ArticleThe Journal of cell biology2000
A specific activation of the mitogen-activated protein kinase kinase 1 (MEK1) is required for Golgi fragmentation during mitosis.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 99 citations in OpenAlex.
- The Impact of Golgi Organization on Cell Cycle and Cancer Development.Sub-cellular biochemistry · 2026Review
- Suppression of autophagy during mitosis via CUL4-RING ubiquitin ligases-mediated WIPI2 polyubiquitination and proteasomal degradation.Autophagy · 2019Article
- Organelle Inheritance Control of Mitotic Entry and Progression: Implications for Tissue Homeostasis and Disease.Frontiers in cell and developmental biology · 2019Review
- Golgi enzymes do not cycle through the endoplasmic reticulum during protein secretion or mitosis.Molecular biology of the cell · 2017Article
- MEK1 inactivates Myt1 to regulate Golgi membrane fragmentation and mitotic entry in mammalian cells.The EMBO journal · 2013Article
- Sequential phosphorylation of GRASP65 during mitotic Golgi disassembly.Biology open · 2012Article
- Golgi biogenesis.Cold Spring Harbor perspectives in biology · 2011Review
- Phosphorylation provides a negative mode of regulation for the yeast Rab GTPase Sec4p.PloS one · 2011Article
- GRASP55 and GRASP65 play complementary and essential roles in Golgi cisternal stacking.The Journal of cell biology · 2010Article
- A non-canonical MEK/ERK signaling pathway regulates autophagy via regulating Beclin 1.The Journal of biological chemistry · 2009Article
- Specific phosphorylation and activation of ERK1c by MEK1b: a unique route in the ERK cascade.Genes & development · 2009Article
- GRASP55 regulates Golgi ribbon formation.Molecular biology of the cell · 2008Article
- The role of GRASP55 in Golgi fragmentation and entry of cells into mitosis.Molecular biology of the cell · 2008Article
- Molecular mechanism of mitotic Golgi disassembly and reassembly revealed by a defined reconstitution assay.The Journal of biological chemistry · 2008Article
- The Golgi mitotic checkpoint is controlled by BARS-dependent fission of the Golgi ribbon into separate stacks in G2.The EMBO journal · 2007Article
- Brain-type creatine kinase BB-CK interacts with the Golgi Matrix Protein GM130 in early prophase.Molecular and cellular biochemistry · 2007Article
- Mitogen-activated protein kinase kinase 1-dependent Golgi unlinking occurs in G2 phase and promotes the G2/M cell cycle transition.Molecular biology of the cell · 2007Article
- Trifunctional norrisolide probes for the study of Golgi vesiculation.Bioorganic & medicinal chemistry letters · 2007Article
- ERK1c regulates Golgi fragmentation during mitosis.The Journal of cell biology · 2006Article
- Extracellular signal-regulated kinase regulates clathrin-independent endosomal trafficking.Molecular biology of the cell · 2006Article
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4 authors at 1 institution in 1 country.
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Abstract
Incubation of permeabilized cells with mitotic extracts results in extensive fragmentation of the pericentriolarly organized stacks of cisternae. The fragmented Golgi membranes are subsequently dispersed from the pericentriolar region. We have shown previously that this process requires the cytosolic protein mitogen-activated protein kinase kinase 1 (MEK1). Extracellular signal-regulated kinase (ERK) 1 and ERK2, the known downstream targets of MEK1, are not required for this fragmentation (Acharya et al. 1998). We now provide evidence that MEK1 is specifically phosphorylated during mitosis. The mitotically phosphorylated MEK1, upon partial proteolysis with trypsin, generates a different peptide population compared with interphase MEK1. MEK1 cleaved with the lethal factor of the anthrax toxin can still be activated by its upstream mitotic kinases, and this form is fully active in the Golgi fragmentation process. We believe that the mitotic phosphorylation induces a change in the conformation of MEK1 and that this form of MEK1 recognizes Golgi membranes as a target compartment. Immunoelectron microscopy analysis reveals that treatment of permeabilized normal rat kidney (NRK) cells with mitotic extracts, treated with or without lethal factor, converts stacks of pericentriolar Golgi membranes into smaller fragments composed predominantly of tubuloreticular elements. These fragments are similar in distribution, morphology, and size to the fragments observed in the prometaphase/metaphase stage of the cell cycle in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.