Relevance of rna synthesis for the early steroidogenic response to acth, dcamp, and phorbol ester in adrenocortical cells (1992)
- Authors:
- Autor USP: ARMELIN, HUGO AGUIRRE - IQ
- Unidade: IQ
- Subjects: BIOQUÍMICA; BIOLOGIA MOLECULAR
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Resumos
- Conference titles: Reuniao Anual da Sociedade Brasileira de Bioquimica e Biologia Molecular
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ABNT
FRIGERI, C K; ARMELIN, Hugo Aguirre. Relevance of rna synthesis for the early steroidogenic response to acth, dcamp, and phorbol ester in adrenocortical cells. Anais.. Sao Paulo: Sbbq, 1992. -
APA
Frigeri, C. K., & Armelin, H. A. (1992). Relevance of rna synthesis for the early steroidogenic response to acth, dcamp, and phorbol ester in adrenocortical cells. In Resumos. Sao Paulo: Sbbq. -
NLM
Frigeri CK, Armelin HA. Relevance of rna synthesis for the early steroidogenic response to acth, dcamp, and phorbol ester in adrenocortical cells. Resumos. 1992 ; -
Vancouver
Frigeri CK, Armelin HA. Relevance of rna synthesis for the early steroidogenic response to acth, dcamp, and phorbol ester in adrenocortical cells. Resumos. 1992 ; - Selection of normal revertants from tumorigenic balb 3t3 mouse cell lines carrying the human ej-ras oncogene
- Role of growth factor inducible early response genes (c-fos, c-iin, c-myc, je, kc) in balb-3t3 cell's growth control and viral transformation
- Como oncogenes modificam a resposta celular a fatores de crescimento ?
- C-fos / c-myc induction pattern in normal revertants of ej-ras transformed 3t3 cells
- Pkc role in acth mechanism of action
- Molecular and cell biology of acth action in adrenocortical cells
- 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
- Investigation of FGFs role in human keratinocyte cell line HaCaT expressing h-RasV12 oncogene
- Alteration in 'G IND.1' phase organization caused by the oncogenese
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