C-Fos protein is a mediator in mitogenic response to ACTH (1998)
- Authors:
- Autor USP: ARMELIN, HUGO AGUIRRE - IQ
- Unidade: IQ
- Assunto: BIOQUÍMICA
- Language: Inglês
- Imprenta:
- Publisher place: Monticello
- Date published: 1998
- Source:
- Título: Endocrine Research
- Volume/Número/Paginação/Ano: v. 24, p. 421-424, 1998
-
ABNT
LOTFI, Claudimara Ferini Pacicco e ARMELIN, Hugo Aguirre. C-Fos protein is a mediator in mitogenic response to ACTH. Endocrine Research, v. 24, p. 421-424, 1998Tradução . . Acesso em: 10 jan. 2026. -
APA
Lotfi, C. F. P., & Armelin, H. A. (1998). C-Fos protein is a mediator in mitogenic response to ACTH. Endocrine Research, 24, 421-424. -
NLM
Lotfi CFP, Armelin HA. C-Fos protein is a mediator in mitogenic response to ACTH. Endocrine Research. 1998 ; 24 421-424.[citado 2026 jan. 10 ] -
Vancouver
Lotfi CFP, Armelin HA. C-Fos protein is a mediator in mitogenic response to ACTH. Endocrine Research. 1998 ; 24 421-424.[citado 2026 jan. 10 ] - Selection of normal revertants from tumorigenic balb 3t3 mouse cell lines carrying the human ej-ras oncogene
- FGF2-citotoxic mechanisms block mitotic entry in a Ras-dependent cell line by activation of G2-M checkpoint and inhibition of CDK1 activity
- FGF2 enhances replicative stress and leads to permanent DDR and G2 cell cycle block selectively in K-Ras transformed cells
- Anti-mitogenic effects of FGF2 in human cells transformed by the RasV12 oncogene
- HMW-FGF2 did not induced the senescence caused by LMW-FGF2 in ras-transformed cells
- FGF2 targets an "Achilles' hell" of Ras-driven mouse malignant cells
- Characterization of keratinocyte responces to FGF1, FGF2 and FGF7
- Molecular mechanisms of cell cycle control in the mouse Y1 adrenal cell line
- FGF2 blocks H-RasV12-dependent proliferation of Balb3T3 mouse fibroblasts
- PMA triggers oxidative stress and apoptosis in H-RASV12-dependent human maligmant keratinocytes
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