Growth and metabolic control of lipid signalling at the Golgi.
Growth and metabolic control of lipid signalling at the Golgi.
复制标题
高尔基体脂质信号的生长和代谢控制。
DOI:
10.1042/bst20110637
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发表时间:
2012
影响因子:
3.9
通讯作者:
Mayinger,Peter
中科院分区:
文献类型:
--
作者:
Piao,Hailan;Mayinger,Peter
PtdIns4Pis a key regulator of the secretory pathway and plays an essential role in trafficking from the Golgi. Our recent work demonstrated that spatial control of PtdIns4Pat the ER (endoplasmic reticulum) and Golgi co-ordinates secretion with cell growth. The central elements of this regulation are specific phosphoinositide 4-kinases and the phosphoinositide phosphatase Sac1. Growth-dependent translocation of Sac1 between the ER and Golgi modulates the levels of PtdIns4Pand anterograde traffic at the Golgi. In yeast, this mechanism is largely dependent on the availability of glucose, but our recent results in mammalian cells suggest that Sac1 phosphatases play evolutionarily conserved roles in the growth control of secretion. Sac1 lipid phosphatase plays also an essential role in the spatial control of PtdIns4Pat the Golgi complex. A restricted pool of PtdIns4Pat the TGN (trans-Golgi network) is required for Golgi integrity and for proper lipid and protein sorting. In mammalian cells, the stress-activated MAPK (mitogen-activated protein kinase) p38 appears to play a critical role in transmitting nutrient signals to the phosphoinositide signalling machinery at the ER and Golgi. These results suggest that temporal and spatial integration of metabolic and lipid signalling networks at the Golgi is required for controlling the secretory pathway.
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DOI:
--
发表时间:
1988-11
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
P. Orlean;C. Albright;P. Robbins
通讯作者:
P. Orlean;C. Albright;P. Robbins
影响因子:
9.2
作者:
Schorr, M;Then, A;Mayinger, P
通讯作者:
Mayinger, P
影响因子:
--
作者:
T. Powers;I. Dilova;C. Chen;K. Wedaman
通讯作者:
K. Wedaman
影响因子:
4.5
作者:
Tahirovic, S;Schorr, M;Mayinger, P
通讯作者:
Mayinger, P
影响因子:
8
作者:
Vicinanza, M.;D'Angelo, G.;De Matteis, M. A.
通讯作者:
De Matteis, M. A.