A5020041044- interferon and immune responses
- Cancer-related Molecular Pathways
- MicroRNA in disease regulation
- Circular RNAs in diseases
- Phagocytosis and Immune Regulation
- Microbial Metabolism and Applications
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Cancer Cells and Metastasis
- Cancer Research and Treatments
- RNA regulation and disease
- Cancer, Hypoxia, and Metabolism
- Cell death mechanisms and regulation
- Adipose Tissue and Metabolism
- Epigenetics and DNA Methylation
- RNA Research and Splicing
- Cerebral Venous Sinus Thrombosis
- Immune cells in cancer
- Pancreatic and Hepatic Oncology Research
- Ocular Diseases and Behçet’s Syndrome
- Retinal and Optic Conditions
- Histone Deacetylase Inhibitors Research
- Nuclear Receptors and Signaling
- Endoplasmic Reticulum Stress and Disease
- Sphingolipid Metabolism and Signaling
Sapienza University of Rome
2020-2024
Fondazione IRCCS Istituto Nazionale dei Tumori
2012
Istituto Dermopatico dell'Immacolata
2004-2010
Istituti di Ricovero e Cura a Carattere Scientifico
2009-2010
Centro Cardiologico Monzino
2004-2006
MicroRNA-210 (miR-210) induction is a virtually constant feature of the hypoxic response in both normal and transformed cells, regulating several key aspects cardiovascular diseases cancer. We found that miR-210 was induced normoxic myoblasts upon myogenic differentiation vitro vivo. transcription activated an hypoxia-inducible factor 1-α (Hif1a)-dependent manner, chromatin immunoprecipitation experiments show Hif1a bound to promoter only differentiated myotubes. Accordingly, luciferase...
Cholangiocarcinoma (CCA) is a very aggressive cancer showing the presence of high stem cells (CSCs). Doublecortin-like kinase1 (DCLK1) has been demonstrated as CSC marker in different gastroenterological solid tumors. Our aim was to evaluate vitro expression and biological function DCLK1 intrahepatic CCA (iCCA) perihilar (pCCA).Specimens surgically resected human were enzymatically digested, submitted immunosorting for specific markers (LGR5 [leucine-rich repeat-containing G protein-coupled...
Abstract In human endothelial cells, nitric oxide (NO) results in class IIa histone deacetylases (HDACs) activation and marked deacetylation. It is unknown whether similar epigenetic events occur embryonic stem cells (ESC) exposed to NO how this treatment could influence ESC therapeutic potential during tissue regeneration. This study reports that the NO-dependent HDACs subcellular localization activity decreases global acetylation level of H3 histones phenomenon associated with inhibition...
The CCAAT-binding transcription factor NF-Y plays a central role in regulating cellular proliferation by controlling the expression of genes required for cell-cycle progression such as cyclin A, B1, B2, cdc25A, cdc25C, and cdk1. Here we show that unrestricted activity leads to apoptosis an E2F1- wild-type p53 (wtp53)-dependent manner. Unrestricted induced increase E2F1 mRNA protein levels. Furthermore, directly bound promoter this correlated with appearance open chromatin marks. ability...
Laminar Shear Stress (SS) induces cytosolic acidification and protects endothelial cells (ECs) from apoptosis. Our prior studies showed that ECs serum deprivation-induced apoptosis by a mechanism directly involving Axl-receptor activation. Aim of the present study was to determine whether anti-apoptotic action SS involves acidification-dependent Axl activation.Axl mRNA protein levels were significantly higher (5 8 fold, respectively) in exposed (12 dyne/cm2), compared static culture (ST)....
AimsAcidification is associated with a variety of pathological and physiological conditions. In the present study, we aimed at investigating whether acidic pH may regulate endothelial cell (EC) functions via chemokine receptor CXCR4, key modulator EC biological activities.
Behçet's disease is an inflammatory condition, caused by vasculitis of big and small veins arteries in which, although vascular inflammation the basis disease, cardiac involvement rare. We present a rare case man, affected with pulmonary embolism due to floating thrombus right ventricle.
Supplementary Figures 1-2 from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Figures 1-2 from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Methods from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Figures 5-6 from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Figures 3-4 from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Methods from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Figures 3-4 from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
Supplementary Figures 5-6 from Transcription Factor NF-Y Induces Apoptosis in Cells Expressing Wild-Type p53 through E2F1 Upregulation and Activation
<div>Abstract<p>The CCAAT-binding transcription factor NF-Y plays a central role in regulating cellular proliferation by controlling the expression of genes required for cell-cycle progression such as <i>cyclin A</i>, B1</i>, B2</i>, <i>cdc25A</i>, <i>cdc25C</i>, and <i>cdk1</i>. Here we show that unrestricted activity leads to apoptosis an E2F1- wild-type p53 (wtp53)-dependent manner. Unrestricted induced increase E2F1...
<div>Abstract<p>The CCAAT-binding transcription factor NF-Y plays a central role in regulating cellular proliferation by controlling the expression of genes required for cell-cycle progression such as <i>cyclin A</i>, B1</i>, B2</i>, <i>cdc25A</i>, <i>cdc25C</i>, and <i>cdk1</i>. Here we show that unrestricted activity leads to apoptosis an E2F1- wild-type p53 (wtp53)-dependent manner. Unrestricted induced increase E2F1...