We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Joiner et al. reply.
- Authors
Joiner, Mei-ling A.; Li, Jingdong; He, B. Julie; Luczak, Elizabeth D.; Mohler, Peter J.; Koval, Olha M.; Gao, Zhan; Hall, Duane D.; Chen, Biyi; Yang, Jinying; Song, Long-Sheng; Allamargot, Chantal; Fink, Brian D.; Moore, Steven A.; Scholz, Thomas D.; Strack, Stefan; Sivitz, William I.; Anderson, Mark E.
- Abstract
Replying to F. Fieni et al. 513, http://dx.doi.org/10.1038/nature13626 (2014)In our Letter identifying mitochondrial CaMKII as a crucial component of a Ca2+-dependent process of heart disease, we used multiple methods to show that CaMKII modulates mitochondrial Ca2+ homeostasis, as outlined below. First, we carried out electrophysiology of the mitochondrial calcium uniporter (MCU) current in mitoplasts. In our report we did not claim to measure capacitance of the mitoplast separately from the total capacitance of the mitoplast and pipette. Although we concede that the approach of Fieni et al. is preferable, we found that even after removing any correction for capacitance, dialysis with constitutively active CaMKII monomers increased MCU current whereas dialysis with catalytically dead CaMKII monomers did not.
- Subjects
HEART mitochondria; CALCIUM
- Publication
Nature, 2014, Vol 513, Issue 7519, pE3
- ISSN
0028-0836
- Publication type
Article
- DOI
10.1038/nature13627