DUSP3 Signals for proliferation and genomic stability in human cells (2016)
- Autor:
- Autor USP: FORTI, FÁBIO LUÍS - IQ
- Unidade: IQ
- Subjects: CÉLULAS; GENÔMICA
- Language: Inglês
- Imprenta:
- Publisher: EMBO
- Publisher place: Heidelberg
- Date published: 2016
- Source:
- Título: Abstract Book
- Conference titles: The modularity of signalling proteins and networks
-
ABNT
FORTI, Fabio Luis. DUSP3 Signals for proliferation and genomic stability in human cells. 2016, Anais.. Heidelberg: EMBO, 2016. . Acesso em: 13 fev. 2026. -
APA
Forti, F. L. (2016). DUSP3 Signals for proliferation and genomic stability in human cells. In Abstract Book. Heidelberg: EMBO. -
NLM
Forti FL. DUSP3 Signals for proliferation and genomic stability in human cells. Abstract Book. 2016 ;[citado 2026 fev. 13 ] -
Vancouver
Forti FL. DUSP3 Signals for proliferation and genomic stability in human cells. Abstract Book. 2016 ;[citado 2026 fev. 13 ] - 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
- Clonagem do receptor de ACTH de células adrenocorticais Y-1 de camundongos e expressão em fivroblastos 3T3 e celulas AR-1 para elucidação de vias de transdução de sinal
- 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 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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