Transforming growth factor "Beta" and cell cycle regulation in endometrial carcinomas (2002)
- Authors:
- Autor USP: GAMA, PATRICIA - ICB
- Unidade: ICB
- Assunto: HISTOLOGIA
- Language: Inglês
- Imprenta:
- Publisher place: Porto Alegre
- Date published: 2002
- Source:
- Título do periódico: Anais
- Conference titles: Congresso Brasileiro de Biologia Celular
-
ABNT
GAMA, Patrícia; PAREKH, T V; GOLD, L I. Transforming growth factor "Beta" and cell cycle regulation in endometrial carcinomas. Anais.. Porto Alegre: [s.n.], 2002. -
APA
Gama, P., Parekh, T. V., & Gold, L. I. (2002). Transforming growth factor "Beta" and cell cycle regulation in endometrial carcinomas. In Anais. Porto Alegre. -
NLM
Gama P, Parekh TV, Gold LI. Transforming growth factor "Beta" and cell cycle regulation in endometrial carcinomas. Anais. 2002 ; -
Vancouver
Gama P, Parekh TV, Gold LI. Transforming growth factor "Beta" and cell cycle regulation in endometrial carcinomas. Anais. 2002 ; - Avaliação da expressão de TGF'beta" na mucosa gástrica de ratos em desenvolvimento sob tratamento com hidrocortisona: estudo in vivo e in vitro
- Transforming growth factor "Beta" and cell cycle regulation in endometrial carcinomas
- TGF beta signaling in gastric epithelial cells
- Ghrelin and growth hormone secretagogue receptor distribution in the gastric mucosa of early weaned rats: effects on epithelial cell proliferation
- Transforming Growth Factor Beta1 promotes p27kip1 post-transcriptional regulation in gastric cells of suckling rats
- The influence of corticosterone in the maturation of rat gastric mucosa during early weaning
- The effect of early weaning on apoptosis in the gastric epithelium of rats in postnatal development
- MAPK Signaling Pathway Regulates p27 Phosphorylation at Threonin 187 as Part of the Mechanism Triggered by Early-Weaning to Induce Cell Proliferation in Rat Gastric Mucosa
- Ghrelin and GHS-R in the rat gastric mucosa: are they involved in regulation of growth during early weaning?
- Transforming growth factor "Beta" signaling is disabled early in human endometrial carcinogenesis concomitant with loss of growth inhibition
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