ArticleThe Journal of biological chemistry2009
Procaspase 8 and Bax are up-regulated by distinct pathways in Streptococcal pyrogenic exotoxin B-induced apoptosis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- The interplay of cancer-associated fibroblasts and apoptotic cancer cells suppresses lung cancer cell growth through WISP-1-integrin ανβ3-STAT1 signaling pathway.Cell communication and signaling : CCS · 2025Article
- AKR1B1 Represses Glioma Cell Proliferation through p38 MAPK-Mediated Bcl-2/BAX/Caspase-3 Apoptotic Signaling Pathways.Current issues in molecular biology · 2023Article
- Organophosphate pesticide chlorpyrifos impairs STAT1 signaling to induce dopaminergic neurotoxicity: Implications for mitochondria mediated oxidative stress signaling events.Neurobiology of disease · 2018Article
- Zinc Chelation Mediates the Lysosomal Disruption without Intracellular ROS Generation.Oxidative medicine and cellular longevity · 2016Article
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- Host responses to group a streptococcus: cell death and inflammation.PLoS pathogens · 2014Review
- Phosphorylation of signal transducer and activator of transcription 1 reduces bortezomib-mediated apoptosis in cancer cells.Cell death & disease · 2013Article
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- Article
- Caveolae-dependent endocytosis is required for class A macrophage scavenger receptor-mediated apoptosis in macrophages.The Journal of biological chemistry · 2011Article
- Glycogen synthase kinase-3 and p38 MAPK are required for opioid-induced microglia apoptosis.Neuropharmacology · 2010Article
- Bax is upregulated by p53 signal pathway in the SPE B-induced apoptosis.Molecular and cellular biochemistry · 2010Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously identified integrin alpha(v)beta(3) and Fas as receptors for the streptococcal pyrogenic exotoxin B (SPE B), and G308S, a mutant of SPE B that binds to Fas only. In the current study we found that after binding to alpha(v)beta(3), SPE B stimulated the tyrosine phosphorylation of JAK2 and STAT1. STAT1 tyrosine phosphorylation was inhibited by a JAK2 inhibitor, AG490, short interfering RNA (siRNA) silencing of JAK2, and anti-alpha(V)beta(3) antibody. AG490 also decreased the binding of tyrosine-phosphorylated STAT1 to the procaspase 8 promoter, decreasing procaspase 8 expression, suggesting that SPE B up-regulates procaspase 8 expression via the JAK2/STAT1 pathway. Alternatively, both SPE B and G308S increased STAT1 phosphorylation at serine 727, which was inhibited by anti-Fas antibody, a p38 inhibitor, SB203580, and siRNA silencing of p38. In addition, SPE B and G308S increased binding of serine-phosphorylated STAT1 to the Bax promoter and Bax expression, which was decreased by SB203580. SPE B and G308S-stimulated Bax expression was also inhibited by anti-Fas antibody. These findings suggest that Fas mediate SPE B-induced Bax expression through p38. Silencing of JAK2 or p38 by siRNA blocked procaspase 8 expression, whereas only p38 siRNA decreased Bax expression. Furthermore, JAK2 inhibition and p38 inhibition reduced SPE B-induced apoptosis, but only p38 inhibition blocked G308S-induced apoptosis.
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