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SHR Neuro Krebs Kardio Lipid

Waldeck-Weiermair, M; Malli, R; Naghdi, S; Trenker, M; Kahn, MJ; Graier, WF.
The contribution of UCP2 and UCP3 to mitochondrial Ca(2+) uptake is differentially determined by the source of supplied Ca(2+).
Cell Calcium. 2010; 47(5): 433-440.
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Autor/innen der Med Uni Graz:
Graier Wolfgang
Khan Muhammad Jadoon
Malli Roland
Naghdi Shamim
Waldeck-Weiermair Markus

Dimensions Citations:

Plum Analytics:
The transmission of Ca(2+) signals to mitochondria is an important phenomenon in cell signaling. We have recently reported that the novel uncoupling proteins UCP2 and UCP3 (UCP2/3) are fundamental for mitochondrial Ca(2+) uniport (MCU). In the present study we investigate the contribution of UCP2/3 to mitochondrial accumulation of Ca(2+) either exclusively released from the ER or entering the cell via the store-operated Ca(2+) entry (SOCE) pathway. Using siRNA we demonstrate that constitutively expressed UCP2/3 are essentially involved in mitochondrial sequestration of intracellularly released Ca(2+) but not of that entering the cells via SOCE. However, overexpression of UCP2/3 yielded elevated mitochondrial Ca(2+) uptake from both sources, though it was more pronounced in case of entering Ca(2+), indicating that the expression levels of UCP2/3 are crucial for the capacity of mitochondria to sequester entering Ca(2+). Our data point to distinct UCP2/3-dependent and UCP2/3-independent modes of mitochondrial Ca(2+) sequestration, which may meet the various demands necessary for an adequate organelle Ca(2+) loading from different Ca(2+) sources in intact cells.
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Calcium - metabolism
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Mitochondria - metabolism
Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism
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Find related publications in this database (Keywords)
Mitochondrial Ca2+ uptake
Store-operated Ca2+ entry
Ca2+ release
Uncoupling proteins
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