Inhibition of the RhoA GTPase activity increases sensitivity of melanoma cells to UV radiation effects (2016)
- Authors:
- Autor USP: FORTI, FÁBIO LUÍS - IQ
- Unidade: IQ
- DOI: 10.1155/2016/2696952
- Subjects: MELANOMA; RADIAÇÃO ULTRAVIOLETA
- Language: Inglês
- Imprenta:
- Source:
- Título: Oxidative Medicine and Cellular Longevity
- ISSN: 1942-0900
- Volume/Número/Paginação/Ano: v. 2016, p. 1-14 art.2696952, 2016
- Este artigo possui versão em acesso aberto
- URL de acesso aberto
- PDF de acesso aberto
- Versão do Documento: Versão publicada (Published version)
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Status: Artigo aberto em periódico híbrido (Hybrid Open Access) -
ABNT
ESPINHA, Gisele et al. Inhibition of the RhoA GTPase activity increases sensitivity of melanoma cells to UV radiation effects. Oxidative Medicine and Cellular Longevity, v. 2016, p. 1-14 art.2696952, 2016Tradução . . Disponível em: https://doi.org/10.1155/2016/2696952. Acesso em: 15 mar. 2026. -
APA
Espinha, G., Osaki, J. H., Costa, É. T., & Forti, F. L. (2016). Inhibition of the RhoA GTPase activity increases sensitivity of melanoma cells to UV radiation effects. Oxidative Medicine and Cellular Longevity, 2016, 1-14 art.2696952. doi:10.1155/2016/2696952 -
NLM
Espinha G, Osaki JH, Costa ÉT, Forti FL. Inhibition of the RhoA GTPase activity increases sensitivity of melanoma cells to UV radiation effects [Internet]. Oxidative Medicine and Cellular Longevity. 2016 ; 2016 1-14 art.2696952.[citado 2026 mar. 15 ] Available from: https://doi.org/10.1155/2016/2696952 -
Vancouver
Espinha G, Osaki JH, Costa ÉT, Forti FL. Inhibition of the RhoA GTPase activity increases sensitivity of melanoma cells to UV radiation effects [Internet]. Oxidative Medicine and Cellular Longevity. 2016 ; 2016 1-14 art.2696952.[citado 2026 mar. 15 ] Available from: https://doi.org/10.1155/2016/2696952 - Investigação estrutural da via de transdução de sinal da proteína SRC: interação de CSK com caveolina-1 depende do estado redox do domínio SH2
- Measuring the contributions of the Rho pathway to the DNA damage response in tumor epithelial cells
- Proteomic and interactome approaches reveal PAK4, PHB-2, and 14-3-3 eta as targets of overactivated Cdc42 in cellular responses to Genomic instability
- The use of HeLa cells as a model for studying DNA damage and repair
- Revisiting the roles of VHR/DUSP3 phosphatase in human diseases
- The small GTPase RhoA signals to DNA damage repair in tumor cells
- DUSP3 Signals for proliferation and genomic stability in human cells
- DUSP3 maintains genomic stability and cell proliferation by modulating NER pathway and cell cycle regulatory proteins
- Non-canonical role of Cdc42 GTPase and its novel interaction partners in genomic instability conditions
- Overactivated Cdc42 acts through Cdc42EP3/Borg2 and NCK to trigger DNA damage response signaling and sensitize cells to DNA-damaging agents
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