Claudio Brancolini
Claudio Brancolini
affiliation: Università di Udine
research area(s): Cancer Biology, Cell Biology
Course: Biomedical and Biotechnological Sciences
University/Istitution: Università di Udine
Claudio Brancolini was born in Trieste 25/09/1962. He is currently serving as Associate Professor of biology at the Medical School of the University of Udine. After the degree in Biology 110/110 cum laude at University of Trieste he worked as PhD student and as post-doc at ICGEB (International Center for Genetic Engineering and Biotechnology of Trieste (1987-1992) and at LNCIB (1992-1998) of Trieste. He was visiting scientist at the Chinese University of Hong-Kong (1997) and at Cold Spring Harbor Laboratory New-York (1999). He attended various practical courses to acquire new methods and emerging techniques. EMBO course "Antibodies in Cell Biology" EMBL-D (1989), FEBS course "Techniques in Cell Biology" Aarhus University DK (1991) EMBO course " Tissue in situ hybridization in animal developmental biology" University of New Castle Medical School UK (1995). Since 2000 he is the head of a research group at the University of Udine. Claudio Brancolini is member of the editorial board of the following scientific journals: Drug Resistance Updates, AJTR, BMC - Cell Biology, AJCR.
The lab is studying the mechanisms controlling the cell death process. These studies are important for understanding cancer development and chemoresistance. Tumors develop and grow because of mutations in genes controlling the cell death process (apoptosis). Tumors acquire chemoresistance because of mutations in genes controlling the cell death process (apoptosis). Over the past decade the research group has been involved in the study of the apoptotic program and in particular in the comprehension of the role of caspases and of some caspase substrates (Catenins, Gas2, HDAC4). The research group also contributed to dissect apoptosis in response to anti-tumor drugs and to develop a new assay to score caspase activity in vivo at single cell level. More specifically two topics are actually dissected: the TRAIL pathway and its relationships with the type I interferon signaling. The tumor model under investigation for this pathway is glioblastoma. The second topic concerns a family of chromatin remodeling enzymes: the class IIa of histone-deacetylases. In this case the model system to unveil the role of these enzymes in tumorigenesis is breast cancer.
Claudio Brancolini has published 52 peer‐reviewed articles indexed in PubMed. In 26 articles he is listed as corresponding author and in 10 as first author. His publications have received approximately 2.400 citations with an H index of 32. Total impact factor is >300. His most quoted experimental paper [The protein encoded by a growth arrest-specific gene (gas6) is a new member of the vitamin K-dependent proteins related to protein S, a negative coregulator in the blood coagulation cascade. Manfioletti G, Brancolini C, Avanzi G, Schneider C. Mol Cell Biol. 1993 ] has 328 citations. His most quoted first author paper [Microfilament reorganization during apoptosis: the role of Gas2, a possible substrate for ICE-like proteases. Brancolini C, Benedetti M, Schneider C. EMBO J. 1995] ranks 2th with 219 quotes. His most quoted last author paper [Caspase-2 can trigger cytochrome C release and apoptosis from the nucleus. Paroni G, Henderson C, Schneider C, Brancolini C. J Biol Chem. 2002] ranks 4th with 148 quotes.

The five most recent publications excluding reviews are:
Ubiquitin-dependent degradation of HDAC4, a new regulator of random cell motility. Cernotta N, Clocchiatti A, Florean C, Brancolini C. Mol Biol Cell. 2011 Jan;22(2):278-89.

Identification of USP18 as an important regulator of the susceptibility to IFN-alpha and drug-induced apoptosis. Potu H, Sgorbissa A, Brancolini C. Cancer Res. 2010 Jan 15;70(2):655-65

Characterization of caspase-dependent and caspase-independent deaths in glioblastoma cells treated with inhibitors of the ubiquitin-proteasome system. Foti C, Florean C, Pezzutto A, Roncaglia P, Tomasella A, Gustincich S, Brancolini C. Mol Cancer Ther. 2009 Nov;8(11):3140-50

The Isopeptidase Inhibitor G5 Triggers a Caspase-independent Necrotic Death in Cells Resistant to Apoptosis: A COMPARATIVE STUDY WITH THE PROTEASOME INHIBITOR BORTEZOMIB. Fontanini A, Foti C, Potu H, Crivellato E, Maestro R, Bernardi P, Demarchi F, Brancolini C. J Biol Chem. 2009 Mar 27;284(13):8369-81.

PP2A regulates HDAC4 nuclear import. Paroni G, Cernotta N, Dello Russo C, Gallinari P, Pallaoro M, Foti C, Talamo F, Orsatti L, Steinkühler C, Brancolini C. Mol Biol Cell. 2008 Feb;19(2):655-67.
Project Title:
Understanding the contribution of class IIa HDACs to cancer cell growth
This research project is aimed to understand the contribution of this family of enzymes to cancer cell growth and survival. More specifically, it will be tested the ability of class IIa of acting as bona-fide oncogenes, by transforming NIH3T3 cells. The molecular pathways activated by these transcriptional repressors will be investigated by evaluating genes up-regulated and repressed after microarray experiments.