Overactivated Cdc42 acts through Cdc42EP3/Borg2 and NCK to trigger DNA damage response signaling and sensitize cells to DNA-damaging agents (2020)
- Authors:
- Autor USP: FORTI, FÁBIO LUÍS - IQ
- Unidade: IQ
- DOI: 10.1016/j.yexcr.2020.112206
- Assunto: DNA
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Experimental Cell Research
- ISSN: 0014-4827
- Volume/Número/Paginação/Ano: v. 395, p. 1-12 art. 112206, 2020
- Este artigo NÃO possui versão em acesso aberto
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Status: Nenhuma versão em acesso aberto identificada -
ABNT
SILVA, Luiz Eduardo e RUSSO, Lilian Cristina e FORTI, Fabio Luis. Overactivated Cdc42 acts through Cdc42EP3/Borg2 and NCK to trigger DNA damage response signaling and sensitize cells to DNA-damaging agents. Experimental Cell Research, v. 395, p. 1-12 art. 112206, 2020Tradução . . Disponível em: https://doi.org/10.1016/j.yexcr.2020.112206. Acesso em: 14 mar. 2026. -
APA
Silva, L. E., Russo, L. C., & Forti, F. L. (2020). Overactivated Cdc42 acts through Cdc42EP3/Borg2 and NCK to trigger DNA damage response signaling and sensitize cells to DNA-damaging agents. Experimental Cell Research, 395, 1-12 art. 112206. doi:10.1016/j.yexcr.2020.112206 -
NLM
Silva LE, Russo LC, Forti FL. Overactivated Cdc42 acts through Cdc42EP3/Borg2 and NCK to trigger DNA damage response signaling and sensitize cells to DNA-damaging agents [Internet]. Experimental Cell Research. 2020 ; 395 1-12 art. 112206.[citado 2026 mar. 14 ] Available from: https://doi.org/10.1016/j.yexcr.2020.112206 -
Vancouver
Silva LE, Russo LC, Forti FL. Overactivated Cdc42 acts through Cdc42EP3/Borg2 and NCK to trigger DNA damage response signaling and sensitize cells to DNA-damaging agents [Internet]. Experimental Cell Research. 2020 ; 395 1-12 art. 112206.[citado 2026 mar. 14 ] Available from: https://doi.org/10.1016/j.yexcr.2020.112206 - 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
- Inhibition of the RhoA GTPase activity increases sensitivity of melanoma cells to UV radiation effects
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