ArticleThe Journal of cell biology2001
Tyrosine-phosphorylated extracellular signal--regulated kinase associates with the Golgi complex during G2/M phase of the cell cycle: evidence for regulation of Golgi structure.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 67 citations in OpenAlex.
- ERK1/2 Signaling in Intrahepatic Cholangiocarcinoma: From Preclinical Advances to Therapeutic Strategies.Biology · 2025Review
- The GPCR adaptor protein Norbin regulates S1PR1 trafficking and the morphology, cell cycle and survival of PC12 cells.Scientific reports · 2023Article
- Spatiotemporal control of pathway sensors and cross-pathway feedback regulate a differentiation MAPK pathway in yeast.Journal of cell science · 2021Article
- Mitotic HOOK3 phosphorylation by ERK1c drives microtubule-dependent Golgi destabilization and fragmentation.iScience · 2021Article
- Thymosin β4 protects against aortic aneurysm via endocytic regulation of growth factor signaling.The Journal of clinical investigation · 2021Article
- The MEK/ERK Network as a Therapeutic Target in Human Cancer.Molecular cancer research : MCR · 2021Review
- Spatial regulation and generation of diversity in signaling pathways.Journal of biosciences · 2021Review
- Proteins and Proteoforms: New Separation Challenges.Analytical chemistry · 2018Review
- Detection and Differentiation of Threonine- and Tyrosine-Monophosphorylated Forms of ERK1/2 by Capillary Isoelectric Focusing-Immunoassay.Scientific reports · 2015Article
- CaMKKβ-AMPKα2 signaling contributes to mitotic Golgi fragmentation and the G2/M transition in mammalian cells.Cell cycle (Georgetown, Tex.) · 2015Article
- Comparative analysis of Erk phosphorylation suggests a mixed strategy for measuring phospho-form distributions.Molecular systems biology · 2011Article
- The ERK Cascade: Distinct Functions within Various Subcellular Organelles.Genes & cancer · 2011Article
- Monophosphothreonyl extracellular signal-regulated kinases 1 and 2 (ERK1/2) are formed endogenously in intact cardiac myocytes and are enzymically active.Cellular signalling · 2011Article
- RAF associates with phosphorylated nuclear BubR1 during endoreduplication induced by JAK inhibition.Cell cycle (Georgetown, Tex.) · 2010Article
- GRASP55 and GRASP65 play complementary and essential roles in Golgi cisternal stacking.The Journal of cell biology · 2010Article
- Regulation of Golgi function via phosphoinositide lipids.Seminars in cell & developmental biology · 2009Review
- Specific phosphorylation and activation of ERK1c by MEK1b: a unique route in the ERK cascade.Genes & development · 2009Article
- Plk3 interacts with and specifically phosphorylates VRK1 in Ser342, a downstream target in a pathway that induces Golgi fragmentation.Molecular and cellular biology · 2009Article
- Enzymatic activity and substrate specificity of mitogen-activated protein kinase p38alpha in different phosphorylation states.The Journal of biological chemistry · 2008Article
- Activation of extracellular signal-regulated kinase (ERK) in G2 phase delays mitotic entry through p21CIP1.Cell proliferation · 2006Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphorylation of the extracellular signal-regulated kinases (ERKs) on tyrosine and threonine residues within the TEY tripeptide motif induces ERK activation and targeting of substrates. Although it is recognized that phosphorylation of both residues is required for ERK activation, it is not known if a single phosphorylation of either residue regulates physiological functions. In light of recent evidence indicating that ERK proteins regulate substrate function in the absence of ERK enzymatic activity, we have begun to examine functional roles for partially phosphorylated forms of ERK. Using phosphorylation site--specific ERK antibodies and immunofluorescence, we demonstrate that ERK phosphorylated on the tyrosine residue (pY ERK) within the TEY activation sequence is found constitutively in the nucleus, and localizes to the Golgi complex of cells that are in late G2 or early mitosis of the cell cycle. As cells progress through metaphase and anaphase, pY ERK localization to Golgi vesicles is most evident around the mitotic spindle poles. During telophase, pY ERK associates with newly formed Golgi vesicles but is not found on there after cytokinesis and entry into G1. Increased ERK phosphorylation causes punctate distribution of several Golgi proteins, indicating disruption of the Golgi structure. This observation is reversible by overexpression of a tyrosine phosphorylation--defective ERK mutant, but not by a kinase-inactive ERK2 mutant that is tyrosine phosphorylated. These data provide the first evidence that pY ERK and not ERK kinase activity regulates Golgi structure and may be involved in mitotic Golgi fragmentation and reformation.
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