)) into an aberrant isoform (PrP(Sc)). In this work, we characterize the in vitro toxicity of amino-terminally truncated recombinant PrP fragment (amino acids 90-231, PrP90-231), on rat cerebellar granule neurons (CGN), focusing on...
Uploaded on: April 14, 2023 -
2011 (v1)Publication
To define the mechanisms by which hPrP90-231 induces cell death, we analyzed its interaction with living cells and monitored its intracellular fate. Treatment of SH-SY5Y cells with fluorescein-5-isothiocyanate (FITC)-conjugated hPrP90-231 caused the accumulation of cytosolic aggregates of the prion protein fragment that increased in number and...
Uploaded on: April 14, 2023 -
2001 (v1)Publication
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Uploaded on: April 14, 2023 -
2000 (v1)Publication
The mitogen activated protein (MAP) kinase cascade represents one of the major regulator of cell growth by hormones and growth factors. However, although the activation of this intracellular pathway has been often regarded as mediator of cell proliferation, in many cell types the increase in MAP kinase (also called extra-cellular signal...
Uploaded on: April 14, 2023 -
2000 (v1)Publication
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Uploaded on: April 14, 2023 -
2012 (v1)Publication
Alzheimer disease (AD) is a heterogeneous neurodegenerative disorder characterized by (1) progressive loss of synapses and neurons, (2) intracellular neurofibrillary tangles, composed of hyperphosphorylated Tau protein, and (3) amyloid plaques. Genetically, AD is linked to mutations in few proteins amyloid precursor protein (APP) and presenilin...
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1999 (v1)Publication
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Uploaded on: April 14, 2023 -
2003 (v1)Publication
BACKGROUND: Previous studies showed that the subtype 2 of somatostatin receptors (sstr2) is generally expressed by soft tissue sarcomas. MATERIALS AND METHODS: Using reverse transcription-polymerase chain reaction (RT-PCR), the present study evaluated the expression of sstr mRNA in 31 human intermediate and malignant soft tissue tumors. In 8...
Uploaded on: April 14, 2023 -
2004 (v1)Publication
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Uploaded on: March 31, 2023 -
2012 (v1)Publication
Among the different species of water-soluble beta-peptides (Abeta1-42, Abeta1-40 and N-terminal truncated Abeta-peptides), Abetapy3-42 is thought to play a relevant role in Alzheimer's pathogenesis due to its abundance, resistance to proteolysis, fast aggregation kinetics, dynamic structure and high neurotoxicity. To evaluate the specific...
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2016 (v1)Publication
A wide consensus based on robust experimental evidence indicates pyroglutamylated amyloid-β isoform (AβpE3-42) as one of the most neurotoxic peptides involved in the onset of Alzheimer's disease. Furthermore, AβpE3-42 co-oligomerized with excess of Aβ1-42, produces oligomers and aggregates that are structurally distinct and far more cytotoxic...
Uploaded on: April 14, 2023