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Francesco Blasi (born 19 October 1937 in Naples) is an Italian biologist.[MS1]

Francesco Blasi was born in Naples, Italy, on 19 October 1937, where he studied Medicine and Surgery, graduating with honors from the University of Naples Federico II in 1961.

He started to deal with scientific research from the third year of the course while he was an intern at the Institute of General Pathology of the University of Naples. After graduating, he worked for two years (1962-64) in post-war Germany in Frankfurt am Main at the Max Planck Institut für Biophysik. In 1968 he went to the United States where he worked for two years in the NIAMD Laboratory of Chemical Biology at the National Institutes of Health (NIH), in Bethesda, Md (1968-70), in the section headed by Bob Goldberger. At the time the Laboratory of Chemical was headed by Christian B. Anfinsen who, a few years later, won the Nobel Prize in Chemistry. After this period, Blasi then returned to the US for subsequent sabbaticals which included returning to the NIH (1983-84) and visiting Columbia University in New York (1986-87).

Between 1970-1980 Blasi became an associate professor of Genetics at the University of Naples Federico II, Second Faculty of Medicine, and then researcher in the italian National Research Council.

In 1980 Blasi won a national competition and was appointed professor of Human Genetics at the second Faculty of Medicine of the University of Naples. In the same year, he was also appointed director of the CNR Institute of Genetics and Biophysics in Naples.

In 1987 Blasi moved to Denmark as Professor of Molecular Biology at the Mikrobiologisk Institut of the University of Copenhagen, and Director of the Center of Molecular Cell Biology. He remained in Copenhagen until the summer of 1992.

In 1992 Blasi returned to Italy, to Milan, as professor of Genetics at the University of Milan and director of the Molecular Genetics Unit in the newly built H.S. Raffaele (HSR). At HSR Blasi later on headed the Department of Molecular Biology and Functional Genomics, became Professor of Molecular Biology at the new HSR Private University and coordinator of the PhD program in Molecular and Cellular Biology,

In 2004 Blasi started the laboratory of "Transcription regulation in development and cancer", in the brand new Institute IFOM (AIRC Institute of Molecular Oncology) where he then moved definitively in 2009, becoming also deputy scientific director.

Research activity

Blasi's scientific interests range from the purification and structure of proteins, to the mechanisms of regulation of gene expression in bacteria, to the study of extracellular proteases and their receptors in the migration of eukaryotic cells and more recently to the study of homeobox transcription factors in the embryonic development of mouse and cancer.

After the first two postgraduate years spent at to the then Max Planck Institut für Biophysik in Frankfurt am Main, Blasi returned to Naples and began working on the biosynthesis of thyroid hormones by identifying and purifying some enzymes. When he moved to the U.S.A. in 1968, Blasi worked with Bob Goldberger on the regulation of the expression of histidine biosynthesis enzymes in the bacterium Salmonella typhimurium, encoded by His Operon. Returned to Italy in 1970, he worked for several years to understand the genetic regulatory mechanism of the His Operon. His studies led to the definition of the Attenuator, a DNA sequence that is transcribed but can be translated or not based on the presence or absence of histidine. In fact, the mRNA of the Attenuator takes on a different conformation that allows or does not allow further transcription and therefore the expression of the entire group of enzymes. In the absence of histidine, the ribosomes remain blocked on the Attenuator and this allows further transcription to continue1. In the presence of histidine, however, the assumed form makes mRNA a target for transcription terminators that destroy it. The discovery of this mechanism required the development in a pioneering era of methods such as the production of bacteriophages transducing the histidine operon, their molecular cloning and sequencing.

Between 1980 and 1992 (between Naples and Copenhagen) Blasi worked on the role of proteases in cancer, following the idea that extracellular proteases could facilitate cell migration and thus possibly influence the malignancy of tumors (metastases). Blasi identified, cloned and studied the regulation of the urokinase plasminogen activator (uPA) and its specific inhibitor PAI-1; then he discovered the existence of a specific receptor for uPA, (uPAR) in 1985, the first receptor for an extracellular protease to be identified, which concentrates the proteolytic activity of the cell on the cell membrane. In the following years, in Milan at the HSR, Blasi's laboratory studied the structure, function and regulation of this receptor.

