1,721,062 research outputs found
Shift of DNA polymerase alpha nuclear distribution and activity in apoptotic human leukaemia cells.
No full textThe changes in the distribution of DNA polymerase alpha in nuclei from HL-60 cells treated with Methotrexate (MTX) for up to 15 hr. were checked by means of both confocal analysis and electron microscopy analysis. The results provided evidence that, relative to controls, in the MTX treated cells the enzyme undergoes a topographical rearrangement throughout the nucleus, showing a pattern of distribution which calls to mind the nuclear matrix structure. The "in vitro" analysis of DNA polymerases alpha, beta, and gamma activities revealed that, in nuclei from control cells, DNA polymerase alpha was the principal DNA polymerase driving this "in vitro" system, while after 15 hr. of MTX treatment its activity was largely decreased and replaced by DNA polymerase beta, which is believed to be associated with DNA repair. Taken together, these results suggest that among the intracellular processes elicited by MTX-induced apoptosis in HL60 cells, the redistribution of DNA polymerase alpha and the stimulation of DNA polymerase beta activity might represent an extreme attempt of the cell to preserve the replicative machinery during fragmentation and chromatin margination
Interferon alpha modulates phosphatidylinositol-3-kinase expression and distribution in Daudi lymphoma cells
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Phospholipase C gamma 1 overexpression and activation induced by interferon beta in human T lymphocytes: an ISGF3-independent response.
No full textInterferons exert their antiviral, antiproliferative and immunoregulatory activities by stimulating the expression of several genes. Such genes disclose a common element within their promoters, defined Interferon Stimulated Response Element (ISRE), which binds a nuclear factor(s) translocated from the cytoplasm to the nucleus (ISGF3) after the binding of interferon (IFN) to the specific receptor. Here we report the induction of the synthesis and of the hydrolytic activity of phospholipase C gamma 1 (PLC gamma 1) in human T lymphocytes by IFN-beta. The increased level of PLC gamma 1 becomes evident after 90 min of IFN-beta treatment and is still detectable after 24 h. Neither the PLC gamma 1 overexpression induced by IFN nor the increased hydrolytic activity of the enzyme appear to be affected by pretreatment of the cells with the protein tyrosine kinase inhibitor genistein, which is known to prevent the association of ISGF3 components. These results suggest that in human T lymphocytes IFN-beta can activate other transcription factor(s) distinct from ISGF3 to regulate PLC gamma 1 expression. In addition, the ability of this enzyme to hydrolyse PIP2, also in the presence of genistein, implies the possibility that this enzyme can exert its hydrolytic activity independently of protein tyrosine kinase activation
Attività motoria e rischio cardiovascolare. Parte seconda – Attività Motoria, salute-malattia e disabilità. In: Il guadagno di salute attraverso la promozione dell’attività fisica. Evidenze scientifiche e attività di campo. Gruppo di Lavoro Scienze Motorie per la Salute.
No full textPoiché le patologie cardiovascolari rappresentano una delle principali cause di morbilità e mortalità in tutti i paesi industrializzati, nelle ultime decadi l’attenzione e gli sforzi per identi care delle strategie preventive e caci sono stati massimi. Da molti anni, si accumu- lano evidenze scienti che che documentano una stretta relazione tra stile di vita (alimen- tazione, attività sica e abitudini voluttuarie, come fumo e alcool) e patologie cardiova- scolari (2). Negli ultimi due decenni, in particolare, il ruolo dell’attività sica ha suscitato un crescente interesse: da una parte, la sedentarietà è inclusa tra i primi cinque fattori di rischio di eventi cardiovascolari, dall’altra, uno stile di vita attivo e la pratica regolare di esercizio sico rappresentano l’intervento non farmacologico più utile (ed economico) nella gestione del rischio cardiovascolare. Numerosi studi hanno infatti mostrato che sia elevati livelli di attività sica, sia l’esercizio sico vero e proprio agiscono positivamente sul peso corporeo (riducendo il sovrappeso ed i rischi correlati), sul tono vascolare (riducendo il ri- schio di ipertensione, o favorendo la terapia di controllo), sul metabolismo del glucosio (di- minuendo le probabilità e di diabete e/o delle relative complicanze) e dei lipidi (riducendo il rischio di ipercolesterolemia o favorendo la terapia di controllo) (11). Per tali motivi, sia le linee guida europee che statunitensi hanno inserito la pratica costante dell’esercizio sico di forma aerobica in tutti i programmi di prevenzione primaria e secondaria delle patologie cardiovascolari, inclusa la prevenzione dell’obesità adulta e infantile (2, 13).
Per quanto concerne i meccanismi attraverso i quali l’esercizio determina la sua azione bene ca sul rischio cardiovascolare, considerando 100 tale e etto, è stato stimato che l’azione antin ammatoria e sulla funzione endoteliale contribuisce per quasi il 60% (32,6% direttamente; 27,1% tramite la riduzione della pressione arteriosa), l’azione sul metabo- lismo lipidico contribuisce per il 19,1%, la riduzione del peso corporeo per il 10,1%, in ne il decremento dell’emoglobina glicata e l’azione antidiabetica contribuiscono per l’8,9% (11)
Phospholipase C expression during the neoplastic transformation of the human gastric mucosa
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Novel shift of Jak/Stat signalling characterizes the protective effect of aurintricarboxylic acid (ATA) from Tumor Necrosis Factor alpha toxicity in human B lymphocytes
No full textPrevious results demonstrated that the occurrence of death in human peripheral B lymphocytes by TNF-a was paralleled by the activation of the cytoplasmic Jak1 and Tyk2 protein kinases, along with the recruitment of transcription factors Stat3 and Stat5b. In this study we demonstrate that the balance of survival signals in the presence of TNF-alpha was altered by the addition of a salicylate compound, the endonuclease inhibitor aurintricarboxylic acid (ATA). Apoptosis effected by TNF-alpha alone was suppressed by ATA and this event was paralleled by phosphorylation and nuclear translocation of Jak2, Stat2, Stat4 and NF-kB, along with inhibition of caspase activation. These results confirm that among the different cellular responses evoked by TNF-alpha in human B cells, recruitment of Jak/Stat proteins and possible related gene modulation represent contributing factors and address the issue of the development of potential therapeutic strategies aimed at the control of systemic or local effects produced by TNF-alpha
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