Search results for "Genetica"

showing 10 items of 906 documents

IL-1β maintains the DNA hypermethylation of anti-inflammatory IL-10 gene in a human intestinal epithelial cell line

2014

Intestinal inflammation is a natural process crucial to maintain gut integrity, but its deregulation is involved in the pathogenesis of severe intestinal disorders[1]. Intestinal epithelial cells play a crucial role in the inflammatory response, modulating the immune cell exposure to antigens and by their ability to secrete many inflammatory mediators. IL-1β represents a pivotal player: secreted by infiltrated leucocytes, it induces the expression of several pro-inflammatory genes. Also the anti-inflammatory IL-10, whose function is to terminate the inflammatory process, modulates the intestinal physiology[2]. Recent clinical reports showed that patients with ulcerative colitis in remission…

Settore BIO/18 - GeneticaIL1-beta; DNA MethylationSettore BIO/10 - BiochimicaDNA MethylationIL1-beta
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Ruolo del rimodellatore della cromatina ATP-dipendente ISWI nel controllo del ciclo cellulare e del differenziamento. ISBN 978-1-4457-9586-7

2011

Settore BIO/18 - GeneticaISWI Drosophila GeneticaSettore BIO/11 - Biologia Molecolare
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Jay Amin Hydroxamic Acid (JAHA), a histone deacetylase inhibitor with cytotoxic activity and the property to increase DNA repair of triple-negative M…

2017

Jay Amin Hydroxamic Acid (JAHA; N8-ferrocenylN1-hydroxy-octanediamide) is a ferrocene-containing analogue of the histone deacetylase inhibitor (HDACi) suberoylanilide hydroxamic acid (SAHA). JAHA’s cytotoxic activity on MDA-MB231 triple negative breast cancer (TNBC) cells at 72 h has been previously demonstrated with an IC50 of 8.45 M. JAHA’s lethal effect was found linked to perturbations of cell cycle, mitochondrial activity, signal transduction and autophagy mechanisms. In order to glean novel insights on how MDA-MB231 breast cancer cells respond to the cytotoxic effect induced by JAHA, and to compare the biological effect with the related compound SAHA, we have employed a combination o…

Settore BIO/18 - GeneticaJAHA SAHA comet assay DNA methylationSettore BIO/06 - Anatomia Comparata E Citologia
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Investigating the inhibition of FTSJ1 a tryptophan tRNA-specific 2’-O-methyltransferase by NV TRIDs, as a mechanism of readthrough in nonsense mutate…

2023

Abstract: Cystic Fibrosis (CF) is an autosomal recessive genetic disease caused by mutations in the CFTR gene, coding for the CFTR chloride channel. About 10% of the CFTR gene mutations are "stop" mutations, which generate a Premature Termination Codon (PTC), thus synthesizing a truncated CFTR protein. A way to bypass PTC relies on ribosome readthrough, which is the ri-bosome’s capacity to skip a PTC, thus generating a full-length protein. “TRIDs” are molecules exerting ribosome readthrough; for some, the mechanism of action is still under debate. We in-vestigate a possible mechanism of action (MOA) by which our recently synthesized TRIDs, namely NV848, NV914, and NV930, could exert their r…

Settore BIO/18 - GeneticaKeywords: FTSJ1 methyltransferase tRNA readthrough stop codon mutation small molecules docking molecular dynamics MM-GBSASettore CHIM/06 - Chimica OrganicaSettore CHIM/08 - Chimica Farmaceutica
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p14ARF re-expression induces apoptosis in aneuploid HCT116 cells

2012

Weakening the Spindle Assembly Checkpoint by reduced expression of its components such as MAD2, BubR1 and MPS1 induces chromosome instability and aneuploidy both hallmarks of cancer cells. p14ARF that is found frequently altered in human cancers, is overexpressed in response to oncogenic stimuli to stabilize p53 halting cell progression. Previously, we determined that lack or reduced expression of p14ARF is involved in the maintenance of aneuploid cells suggesting that it could be part of a pathway controlling proliferation of aneuploidy cells. To investigate further this aspect of p14ARF function it was ectopically expressed in HCT116 cells, a stable near diploid cell line, after MAD2 depl…

Settore BIO/18 - GeneticaMAD2 Aneuploidy P14ARF
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Simultaneous reduction of MAD2 and BUBR1 expression induces mitotic spindle alterations associated with p53 dependent cell cycle arrest and death

2014

Settore BIO/18 - GeneticaMAD2 BUBR1 aneuploidy MITOTIC CHECKPOINT
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RNA interference of MAD2 and BUBR1 genes causes mitotic spindle alterations, aneuploidy and cell cycle arrest p53-dependent.

2009

The Spindle Assembly Checkpoint (SAC) is a cellular surveillance mechanism that functions to ensure faithful chromosome segregation during mitosis. Failure of this checkpoint or alteration in expression of SAC proteins (MAD2, BUB1, BUBR1 and others) can result in aneuploidy, a state of having abnormal numbers of chromosomes. MAD2 haploinsufficiency resulted in aneuploidy in MEFs and colon cancer cells in culture. Thus, spindle checkpoint components might have additional functions not-checkpoint-related functions that when disrupted contribute to tumorigenesis. Here we investigated the effects of MAD2 or BUBR1 transcriptional silencing in HCT-116 cells. Transient reduction of MAD2 (40%) and …

Settore BIO/18 - GeneticaMAD2 BUBR1 mitotic spindle
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Identification of a prognostic gene signature associated with MBP-1 expression in ErbB2-negative breast carcinomas

2014

The ENO1 transcript, which encodes the glycolitic enzyme alpha-enolase, can be translated into a shorter nuclear protein called Myc-promoter Binding Protein-1 (MBP-1) by using an alternative translation start site. MBP-1 acts as a negative regulator of c-Myc, ErbB2 and Cox2 genes (1). Several evidences indicate that MBP-1 acts as a tumor suppressor in breast carcinoma and prostate cancer and its expression results in a reduced invasive ability (2). In our previous studies, we showed that MBP-1 is expressed and easily detectable in normal breast epithelial cells, but a loss of expression occurs in most primary invasive ductal carcinomas (IDC) of the breast. Furthermore, in these tumors MBP-1…

Settore BIO/18 - GeneticaMBP-1 Breast cancer mRNA expression profiles
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Relazione tra l’espressione del repressore trascrizionale MBP-1 e di miRNAs nel carcinoma mammario

2013

MBP-1 (Myc-promoter-binding-protein-1) è una proteina di 37 kDa, prodotta dalla traduzione alternativa del mRNA del gene ENO1, codificante per l’enzima glicolitico α-enolasi. MBP-1 svolge il ruolo di repressore trascrizionale agendo direttamente sul promotore di c-MYC, ERBB2 e COX2, tutti geni coinvolti in diverse fasi della progressione tumorale (1-3). Nei carcinomi duttali infiltranti della mammella (IDC), l’espressione di MBP-1 è inversamente correlata alla comparsa di metastasi linfonodali e di recidive (4). In diverse linee cellulari tumorali l’overespressione di MBP-1 risulta nella riduzione della proliferazione cellulare e dell’invasività e in un aumento nella morte cellulare per apo…

Settore BIO/18 - GeneticaMBP-1miRNA
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ONCOSUPPRESSOR ACTIVITY OF TRANSCRIPTIONAL REPRESSOR MBP-1 IN NEUROBLASTOMA LAN-5 CELLS

2014

Settore BIO/18 - GeneticaMYCNNEUROBLASTOMAMBP-1
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