Regulation of autophagy by the inositol trisphosphate receptor (Cell Death and Differentiation, 2007, 14:1029-1039)

報告日期: 2007/11/16
報告時間: 16:00/16:50
報告學生: 藍昇輝
講評老師: 呂佩融
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Regulation of autophagy by the inositol trisphosphate receptor

Cell Death and Differentiation (2007) 14, 1029–1039

 

Speaker: 藍昇輝

Commentator: 呂佩融 老師

Time:2007/11/16 16:00~16:50

Place: Room 602

 

Abstract:

Autophagy could be induced by various stimuli,and the process of autophagy is controlled by a series of evolutionary conserved genes, the atg genes, whose products are essential for specific steps of the autophagic process. Suppression of autophagy by chemical inhibitors or knockdown of the essential genes can inhibit the formation of autophagy. One of the strongest triggers of autophagy is nutrient stress. Previous study suggested that myo-inositol-1,4,5-trisphosphate (IP3) could also regulate autophagy. IP3 acts on the IP3 receptor (IP3R),which is known to play a major role within the Ca2+ microdomains that transmit Ca2+ spikes generated by the ER to mitochondria. This study unravels the note of IP3R in autophagy. The authors observed that inhibited IP3R is a strong stimulus for the induction of autophagy. The mechanism of IP3R related autophagy is similar to that of the starvation-induced autophagy, but is different to that of ER stress-induced autophagy. Autophagy promoted by IP3R inhibition could not be attributed to a modulation of steady-state Ca2+ levels in the ER or in the cytosol. Altogether, these results strongly suggest that IP3R exerts a major role in the physiological control of autophagy.

 

References:

Levine B, Yuan J. Autophagy in cell death: an innocent convict? J Clin Invest 2005; 115: 2679–2688.

Yorimitsu T, Klionsky DJ. Autophagy: molecular machinery for self-eating. Cell Death Differ 2005; 12 (Suppl 2): 1542–1552.