| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
The endoplasmic reticulum (ER) is the place of protein synthesis and the starting point of vesicular transport. In addition to these roles, the ER sends out intracellular signals that include those for cell fate decision. This study focuses on the ER signaling that we have already found to be involved in skeletal muscle formation from the progenitor cells (myoblasts) by cell fusion. We have found that ER calcium depletion occurs in differentiating myoblasts, just prior to cell fusion. Because critical enzymes that assist protein folding in the ER require calcium for their activity, calcium depletion causes ER stress. This result suggests that ER stress evoked by calcium depletion activates ATF6, a stress sensor, and caspases in a specific manner. We have also identified a substrate candidate of caspase-12 which was previously shown as the ER stress-specific caspase by us.
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