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	Provedor de dados BJMBR (2) Autor Xia,D.Y. (2) Chen,R.A. (1) Hao,M.W. (1) Li,W. (1) Liang,Y.M. (1) Liu,J.G. (1) Liu,L. (1) Liu,Q. (1) Qi,X.K. (1) Qian,H.R. (1) Yao,S. (1) Mais... Palavra-chave Apoptosis (1) Apoptosis Chronic myeloid leukemia p15INK4B STI571 (Gleevec (1) Autophagy (1) Focal cerebral ischemic reperfusion (1) Imatinib) (1) Ischemic preconditioning (1) Mais... Tipo do documento Info:eu-repo/semantics/article (2) Ano 2014 (1) 2013 (1) País Brazil (2) Idioma Inglês (2)		Ordenar por:  Relevância Autor Título Ano Registros recuperados: 2 Primeira ... 1 ... Última Ischemia preconditioning is neuroprotective in a rat cerebral ischemic injury model through autophagy activation and apoptosis inhibition BJMBR Xia,D.Y.; Li,W.; Qian,H.R.; Yao,S.; Liu,J.G.; Qi,X.K.. Sublethal ischemic preconditioning (IPC) is a powerful inducer of ischemic brain tolerance. However, its underlying mechanisms are still not well understood. In this study, we chose four different IPC paradigms, namely 5 min (5 min duration), 5×5 min (5 min duration, 2 episodes, 15-min interval), 5×5×5 min (5 min duration, 3 episodes, 15-min intervals), and 15 min (15 min duration), and demonstrated that three episodes of 5 min IPC activated autophagy to the greatest extent 24 h after IPC, as evidenced by Beclin expression and LC3-I/II conversion. Autophagic activation was mediated by the tuberous sclerosis type 1 (TSC1)-mTor signal pathway as IPC increased TSC1 but decreased mTor phosphorylation. Terminal deoxynucleotidyl transferase dUTP nick end... Tipo: Info:eu-repo/semantics/article Palavras-chave: Ischemic preconditioning; Autophagy; Apoptosis; Focal cerebral ischemic reperfusion. Ano: 2013 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2013000700580 A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia BJMBR Xia,D.Y.; Liu,L.; Hao,M.W.; Liu,Q.; Chen,R.A.; Liang,Y.M.. p15INK4B, a cyclin-dependent kinase inhibitor, has been recognized as a tumor suppressor. Loss of or methylation of the p15INK4B gene in chronic myeloid leukemia (CML) cells enhances myeloid progenitor formation from common myeloid progenitors. Therefore, we examined the effects of overexpressed p15INK4B on proliferation and apoptosis of CML cells. Overexpression of p15INK4B inhibited the growth of K562 cells by downregulation of cyclin-dependent kinase 4 (CDK4) and cyclin D1 expression. Overexpression of p15INK4B also induced apoptosis of K562 cells by upregulating Bax expression and downregulating Bcl-2 expression. Overexpression of p15INK4B together with STI571 (imatinib) or BCR-ABL1 small interfering RNA (siRNA) also enhanced growth inhibition and... Tipo: Info:eu-repo/semantics/article Palavras-chave: Apoptosis Chronic myeloid leukemia p15INK4B STI571 (Gleevec; Imatinib). Ano: 2014 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014001201096 Registros recuperados: 2 Primeira ... 1 ... Última

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