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Mauro Piacentini

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Biography

Detail

  • Name: Mauro Piacentini
  • Email: mauro.piacentini@uniroma2.it

The Prof. Piacentini directs two research laboratories in Rome, the Laboratory of Cellular and Developmental Biology at the Department of Biology of the University of Rome “Tor Vergata and the Laboratory of Cell Biology and Electron Microscopy at the National Institute for Infectious Diseases IRCCS “Lazzaro Spallanzani”

The research interests of Prof. Mauro Piacentini are focused on the understanding of the molecular mechanisms of autophagy/cell death and their involvement in human diseases pathogenesis:

  1. Role of Ambra1 in the regulation of autophagy under normal and pathological conditions.

  2. Role of autophagy in the control of particular regards to HIV and Mycobactrium Tubercolosis pathogenesis.

  3. Regulation of cellular proteostasis by Transglutaminase type 2 in Cystic Fibrosis.

  4. Role of Transglutaminase type 2 in the development of Hepatocellular carcinoma

Prof. Mauro Piacentini has over 30 years experience working in the cell death/autophagy field and their application to major human diseases with particular regards to cancer and infectious diseases development. He is author of more than 280 papers.
The published papers include articles in PNAS, Nature, Nature Medicine, Nature Cell Biology, Science, Molecular Cell,
Developmental Cell, Journal of Experimental Medicine. Among his major scientific accomplishments it is imortant to mention the discovery (Fimia et al. Nature 2007) and the characterization (Antonioli et al. Dev. Cell 2014 and Trends in Biochem. Sci. 2017) of the key role of the gene Ambra1 in the regulation of autophagy in normal and neoplastic cells (Cianfanelli et al. Nat Cell Biol. 2015). Of note, it is the contribution of the Prof. Piacentini’s lab to the characterization of the molecular mechanisms at the basis of the “Immungenic Cell Death” which plays a key role in the immune system-dependent eradication of tumors (Obeid et al. Nature Medicine 2007) as well as the role played by autophagy in melanomagenesis with particular regards to the BRAF mutation and ER stress induction (Corazzari et al. Cell Death Differ. 2015; Pagliarini et al. J. Cell Sci. 2015). Another important contribution (more than 100 pubblications) is the dissection of the role of the Transglutaminase type 2 (TG2) in apoptosis and more recently in the autophagic pathway under physiological and pathological conditions (D’Eletto et al. Autophagy 2009 and Cell Death Differ. 2012). Prof Piacentini is the most cited scientist worldwide on TG2 (source ISI) and in 2015 he has been included among the 25 most cited authors in Cell Biology in Europe (source LabTimes).

Mauro Piacentini is author of more than 280 papers with a total number of citations above 31,000, total impact above 2000 and an H-index of 75 according to Google scholar, 67 according to Web of Science.

Editorials about Prof. Piacentini scientific publications have been published on the following journals:
Journal of National Cancer Institute, September, 2004;
Cell Death and Differentiation, November, 2004;
Nature Cell Biology, July 2007.
Nature Business Exchange, September 2011.

Skills

Education & Training

  • 2017

    • Emerging Mechanisms in Initiating and Terminating Autophagy. Antonioli M, Trends Biochem Sci. 42(1):28-41. • Role of autophagy in HIV infection and pathogenesis. Nardacci R, J Intern Med. Jan 31. doi: 10.1111/joim.12596. • Control of Mitochondrial Remodeling by the ATPase Inhibitory Factor 1 Unveils a Pro-survival Relay via OPA1. Faccenda D, Cell Rep. 18(8):1869-1883. • Molecular definitions of autophagy and related processes Galluzzi L, EMBO J. Jun 8. pii: e201796697. • Transglutaminase type 2 plays a key role in the pathogenesis of Mycobacterium tuberculosis infection. Palucci I, J Intern Med. 2017 Dec 4. doi: 10.1111/joim.12714.

  • 2016

    • Induction of autophagy promotes the growth of early preneoplastic rat liver nodules. Kowalik MA, et al. Oncotarget 7(5):5788-99. • Transglutaminase type 2-dependent selective recruitment of proteins into exosomes under stressful cellular conditions. Diaz-Hidalgo L, Biochim Biophys Acta. pii: S0167-4889(16)30139-2. doi: 10.1016/j.bbamcr.2016.05.005. • Molecular mechanisms of Hepatitis C virus-induced hepatocellular carcinoma. Vescovo T, Clin Microbiol Infect. pii: S1198-743X(16)30243-9.

  • 2015

    • AMBRA1 links autophagy to cell proliferation and tumorigenesis by promoting c-Myc dephosphorylation and degradation. Cianfanelli V, et al. Nat Cell Biol.17(1):20-30. • Down-regulation of E2F1 during ER stress is required to induce apoptosis. Pagliarini V, et al. J Cell Science 128(6):1166-79. • . Autophagy in malignant transformation and cancer progression. Galluzzi L, et al. EMBO J. 34(7):856-80. • Interaction between AIF and CHCHD4 Regulates Respiratory Chain Biogenesis. Hangen E, et al. Molecular Cell 58(6):1001-14.

  • 2014

    • Impaired autophagic flux is associated with increased endoplasmic reticulum stress during the development of NAFLD. • Transglutaminase 2 ablation leads to mitophagy impairment associated with a metabolic shift towards aerobic glycolysis. Rossin F, et al. Cell Death Differ. 22(3):408-18. • Oncogenic BRAF induces chronic ER stress condition resulting in increased basal autophagy and apoptotic resistance of cutaneous melanoma. Corazzari M, et al. Cell Death Differ. 22(6):946-58. • . AMBRA1 Interplay with Cullin E3 Ubiquitin Ligases Regulates Autophagy Dynamics. Antonioli M, et al. Developmental Cell 31(6):734-46.

  • 2013

    • mTOR inhibits autophagy by controlling ULK1 ubiquitylation, self-association and function through AMBRA1 and TRAF6. Nazio F, et al. Nature Cell Biology 15(4):406-16. • Why is Autophagy Important for Melanoma? Molecular Mechanisms and Therapeutic Implications. Corazzari M, et al. Seminar Cancer Biol doi:pii: S1044-579X(13)00063-1. 10.1016. • The Fragile X Protein binds mRNAs involved in cancer progression and modulates metastasis formation. Lucá R, et al. EMBO Mol Med. 5(10):1523-1536.

  • 2012

    •. Autophagy Protects Cells from HCV-Induced Defects in Lipid Metabolism. Vescovo T, et al. Gastroenterology. 142(3):644-653.e3. • Liver protein profiling in chronic hepatitis C: Identification of potential predictive markers for interferon therapy outcome. Basulto Perdomo A, et al. J Proteome Res. 11(2):717-27. •. Type 2 transglutaminase is involved in the autophagy-dependent clearance of ubiquitinated proteins. D'Eletto M, et al. Cell Death Differ. 19(7):1228-38. • Proteolysis of Ambra1 during apoptosis has a role in the inhibition of the autophagic pro-survival response. Pagliarini V, et al. Cell Death Differ. 19(9):1495-504. •. An Immunosurveillance Mechanism Controls Cancer Cell Ploidy Senovilla L, et al.Science. 337(6102):1678-84. • Ambra1 at the crossroad between autophagy and cell death. Fimia GM, et al.Oncogene 32(28):3311-8.

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