有丝分裂期间高尔基体碎片化需要通过丝裂原活化蛋白激酶激酶（MEK1）进行信号传导。
Signaling via mitogen-activated protein kinase kinase (MEK1) is required for Golgi fragmentation during mitosis.
作者信息
Acharya U, Mallabiabarrena A, Acharya J K, Malhotra V
机构信息
Department of Biology, University of California, San Diego, La Jolla 92093-0347, USA.
出版信息
Cell. 1998 Jan 23;92(2):183-92. doi: 10.1016/s0092-8674(00)80913-7.
We have developed an assay using permeabilized cells to monitor fragmentation of the Golgi complex that occurs during mitosis. Golgi stacks, in permeabilized interphase normal rat kidney (NRK) cells, upon incubation with mitotic extracts undergo extensive fragmentation, and the fragmented Golgi membranes are dispersed throughout the cytoplasm. We find that the continued presence of p34cdc2, the mitosis initiation kinase, is not necessary for Golgi fragmentation. Instead, fragmentation depends on cytosolic mitogen-activated protein kinase kinase 1 (MEK1 or MAPKK1). However, the known cytoplasmic substrates for MEK1, ERK1, and ERK2 are not required for this process. Interestingly, we find a Golgi-associated ERK, which we propose as the likely target for MEK1 in Golgi fragmentation.
我们开发了一种利用通透细胞来监测有丝分裂期间高尔基体复合体碎片化的检测方法。在通透的间期正常大鼠肾（NRK）细胞中，高尔基体堆栈与有丝分裂提取物一起孵育后会发生广泛的碎片化，并且碎片化的高尔基体膜会分散在整个细胞质中。我们发现，有丝分裂起始激酶p34cdc2的持续存在对于高尔基体碎片化并非必需。相反，碎片化依赖于胞质丝裂原活化蛋白激酶激酶1（MEK1或MAPKK1）。然而，MEK1的已知胞质底物ERK1和ERK2并非此过程所必需。有趣的是，我们发现了一种与高尔基体相关的ERK，我们认为它可能是MEK1在高尔基体碎片化过程中的作用靶点。
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