BRYAN ERIC STRAUSS

(Fonte: Lattes)
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Instituto do Câncer do Estado de São Paulo, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder

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Colaboração internacional: Argentina ×

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  • article 10 Citação(ões) na Scopus
    Current Status of Canine Melanoma Diagnosis and Therapy: Report From a Colloquium on Canine Melanoma Organized by ABROVET (Brazilian Association of Veterinary Oncology)
    (2021) FONSECA-ALVES, Carlos Eduardo; FERREIRA, Enio; MASSOCO, Cristina de Oliveira; STRAUSS, Bryan Eric; FAVARO, Wagner Jose; DURAN, Nelson; CRUZ, Natalia Oyafuso da; CUNHA, Simone Carvalho dos Santos; CASTRO, Jorge Luiz Costa; RANGEL, Marcelo Monte Mor; BRUNNER, Carlos Henrique Maciel; TELLADO, Matias; ANJOS, Denner Santos dos; FERNANDES, Simone Crestoni; NARDI, Andrigo Barbosa de; BIONDI, Luiz Roberto; DAGLI, Maria Lucia Zaidan
  • article 39 Citação(ões) na Scopus
    Predominant role of DNA polymerase eta and p53-dependent translesion synthesis in the survival of ultraviolet-irradiated human cells
    (2017) LERNER, Leticia K.; FRANCISCO, Guilherme; SOLTYS, Daniela T.; ROCHA, Clarissa R. R.; QUINET, Annabel; VESSONI, Alexandre T.; CASTRO, Ligia P.; DAVID, Taynah I. P.; BUSTOS, Silvina O.; STRAUSS, Bryan E.; GOTTIFREDI, Vanesa; STARY, Anne; SARASIN, Alain; CHAMMAS, Roger; MENCK, Carlos F. M.
    Genome lesions trigger biological responses that help cells manage damaged DNA, improving cell survival. Pol eta is a translesion synthesis (TLS) polymerase that bypasses lesions that block replicative polymerases, avoiding continued stalling of replication forks, which could lead to cell death. p53 also plays an important role in preventing cell death after ultraviolet (UV) light exposure. Intriguingly, we show that p53 does so by favoring translesion DNA synthesis by pol eta. In fact, the p53-dependent induction of pol eta in normal and DNA repair-deficient XP-C human cells afterUV exposure has a protective effect on cell survival after challenging UV exposures, which was absent in p53-and Pol H-silenced cells. Viability increase was associated with improved elongation of nascent DNA, indicating the protective effect was due to more efficient lesion bypass by pol eta. This protection was observed in cells proficient or deficient in nucleotide excision repair, suggesting that, from a cell survival perspective, proper bypass of DNA damage can be as relevant as removal. These results indicate p53 controls the induction of pol eta in DNA damaged human cells, resulting in improved TLS and enhancing cell tolerance to DNA damage, which parallels SOS responses in bacteria.