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Activation of Erk1/Erk2 and transiently increased p53 levels together may account for p21 expression associated with phorbol ester-induced transient growth inhibition in HepG2 cells

机译:Erk1 / Erk2的激活和p53的瞬时升高可能一起解释了佛波酯诱导的HepG2细胞中瞬时生长抑制相关的p21表达

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In HepG2 cells grown in the presence of serum, enhanced Raf-activation correlated with transient growth inhibition. The activation of Raf was increased either by the phorbol ester-induced activation of protein kinase C (PKC) or by the addition of the PKC inhibitor bisindolylmaleimide I (BIM). Either of these treatments increased the cellular levels of p21 by an Erk1/Erk-2 MAP kinase cascade-dependent way, since this increase was prevented by the MEK-inhibitor PD98059. Nevertheless, the growth inhibition correlated with the transient increase of p53 levels as well. Either the activation of PKC with phorbol ester or the addition of BIM to cells growing in serum induced a rapid but transient increase of p53 levels, which preceded growth inhibition. This increase of p53 levels was probably due to the transient stabilisation of p53 and did not require the activation of Erk1/Erk2. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 23]
机译:在血清存在下生长的HepG2细胞中,Raf活化增强与瞬时生长抑制相关。 Raf的激活通过佛波酯诱导的蛋白激酶C(PKC)的激活或通过添加PKC抑制剂双吲哚基马来酰亚胺I(BIM)来增加。这些方法中的任何一种都通过Erk1 / Erk-2 MAP激酶级联依赖的方式增加了p21的细胞水平,因为这种增加被MEK抑制剂PD98059阻止了。然而,生长抑制也与p53水平的瞬时增加相关。用佛波酯酯激活PKC或在血清中生长的细胞中添加BIM都会引起p53水平的快速但短暂的升高,这先于生长抑制。 p53水平的这种升高可能是由于p53的瞬时稳定所致,不需要激活Erk1 / Erk2。 (C)2002 Elsevier Science Inc.保留所有权利。 [参考:23]

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