Barbara Pascucci

 

Barbara Pascucci Barbara Pascucci

Tel. 0039 06 90672631 / 0039 06 49902560
Fax 0039 06 90672630 / 0039 06 49903650
E-mail : barbara.pascucciATic.cnr.it
Address :
Via Salaria, km 29.300, Monterotondo Stazione, Roma

 

 

Present position :


- Researcher.

 

Short CV :


1991-1993: Experimental work for the preparation of her thesis, advisor Prof. Antonio Fantoni, Sez. Biologia Cellulare, Dip. Biopatologia Umana, Univ. of Rome "La Sapienza"
1993-1994: Research Assistant in the same institution, working at the construction and characterization of a new Factor XII recombinant protein. Working visit in the lab of C.E. Hack, University of Amsterdam, working on human Factor XII molecule.
January 1995-December 1996: E.E.C. research contract. Title of the project: "Mutagenesis and DNA repair in mitochondria." Scientific supervisor Dr. Eugenia Dogliotti. National Health Institute
November 1996: Working visit in the lab directed by R.P.P.Fuchs, Cancérogenese et Mutagenése Moleculaire et Structurale, Unité Prope de Recherche du Centre National de la Recherche Scientifique - CNRS, working on the MAMA/PCR method setting up. Funded by the DNA Repair Network.
September 1997: Winner of the SIMA (Italian Society Enviromental Mutagenesis) prize 1997 for the best paper published in international journals in 1997 by a young researcher.
April 1997-February 1998: Visiting scientist in the lab directed by R.P.P.Fuchs, Cancérogenese et Mutagenése Moleculaire et Structurale, Unité Prope de Recherche du Centre National de la Recherche Scientifique - CNRS. Title of the project: "An experimental strategy for detection of low frequency mutations in human DNA: towards an application in molecular epidemiology". Granted by the Ligue Nationale Contre le Cancer
May-June 1998: Visiting scientist in the lab directed by U. Hubscher, University of Zurich, working on the in vitro reconstitution of the long-patch baseexcision repair. Funded by the EU Concerted Action Commettee
June 1998-December 2000: Research contract from the Environment Department. Scientific supervisor Dr. Angelo Carere. National Health Institute
September-October 1998: Visiting scientist in the lab directed by U. Hubscher, University of Zurich, working on the in vitro reconstitution of the long-patch base excision repair. Funded by the University of Zurich
December 2000-May 2001: E.E.C. research contract. Title of the project "Role of the Mismatch Repair in the repair of DNA lesions induced by oxidative stress", Scientific supervisor Dr. Margherita Bignami, National Health Institute
Juanary 2001-December 2002: Grant form the Fondazione Italiana per la Ricerca sul Cancro
December 2001: Winner of a permanent position, as a researcher, in the Institute of Cristallography at the CNR

 

Research Activity :

The main objective of this research activity is to gain insights into the molecular etiology of Cockayne syndrome (CS), a cancer-free multi-system disorder defective in both transcription and DNA repair and characterized by neurological abnormalities.
Specific aims are: 1) to further clarify the functions of CSA and CSB proteins in normal cell metabolism and under oxidative stress by using as model systems human and mice defective fibroblasts; 2) to evaluate the role of CSA and CSB in the processing of oxidative
DNA damage in a clinically relevant cell system such as human neural precursor cells; 3) to resolve the crystallographic structure of WT CSA protein and mutated forms.
The molecular mechanisms responsible for the peculiar clinical features of CS-namely, mental and physical retardation, developmental abnormalities and ageing-are still largely unknown. We intend to verify whether alterations in oxidative DNA damage responses might be somehow implicated. To this regard new designed anti-oxidant drugs targeted to mitochondrial reactive oxygen species will be also available to be tested. The response to oxidative DNA damage and its mechanistic basis will be explored in CS primary human and mice fibroblasts as well as in human neural precursor cells where the CS genes have been silenced. Moreover, the elucidation of the crystal structure of the CSA protein would certainly be helpful to understand the functional consequences of the mutations found in patients.
The knowledge derived from this study should shed light on the strategies of response to oxidative stress in human cells, and on the processes/lesions that ultimately cause the specific features of CS.

 

Selected publications :

Selected publications
- DNA repair of UV photoproducts and mutagenesis in human mitochondrial DNA
Barbara Pascucci, A, Varsteegh, A. van der Leer-van Hoffen, A.A. van Zeeland, L.H.F. Mullenders and E. Dogliotti
Journal of Molecular Biology, Oct 24; 273 (2): 417-427, 1997

- Long patch base excision repair with purified human proteins: DNA ligase I as patch size mediator for DNA polymerase δ and ε
Barbara Pascucci, Manuel Stucki, Zophonìas Jònsson, Eugenia Dogliotti and Ulrich Hubscher
Journal of Biological Chemistry, 274, 47, Nov. 19, 33696-33702, 1999

- Short-patch base excision repair at 7,8-dihydroxy-8-oxoguanines by DNA polymerase β is dependent on the recruitment of DNA ligase I at the lesion site
B. Pascucci, G. Maga, U. Hubscher, M.Bjoras, E. Seeberg, I.D.Hickson, G. Villani, C. Giordano, L. Cellai, and E. Dogliotti
Nucleic Acid Research, 30, 10, 2124-2130, 2002

- The accumulation of MMS-induced single strand breaks in G1 phase is recombinogenic in DNA polymerase β defective mammalian cells
Barbara Pascucci, Maria Teresa Russo, Marco Crescenzi, Margherita Bignami, and Eugenia Dogliotti
Nucleic Acid Research, 33 (1), 280-288, 2005

- Large scale analysis of transcription factor TTF-1/NKX2.1 target genes in GnRH secreting cell line GT1-7
Claudia Provenzano, Barbara Pascucci, Eliana Lupari and Donato Civitareale
Molecular and Cellular Endocrinology, 29;323(2):215-23, 2010

 

Last Updated (Monday, 22 September 2014 15:54)