mCICR is required for AsO-induced permeability transition pore opening and cytochrome c release from mitochondria
Molecular and Cellular Biochemistry, ISSN: 0300-8177, Vol: 277, Issue: 1-2, Page: 33-42
2005
- 12Citations
- 3Captures
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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
- Citations12
- Citation Indexes12
- 12
- CrossRef10
- Captures3
- Readers3
Article Description
The permeability transition pore (PTP) is central for apoptosis by acting as a good candidate pathway for the release of Cyt. c and apoptosis induction factors (AIF). Arsenite induces apoptosis via a direct effect on PTP. To characterize the exact mechanism for arsenite induces PTP opening, the effect of Ca on As O-induced PTP opening, the relationship between AsO-induced PTP opening and Cyt. c release from mitochondria and calcium-induced calcium release from mitochondria (mCICR), and the effects of AsO on Ca-induced PTP opening were studied. The results showed AsO induces Cyt. c release by triggering PTP opening. Ca is necessary for AsO -induced PTP opening. AsO-induced PTP opening and Cyt. c release depends on mCICR. AsO promotes PTP opening by lowering Ca-threshold. These results indicated AsO induce Cyt. c release from mitochondria by lowering Ca-threshold for PTP and triggering mCICR-dependent PTP opening. Suggesting that it is possible to control apoptosis by altering Ca threshold and mCICR to modulate PTP opening and Cyt. c release. © Springer Science + Business Media, Inc. 2005.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=24144448091&origin=inward; http://dx.doi.org/10.1007/s11010-005-4818-x; http://www.ncbi.nlm.nih.gov/pubmed/16132712; http://link.springer.com/10.1007/s11010-005-4818-x; http://www.springerlink.com/index/10.1007/s11010-005-4818-x; http://www.springerlink.com/index/pdf/10.1007/s11010-005-4818-x; https://dx.doi.org/10.1007/s11010-005-4818-x; https://link.springer.com/article/10.1007/s11010-005-4818-x
Springer Science and Business Media LLC
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