Alessandra Pelegrini

From Laboratório de Reparo de DNA

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-|BSc, <b>Biological Sciences</b>, <b>Universidade Federal do Rio Grande do Sul – UFRGS</b>,(2001/2005).<br>MSc, <b>Celular and Molecular Biology</b>, <b>Universidade Federal do Rio Grande do Sul – UFRGS</b>, (2006/2007).<br>PhD, <b>Celular and Molecular Biology</b>, <b>Universidade Federal do Rio Grande do Sul - UFRGS and Universidade de São Paulo – USP</b>, ( 2007/2012).<br>Post-doctoral Fellowship, <b> Cancer Research Center of Toulouse – CRCT</b> (2016/2018)<br>Post-doctoral Fellowship in DNA Repair Lab - <b>Institute of Biological Sciences at University of São Paulo - USP</b> (2013 – Current)<br><br>Has experience in Cell Biology, Molecular Biology and Next Generation Sequencing (NGS) on the identification of causative mutations for Mendelian diseases related to DNA repair deficiencies.<br><br> The researcher has experience in cell and molecular biology, culture of human and animal cells, proteomics and mass spectrometry, microscopy and immunofluorescence, drug testing and cytotoxicity.<br> Research keywords: <b>Cancer</b>, <b>DNA repair</b>, <b>Replicative stress</b>, <b>Genetic instability</b> and <b>Chemotherapy and Therapeutic resistance</b><br> [http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4463877A9 Lattes]. +|BSc, <b>Biological Sciences</b>, <b>Universidade Federal do Rio Grande do Sul – UFRGS</b>,(2001/2005).<br>MSc, <b>Celular and Molecular Biology</b>, <b>Universidade Federal do Rio Grande do Sul – UFRGS</b>, (2006/2007).<br>PhD, <b>Celular and Molecular Biology</b>, <b>Universidade Federal do Rio Grande do Sul - UFRGS and Universidade de São Paulo – USP</b>, ( 2007/2012).<br>Post-doctoral Fellowship, <b> Cancer Research Center of Toulouse – CRCT</b> (2016/2018)<br>Post-doctoral Fellowship in DNA Repair Lab - <b>Institute of Biological Sciences at University of São Paulo - USP</b> (2013 – Current)<br><br>The researcher has experience in cell and molecular biology, culture of human and animal cells, proteomics and mass spectrometry, microscopy and immunofluorescence, drug testing and cytotoxicity<br><br> The researcher has experience in cell and molecular biology, culture of human and animal cells, proteomics and mass spectrometry, microscopy and immunofluorescence, drug testing and cytotoxicity.<br> Research keywords: <b>Cancer</b>, <b>DNA repair</b>, <b>Replicative stress</b>, <b>Genetic instability</b> and <b>Chemotherapy and Therapeutic resistance</b><br> [http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4463877A9 Lattes].
<b>Contato:</b> aleepelegrini[at]gmail.com <b>Contato:</b> aleepelegrini[at]gmail.com
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Revisão de 14:25, 23 Abril 2018

BSc, Biological Sciences, Universidade Federal do Rio Grande do Sul – UFRGS,(2001/2005).
MSc, Celular and Molecular Biology, Universidade Federal do Rio Grande do Sul – UFRGS, (2006/2007).
PhD, Celular and Molecular Biology, Universidade Federal do Rio Grande do Sul - UFRGS and Universidade de São Paulo – USP, ( 2007/2012).
Post-doctoral Fellowship, Cancer Research Center of Toulouse – CRCT (2016/2018)
Post-doctoral Fellowship in DNA Repair Lab - Institute of Biological Sciences at University of São Paulo - USP (2013 – Current)

The researcher has experience in cell and molecular biology, culture of human and animal cells, proteomics and mass spectrometry, microscopy and immunofluorescence, drug testing and cytotoxicity

The researcher has experience in cell and molecular biology, culture of human and animal cells, proteomics and mass spectrometry, microscopy and immunofluorescence, drug testing and cytotoxicity.
Research keywords: Cancer, DNA repair, Replicative stress, Genetic instability and Chemotherapy and Therapeutic resistance
Lattes.

Contato: aleepelegrini[at]gmail.com


Current Project

Cancer is currently the leading cause of morbidity and mortality worldwide which it is characterized by abnormal and uncontrolled cell growth in addition to genetic instability. It is very likely that genetic instability accelerates and even possibly initiates the proliferation of cancer cells by favoring the emergence of variant cells. Indeed, alterations of genes involved in genome maintenance promote carcinogenesis. This process is predominantly generated in S phase, during the DNA synthesis and relies on a replication stress activated by oncogenes. During the replication, the fork can be stalled for several reasons, such as DNA damage, structured DNA, nucleotide depletion and encounters with the transcription machinery, characterizing replication stress. In this way, replication stress contributes to chromosomal instability since stalled forks may eventually collapse, producing a broken DNA end. Up until recently, the mechanisms leading to fork collapse were only described after prolonged exposition of DNA replication stress sources (24 hours) by Mus81 activity. However, we have been described a phenomenon in which DNA replication forks stalls in response to DNA replication stress and are rapidly converted into DSBs, which we refer to as rapid replication fork breakage (RRFB) and it is dependent of XPF and Artemis nucleases. In this project, i have investigated the role of that endonuclease and its partner, ERCC1, in interstrand crosslink (ICLs) repair and its evolvement in chemotherapy sensitivity. Since the ICLs may cause persistent fork stalling, the proposed objective for this research is understanding how the XPF-ERCC1 complex and each of these separate protein participate in DNA replication stress, exploring their roles from the regulation of fork collapse to repair mechanisms, and evaluating the importance of these early events in the development of genetic instability from chromosomal aberrations.



Publications

Munford V*, Castro LP*, Souto R, Lerner LK, Vilar JB, Quayle C, Asif H, Schuch AP, de Souza TA, Ienne S, Alves FIA, Moura LMS, Galante PAF, Camargo AA, Liboredo R, Pena SDJ, Sarasin A, Chaibub SC, Menck CFM (2017). A genetic cluster of patients with variant xeroderma pigmentosum with two different founder mutations. British Journal of Dermatology. 176 (5), 1270-1278.
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Pedroso JL, Munford V, Bastos AU, Castro LP, Marussi VHR, Silva GS, Arita JH, Menck CFM, Barsottini OG (2017). LMNB1 mutation causes cerebellar involvement and a genome instability defect. Journal of the Neurological Sciences. 379:249-252.
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Lerner LK, Francisco G, Soltys DT, Rocha CR, Quinet A, Vessoni AT, Castro LP, David TI, Bustos SO, Strauss BE, Gottifredi V, Stary A, Sarasin A, Chammas R, Menck CF (2016). Predominant role of DNA polymerase eta and p53-dependent translesion synthesis in the survival of ultraviolet-irradiated human cells. Nucleic Acids Research. 45 (3), 1270-1280.
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