Modulation of RhoA GTPase activity sensitizes human cervix carcinoma cells to gamma-radiation by attenuating DNA repair pathways (2016)
- Authors:
- Autor USP: FORTI, FÁBIO LUÍS - IQ
- Unidade: IQ
- DOI: 10.1155/2016/6012642
- Subjects: CARCINOMA; RADIOTERAPIA
- Language: Inglês
- Imprenta:
- Source:
- Título: Oxidative Medicine and Cellular Longevity
- ISSN: 1942-0900
- Volume/Número/Paginação/Ano: p. 1-11 art. 6012642, 2016
- Este artigo possui versão em acesso aberto
- URL de acesso aberto
- PDF de acesso aberto
- Versão do Documento: Versão publicada (Published version)
-
Status: Artigo aberto em periódico híbrido (Hybrid Open Access) -
ABNT
OSAKI, Juliana Harumi et al. Modulation of RhoA GTPase activity sensitizes human cervix carcinoma cells to gamma-radiation by attenuating DNA repair pathways. Oxidative Medicine and Cellular Longevity, p. 1-11 art. 6012642, 2016Tradução . . Disponível em: https://doi.org/10.1155/2016/6012642. Acesso em: 14 mar. 2026. -
APA
Osaki, J. H., Espinha, G., Magalhães, Y. T., & Forti, F. L. (2016). Modulation of RhoA GTPase activity sensitizes human cervix carcinoma cells to gamma-radiation by attenuating DNA repair pathways. Oxidative Medicine and Cellular Longevity, 1-11 art. 6012642. doi:10.1155/2016/6012642 -
NLM
Osaki JH, Espinha G, Magalhães YT, Forti FL. Modulation of RhoA GTPase activity sensitizes human cervix carcinoma cells to gamma-radiation by attenuating DNA repair pathways [Internet]. Oxidative Medicine and Cellular Longevity. 2016 ; 1-11 art. 6012642.[citado 2026 mar. 14 ] Available from: https://doi.org/10.1155/2016/6012642 -
Vancouver
Osaki JH, Espinha G, Magalhães YT, Forti FL. Modulation of RhoA GTPase activity sensitizes human cervix carcinoma cells to gamma-radiation by attenuating DNA repair pathways [Internet]. Oxidative Medicine and Cellular Longevity. 2016 ; 1-11 art. 6012642.[citado 2026 mar. 14 ] Available from: https://doi.org/10.1155/2016/6012642 - 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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