ArticleMolecular and cellular biochemistry2010
Bax is upregulated by p53 signal pathway in the SPE B-induced apoptosis.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Cordycepin Induces Apoptosis through JNK-Mediated Caspase Activation in Human OEC-M1 Oral Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Role of JNK activation in paclitaxel-induced apoptosis in human head and neck squamous cell carcinoma.Oncology letters · 2021Article
- Estradiol Prevents High Glucose-Induced β-cell Apoptosis by Decreased BTG2 Expression.Scientific reports · 2018Article
- Curcumin suppresses gastric tumor cell growth via ROS-mediated DNA polymerase γ depletion disrupting cellular bioenergetics.Journal of experimental & clinical cancer research : CR · 2017Article
- Host responses to group a streptococcus: cell death and inflammation.PLoS pathogens · 2014Review
- Role of Bax/Bcl-2 family members in green tea polyphenol induced necroptosis of p53-deficient Hep3B cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Regulation of lung injury and fibrosis by p53-mediated changes in urokinase and plasminogen activator inhibitor-1.The American journal of pathology · 2013Article
- INMAP, a novel truncated version of POLR3B, represses AP-1 and p53 transcriptional activity.Molecular and cellular biochemistry · 2013Article
- Insights into the structural stability of Bax from molecular dynamics simulations at high temperatures.Protein science : a publication of the Protein Society · 2011Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We identify integrin α(v)β(3) and Fas as receptors for the streptococcal pyrogenic exotoxin B (SPE B), and G308S (SPE B mutant, glycine at residue 308 is changed to serine), which interacts with Fas only, in our previous study. Here, we explore the signal pathways that regulate proapoptotic protein expression after SPE B stimulation. We find that both SPE B and G308S can stimulate the serine phosphorylation of p53, and p53 phosphorylation is inhibited by the anti-Fas antibody but not by anti-α(V)β(3) antibody. p38 inhibitor and siRNA decrease the activation and translocation of p53 into the nucleus, which executes its transcription activity. These results indicate that after SPE B treatment, p53 is activated and p38 is the upstream of p53. p38 siRNA also decreases the binding of p53 to the bax promoter and interferes with the association of p53 and STAT1. p53, p38, and STAT1 siRNAs downregulate SPE B-induced Bax expression. This shows that SPE B activates the bax promoter via p38/p53 signal pathways through the Fas receptor, and that STAT1 acts as a coactivator of p53. In addition, p38 and p53 siRNAs inhibit SPE B-induced apoptosis. This is consistent with the findings that SPE B upregulates Bax expression through p38/p53 signal pathways that enhance cell apoptosis.
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