At the beginning of the new century, Blasi began to take an interest in developmental biology, thanks to the discovery of a new transcription factor, PREP1, belonging to the group of those containing a homeodomain; PREP1 is essential in embryonic development, but in adults it acts as a tumor suppressor in both mice and humans. The mechanism underlying these functions is that of safeguarding the integrity of the genome.

Assignments

In 1979 Blasi was elected a member of the European Molecular Biology Organization (EMBO), in 1987 of the Danish Scientific Academy and in 1993 of the European Academy. In the EMBO, Blasi was a member of the EMBO Council, of the Course Committee and from 1999 to 2004 of the Fellowships Committee.

Furthermore, Blasi has been a member for several years of the Scientific Advisory Committee of the European Molecular Biology Laboratory (EMBL) of Heidelberg, of the Institutes of Developmental Biology and of Genetics and Biophysics of the CNR, in Naples, and of the InSTEM, Bangalore (India).

Blasi was also a member of the Review Committee of the Weizmann Institute of Science, (1995) and in 1994 of the Review Committee set up by EMBO for the evaluation of Biochemistry and Cell Biology in the Republic of Austria.

Awards and Honours

In 1993, Blasi was awarded the title of Dr. Med. Honoris Causa by the University of Copenhagen.

In 1983-84 Blasi was awarded the Fogarty International Scholarship of the National Cancer Institute, Bethesda, MD; in 1993, he was honoured by the ISFT (International Society of Fibrinolysis and Thrombolysis) with the prize for the discovery of the urokinase receptor.

Publications

Di Nocera, PP, Blasi,F, Di Lauro,R, Frunzio,R & Bruni, CB. Nucleotide sequence of the attenuator region of the histidine operon of Escherichia coli K12. Proc. Natl. Acad. Sci.USA, 75, 4276, 1978. Stoppelli, MP, Tacchetti, C, Cubellis, MV, Corti, A, Hearing, VJ, Cassani, G, Appella, E & Blasi, F. Autocrine saturation of pro-urokinase receptors on human A431 cells. Cell, 45, 675-684, 1986. Blasi, F, Vassalli, JD & Danø, K. Urokinase-type plasminogen activator: proenzyme, receptor and inhibitors. J. Cell Biol. 104, 801-804, 1987. Blasi, F. and Carmeliet, P. (2002). uPAR: a versatile signaling orchestrator. Nature Rev. Mol. Biol. 3, 932-943. Berthelsen, J., Zappavigna, V., Ferretti, E., Mavilio, F. and Blasi, F. Prep1, a novel partner of Pbx proteins, modifies Pbx-Hox protein cooperativity. EMBO J., 17, 1434-1445 (1998). Ferretti, E., J.Carlos Villaescusa, Patrizia Di Rosa, Luis C. Fernandez-Diaz, Elena Longobardi, Roberta Mazzieri, Annarita Miccio, Nicola Micali, Licia Selleri, Giuliana Ferrari and Francesco Blasi. Hypomorphic mutation of the TALE gene Prep1 (pKnox1) causes a major reduction of Pbx and Meis proteins and a pleiotropic embryonic phenotype. (2006). Mol. Cell. Biol. 26:5650-5662. Fernandez-Diaz, L. C., Laurent, A., Girasoli, S., Turco, M., Longobardi, E., Iotti, G., Jenkins, N. A., Fiorenza, M.T., Copeland, N. G. and Blasi, F... The absence of Prep1 causes p53-dependent apoptosis of pluripotent epiblast cells. Development, 137:3393-3403, 2010. F. Blasi, C. Bruckmann, D. Penkov, L. Dardaei. 2017. A tale of TALE. PREP1, PBX1 and MEIS1: interconnections and competition in cancer. BioEssays. May;39(5). doi: 10.1002/bies.201600245.