ArticleThe EMBO journal2006
PDGF regulates the actin cytoskeleton through hnRNP-K-mediated activation of the ubiquitin E3-ligase MIR.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Construction of an E3 Ubiquitin Ligase Gene Model to Predict the Prognosis of Idiopathic Pulmonary Fibrosis Patients Using Integrated Bioinformatics Analysis.Current medicinal chemistry · 2026Article
- Platelet-derived growth factor signaling in porcine testicular tubular somatic cells.Cell and tissue research · 2025Article
- Role of MARCH E3 ubiquitin ligases in cancer development.Cancer metastasis reviews · 2024Review
- Pervasive compartment-specific regulation of gene expression during homeostatic synaptic scaling.EMBO reports · 2021Article
- Overexpression of α-Synuclein Reorganises Growth Factor Profile of Human Astrocytes.Molecular neurobiology · 2021Article
- Spontaneous regression of micro-metastases following primary tumor excision: a critical role for primary tumor secretome.BMC biology · 2020Article
- Glycosaminoglycan-Mediated Downstream Signaling of CXCL8 Binding to Endothelial Cells.International journal of molecular sciences · 2017Article
- Myosin light chains: Teaching old dogs new tricks.Bioarchitecture · 2014Review
- Functional proteomic analysis of long-term growth factor stimulation and receptor tyrosine kinase coactivation in Swiss 3T3 fibroblasts.Molecular & cellular proteomics : MCP · 2012Article
- Fibroblast growth factor-21 (FGF21) regulates low-density lipoprotein receptor (LDLR) levels in cells via the E3-ubiquitin ligase Mylip/Idol and the Canopy2 (Cnpy2)/Mylip-interacting saposin-like protein (Msap).The Journal of biological chemistry · 2012Article
- Inhibition of platelet-derived growth factor receptor signaling regulates Oct4 and Nanog expression, cell shape, and mesenchymal stem cell potency.Stem cells (Dayton, Ohio) · 2012Article
- PDGF: the nuts and bolts of signalling toolbox.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Review
- Identification of c-Src tyrosine kinase substrates in platelet-derived growth factor receptor signaling.Molecular oncology · 2009Article
- Mylip makes an Idol turn into regulation of LDL receptor.Cellular and molecular life sciences : CMLS · 2009Review
- The sodium-hydrogen exchanger NHE1 is an Akt substrate necessary for actin filament reorganization by growth factors.The Journal of biological chemistry · 2009Article
- N-methyl-D-aspartate receptor subunits are non-myosin targets of myosin regulatory light chain.The Journal of biological chemistry · 2009Article
- The phosphorylation of myosin II at the Ser1 and Ser2 is critical for normal platelet-derived growth factor induced reorganization of myosin filaments.Molecular biology of the cell · 2007Article
- Loss-of-function screening by randomized intracellular antibodies: identification of hnRNP-K as a potential target for metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PDGF is a potent chemotactic mitogen and a strong inductor of fibroblast motility. In Swiss 3T3 fibroblasts, exposure to PDGF but not EGF or IGF-1 causes a rapid loss of actin stress fibers (SFs) and focal adhesions (FAs), which is followed by the development of retractile dendritic protrusions and induction of motility. The PDGF-specific actin reorganization was blocked by inhibition of Src-kinase and the 26S proteasome. PDGF induced Src-dependent association between the multifunctional transcription/translation regulator hnRNP-K and the mRNA-encoding myosin regulatory light-chain (MRLC)-interacting protein (MIR), a E(3)-ubiquitin ligase that is MRLC specific. This in turn rapidly increased MIR expression, and led to ubiquitination and proteasome-mediated degradation of MRLC. Downregulation of MIR by RNA muting prevented the reorganization of actin structures and severely reduced the migratory and wound-healing potential of PDGF-treated cells. The results show that activation of MIR and the resulting removal of diphosphorylated MRLC are essential for PDGF to instigate and maintain control over the actin-myosin-based contractile system in Swiss 3T3 fibroblasts. The PDGF induced protein destabilization through the regulation of hnRNP-K controlled ubiquitin -ligase translation identifies a novel pathway by which external stimuli can regulate phenotypic development through rapid, organelle-specific changes in the activity and stability of cytoskeletal regulators.
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