Gioacchino Natoli

ORCID: 0000-0003-0711-2411
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Epigenetics and DNA Methylation
  • NF-κB Signaling Pathways
  • Immune cells in cancer
  • Hepatitis B Virus Studies
  • RNA Research and Splicing
  • Genomics and Chromatin Dynamics
  • Cytokine Signaling Pathways and Interactions
  • interferon and immune responses
  • Hepatitis C virus research
  • Inflammatory mediators and NSAID effects
  • Cancer Genomics and Diagnostics
  • Cancer-related gene regulation
  • Pancreatic and Hepatic Oncology Research
  • RNA modifications and cancer
  • RNA and protein synthesis mechanisms
  • Liver Disease Diagnosis and Treatment
  • Cell death mechanisms and regulation
  • HIV Research and Treatment
  • Phagocytosis and Immune Regulation
  • Immune responses and vaccinations
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • COVID-19 Clinical Research Studies
  • Cancer-related molecular mechanisms research

European Institute of Oncology
2015-2025

Istituti di Ricovero e Cura a Carattere Scientifico
2019-2025

Humanitas University
2017-2022

Humanitas (United States)
2019

Institute of Oncology Research
2003-2006

California Institute of Technology
2005

Howard Hughes Medical Institute
2005

University of California, Los Angeles
2005

Walter and Eliza Hall Institute of Medical Research
2005

University of California, San Diego
1998-2005

Mammalian genomes are pervasively transcribed outside mapped protein-coding genes. One class of extragenic transcription products is represented by long non-coding RNAs (lncRNAs), some which result from Pol_II bona-fide RNA Whether all lncRNAs described insofar genes, however, still unclear. Here we have characterized sites located genes in a highly regulated response, macrophage activation endotoxin. Using chromatin signatures, could unambiguously classify binding as belonging to either...

10.1371/journal.pbio.1000384 article EN cc-by PLoS Biology 2010-05-11

The human homologue of Drosophila Toll (hToll) is a recently cloned receptor the interleukin 1 (IL-1R) superfamily, and has been implicated in activation adaptive immunity. Signaling by hToll shown to occur through sequential recruitment adapter molecule MyD88 IL-1R–associated kinase. Tumor necrosis factor receptor–activated 6 (TRAF6) nuclear κB (NF-κB)–inducing kinase (NIK) are both involved subsequent steps NF-κB activation. Conversely, dominant negative version TRAF6 failed block...

10.1084/jem.187.12.2097 article EN The Journal of Experimental Medicine 1998-06-15

Cells of the monocyte-macrophage lineage play a central role in orchestration and resolution inflammation. Plasticity is hallmark mononuclear phagocytes, response to environmental signals these cells undergo different forms polarized activation, extremes which are called classic or M1 alternative M2. NF-kappaB key regulator inflammation resolution, its activation subject multiple levels regulation, including inhibitory, finely tune macrophage functions. Here we identify p50 subunit as...

10.1073/pnas.0809784106 article EN Proceedings of the National Academy of Sciences 2009-08-18

Interaction of the p55 tumor necrosis factor receptor 1 (TNF-R1)-associated signal transducer TRADD with FADD signals apoptosis, whereas TNF receptor-associated 2 protein (TRAF2) is required for activation nuclear transcription kappa B. TNF-induced stress-activated kinase (SAPK) was shown to occur through a noncytotoxic TRAF2-dependent pathway. TRAF2 both sufficient and necessary SAPK by TNF-R1; conversely, expression dominant-negative mutant, which blocks did not interfere activation....

10.1126/science.275.5297.200 article EN Science 1997-01-10

Histone deacetylases (HDACs) regulate inflammatory gene expression, as indicated by the potent antiinflammatory activity of pan-HDAC inhibitors. However, specific contribution each 11 HDAC proteins to expression program is unknown. Using an integrated genomic approach, we found that Hdac3-deficient macrophages were unable activate almost half when stimulated with LPS. A large part activation defect was attributable loss basal and LPS-inducible IFN-β, which maintains Stat1 protein levels in...

10.1073/pnas.1121131109 article EN Proceedings of the National Academy of Sciences 2012-07-16

ADP‐ribosylation, a modification of proteins, nucleic acids, and metabolites, confers broad functions, including roles in stress responses elicited, for example, by DNA damage viral infection is involved intra‐ extracellular signaling, chromatin transcriptional regulation, protein biosynthesis, cell death. ADP‐ribosylation catalyzed ADP‐ribosyltransferases (ARTs), which transfer ADP‐ribose from NAD + onto substrates. The modification, occurs as mono‐ or poly‐ADP‐ribosylation, reversible due...

10.1111/febs.16142 article EN cc-by-nc-nd FEBS Journal 2021-07-29
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