A model of the cell, population growth and drug effect on the cell cycle (2012)
- Authors:
- USP affiliated authors: NAKANO, FÁBIO - EACH ; ARMELIN, HUGO AGUIRRE - IQ
- Unidades: EACH; IQ
- Assunto: CICLO CELULAR
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq)
- Publisher place: São Paulo
- Date published: 2012
- Source:
- Título: Program and Index
- Conference titles: Annual Meeting of the Brazilian Biochemistry and Molecular Biology Society (SBBq)
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ABNT
NAKANO, Fábio e DIAS, Matheus Henrique dos Santos e ARMELIN, Hugo Aguirre. A model of the cell, population growth and drug effect on the cell cycle. 2012, Anais.. São Paulo: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq), 2012. . Acesso em: 11 fev. 2026. -
APA
Nakano, F., Dias, M. H. dos S., & Armelin, H. A. (2012). A model of the cell, population growth and drug effect on the cell cycle. In Program and Index. São Paulo: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq). -
NLM
Nakano F, Dias MH dos S, Armelin HA. A model of the cell, population growth and drug effect on the cell cycle. Program and Index. 2012 ;[citado 2026 fev. 11 ] -
Vancouver
Nakano F, Dias MH dos S, Armelin HA. A model of the cell, population growth and drug effect on the cell cycle. Program and Index. 2012 ;[citado 2026 fev. 11 ] - Mathematical modeling of RAs/MAPK signalling network kinetics provides insights into mechanisms of FGF2-induced cell cycle arrest in the K-K-ras-driven mouse Y1 adrenocortical tumor cells
- Modeling the kinetics of Ras/MAPK and PI3K/AKT signaling pathways in the K-Ras-driven mouse Y1 adrenocortical tumor cells: novel insights into the mechanisms of FGF2-driven cell cycle arrest
- Mathematical modeling of the Ras/MAPK and PI3K/AKT signaling networks in the K-Ras-driven mouse Y1 adrenocortical tumor cells
- Solver de alto desempenho para problemas na forma angular blocada aninhada
- Um novo modelo para cálculo de probabilidade de paternidade: concepção e implementação
- Selection of normal revertants from tumorigenic balb 3t3 mouse cell lines carrying the human ej-ras oncogene
- Selection of FGF2-resistant cell sublines led to separation between classical mitogenic signaling and novel cytostatic mechanisms of FGF2 in K-Ras-driven mouse Y1 adrenocortical tumor cells
- Regulation of 'G IND.0'-> 'G IND.1'-> s transition a genetic approach
- Antiproliferative effects of FGF2 on human embryonic kidney cell lines (HEK293) displaying a ras-dependent malignant phenotype
- Pkc role in acth mechanism of action
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