William Kleber Martins Vieira

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|Lic, <b>Biological Sciences</b>, <b>Instituto Federal de Educação, Ciência e Tecnologia de São Paulo (IFSP)</b>.<br><br> Has experience in Cell Biology, Molecular Biology, Atmospheric Pollution, Research teaching and DNA repair deficiencies. <br><br> Will is a master´s degree student in the <b>DNA Repair Lab – Biomedical Sciences Institute at University of Sao Paulo</b> since 2018.<br> Research keywords: <b>XPV</b>, <b>CRISPR</b> and <b>Gene Therapy</b> <br> [http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K8157507T3 Lattes]. |Lic, <b>Biological Sciences</b>, <b>Instituto Federal de Educação, Ciência e Tecnologia de São Paulo (IFSP)</b>.<br><br> Has experience in Cell Biology, Molecular Biology, Atmospheric Pollution, Research teaching and DNA repair deficiencies. <br><br> Will is a master´s degree student in the <b>DNA Repair Lab – Biomedical Sciences Institute at University of Sao Paulo</b> since 2018.<br> Research keywords: <b>XPV</b>, <b>CRISPR</b> and <b>Gene Therapy</b> <br> [http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K8157507T3 Lattes].
<b>Contato:</b> williamklebermartins[at]gmail.com, williamkmv[at]usp.br <b>Contato:</b> williamklebermartins[at]gmail.com, williamkmv[at]usp.br

Revisão de 19:29, 17 Abril 2018

Lic, Biological Sciences, Instituto Federal de Educação, Ciência e Tecnologia de São Paulo (IFSP).

Has experience in Cell Biology, Molecular Biology, Atmospheric Pollution, Research teaching and DNA repair deficiencies.

Will is a master´s degree student in the DNA Repair Lab – Biomedical Sciences Institute at University of Sao Paulo since 2018.
Research keywords: XPV, CRISPR and Gene Therapy
Lattes.

Contato: williamklebermartins[at]gmail.com, williamkmv[at]usp.br

Current Project

Correction of PolH gene mutated in human cells with CRISPR/Cas

Xeroderma pigmentosum (XP) is a rare, autosomal recessive syndrome related to sun hypersensitivity, skin abnormalities, premature aging and high incidence of tumors. Among XP patient groups, there is a syndrome known as Xeroderma Pigmentosum Variant or XP-V, which has a typical XP phenotype, but has generally milder symptoms. In addition, unlike the other XP groups, they are not deficient in nucleotide excision repair (NER). This group corresponds to approximately 20% of the total XP patients and is deficient in the mechanisms of tolerance to the damage, specifically in the translesion synthesis (TLS). This mechanism allows the bypass of DNA tape damage and replication fork release, collaborating for cell survival and preventing replicative stress and breakage generation. There is still no cure for XP, so the treatment involves removing the lesions that appear on the skin and, especially, preventing the appearance of new lesions. However, the present work aims at correcting mutations known in XPV, using recent genomic editing technology known as CRISPR / Cas. In this way, we will try to use this innovative methodology to develop a gene therapy tool aimed at this syndrome.



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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