2013年9月5日 · ROS-JNK-p53 pathways played a crucial role in autophagy via repressing the activation of mTOR in PAB-treated L929 cells. A: The cells were pretreated with pifithrin-α or SP600125 for 1 h, and then co-incubated with 20 µM PAB for 48 h.

2012年2月23日 · In this study, oridonin induced NO production, which medi-ated L929 cell apoptosis and autophagy and led to the activa-tion of ERK and p53. Oridonin was obtained from the Kunming Institute of...

1998年9月11日 · The overexpressed p53 probably contributes to the increased TNF killing in L929 cells. p53 is defined as a tumor suppressor. p53 mediates cell growth arrest by induction of an inhibitor of cyclin dependent kinase (CDK), p21 WAF/CIP-1, whereas under certain circumstances it may induce apoptosis [24]. The mechanism of p53-mediated apoptosis is ...

LAPF表达的沉默消除了磷酸化的p53（Ser（15/18））的溶酶体易位，而p53表达的沉默对LAPF的溶酶体易位没有影响。 与LAPF沉默类似，L929细胞中内源性p53表达的沉默可能显着损害TNF-α诱导的LMP和细胞凋亡。

2012年7月30日 · In this study, oridonin induced NO production, which mediated L929 cell apoptosis and autophagy and led to the activation of ERK and p53. Oridonin was obtained from the Kunming Institute of...

2008年11月21日 · Herein, we found that the treatment of L929 cells with TNFα caused a time-dependent increase in p53 activity. The inhibition of p53 activation reduced TNFα-induced apoptosis and autophagy that were accompanied by the …

In this report, we show a novel suppressive effect of calpeptin, a calpain inhibitor, on TNFα-induced cell death and accumulation of p53 in L929 mouse fibrosarcoma. Exposure to 10 ng/ml TNFα induced cell death in >50% of L929 cells within 12 …

1998年9月11日 · Conceivably, hyaluronidase enhancement of TNF sensitivity in L929 cells is p53-dependent and the matrix inter-alpha-inhibitor contributes a protective role against TNF cytotoxicity. Degradation of extracellular matrix by hyaluronidase increases murine L929 cell sensitivity to tumor necrosis factor (TNF) cytotoxicity.

In our study, we subcloned oridonin-sensitive and low sensitive L929 cells and both types of cells grew at almost the same growth rate. The acquired low sensitivity to oridonin-induced apoptosis was associated with Bcl-2 up-regulation and down-regulation of p53 phosphorylation.

In addition, oridonin (50 μmol/L) activated ERK and p53 in L929 cells, and the interruption of ERK and p53 activation by PD 98059, pifithrin-α, or ERK siRNA decreased oridonin-induced apoptosis and autophagy.