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The MCU complex in cell death

期刊

CELL CALCIUM
卷 69, 期 -, 页码 73-80

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2017.08.008

关键词

Mitochondria; Calcium; Cell death; MCU; MCU complex

资金

  1. University of Padova
  2. Italian Ministries of Health (Ricerca Finalizzata)
  3. Education, University and Research (FIRB)
  4. European Union (ERC mitoCalcium) [294777]
  5. NIH [1P01AG025532-01A1]
  6. Cariparo Foundation
  7. Italian Association for Cancer Research
  8. AIRC
  9. Telethon-Italy [GPP1005A]
  10. Junta de Extremadura - European Regional Development Fund, ERDF [PO14011]
  11. NATIONAL INSTITUTE ON AGING [P01AG025532] Funding Source: NIH RePORTER

向作者/读者索取更多资源

During the 60s, the notion that positively charged Ca2+ ions are rapidly accumulated in energized mitochondria has been first established. In the following decades, mitochondrial Ca2+ homeostasis was shown to control cell metabolism, cell survival and other cell-specific functions through different mechanism. However, the molecular identity of the molecules controlling this process remained a mystery until just few years ago, when both mitochondrial Ca2+ uptake and release systems were genetically dissected. This finally opened the possibility to develop genetic model to directly test the contribution of mitochondrial Ca2+ homeostasis to cellular functions. Although the picture is still far from being clear, we here summarize and critically evaluate the current knowledge on how mitochondrial Ca2+ handling controls cell death.

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