1
These activities of SnoN rely on the ability of SnoN to activate p53.
2
We investigated the ability of LMB to activate p53 in prostatic epithelial cells.
3
Dysfunctional telomeres activate p53 to initiate cellular senescence or apoptosis to suppress tumorigenesis.
4
Previous work demonstrated that prolonged prometaphase and DNA damage during abnormal mitosis can activate p53.
5
However, fewer compounds directly bind to and activate p53.
6
The mature and pro-form of nerve growth factor (NGF) activate p75NTR to trigger motor neuron apoptosis.
7
Recently, many kinds of non-genotoxic stress such as heat shock, cold shock, and low pH also have been found to activate p53 pathway.
8
Thus, LM11A-24 appears to activate p75NTR-linked survival but not death mechanisms, and may interfere with the ability of neurotrophins to induce apoptosis.
9
The results suggested that B4 had a certain protective effect on cisplatin-induced acute kidney injury, and could activate p53 signaling pathway related apoptotic factors.
10
Interestingly, LA treatment did neither activate p53 nor induced genotoxic effects as shown by lack of DNA strand breaks and phosphorylation of histone 2AX.
11
In particular, we over- activate p53 in breast cancer cells, followed by RNA-seq and ChIP-seq, and could identify an extensive up-regulated network controlled directly by p53.
12
Early studies have shown that genotoxic stress activates p53 pathway.
13
Combo treatment also restored normal staining for activated p38.
14
Ferrichrome inhibited the progression of cancer cells via dysregulation of the cell cycle by activating p53.
15
Thus, we have revealed a novel function of SnoN in regulating aging and tumorigenesis by directly activating p53.
16
We now show that TNF activates p42 MAPK in two cell lines whose growth is inhibited by TNF.
