Participation of Intracellular Ca 2+ /Calmodulin and Protein Kinase(s) in the Pathway of Apoptosis Induced by a Drosophila Cell Death Gene, reaper
Molecular Cell Biology Research Communications, ISSN: 1522-4724, Vol: 4, Issue: 5, Page: 307-312
2001
- 6Citations
- 14Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations6
- Citation Indexes6
- CrossRef2
- Captures14
- Readers14
- 14
Article Description
To elucidate the apoptotic signaling pathway, we have generated a cell culture model: S2 cells stably transfected with a Drosophila cell death gene, reaper ( rpr ). Following rpr overexpression, caspase activation-mediated apoptotic cell death was induced in the cells. Apoptosis triggered by rpr required intracellular Ca 2+ ions and calmodulin. Furthermore, protein kinase inhibitors H-7 (a PKC, PKA, PKG, MLCK, and CKI inhibitor), calphostin C (a PKC inhibitor), or H-89 (a PKA and PKG inhibitor) completely blocked apoptosis induced by rpr, suggesting that some kind of serine/threonine protein kinase(s) act upstream of caspase in apoptotic pathway induced by rpr in S2 cells.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1522472401902971; http://dx.doi.org/10.1006/mcbr.2001.0297; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034828792&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11529681; https://linkinghub.elsevier.com/retrieve/pii/S1522472401902971; https://dx.doi.org/10.1006/mcbr.2001.0297
Elsevier BV
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