ArticleProceedings of the National Academy of Sciences of the United States of America2009
Fibroblast growth factor-2 regulates the stability of nuclear bodies.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Chaperoning the chaperones: Proteomic analysis of the SMN complex reveals conserved and etiologic connections to the proteostasis network.bioRxiv : the preprint server for biology · 2024Article
- Proteomic analysis of the SMN complex reveals conserved and etiologic connections to the proteostasis network.Frontiers in RNA research · 2024Article
- NRF2 has a splicing regulatory function involving the survival of motor neuron (SMN) in non-small cell lung cancer.Oncogene · 2023Article
- UsnRNP biogenesis: mechanisms and regulation.Chromosoma · 2017Review
- Deregulation of ZPR1 causes respiratory failure in spinal muscular atrophy.Scientific reports · 2017Article
- Towards an understanding of regulating Cajal body activity by protein modification.RNA biology · 2017Review
- Molecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy.Journal of experimental neuroscience · 2016Review
- A nuclear odyssey: fibroblast growth factor-2 (FGF-2) as a regulator of nuclear homeostasis in the nervous system.Cellular and molecular life sciences : CMLS · 2015Review
- Immobile survival of motoneuron (SMN) protein stored in Cajal bodies can be mobilized by protein interactions.Cellular and molecular life sciences : CMLS · 2013Article
- Signals controlling Cajal body assembly and function.The international journal of biochemistry & cell biology · 2013Review
- Article
- Cooperation of nuclear fibroblast growth factor receptor 1 and Nurr1 offers new interactive mechanism in postmitotic development of mesencephalic dopaminergic neurons.The Journal of biological chemistry · 2012Article
- Analysis of the fibroblast growth factor system reveals alterations in a mouse model of spinal muscular atrophy.PloS one · 2012Article
- Modeling spinal muscular atrophy in Drosophila links Smn to FGF signaling.The Journal of cell biology · 2011Article
- Phosphorylation and the Cajal body: modification in search of function.Archives of biochemistry and biophysics · 2010Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear bodies are distinct subnuclear structures. The survival of motoneuron (SMN) gene is mutated or deleted in patients with the neurodegenerative disease spinal muscular atrophy (SMA). The gene product SMN is a marker protein for one class of nuclear bodies denoted as nuclear gems. SMN has also been found in Cajal bodies, which co-localize with gems in many cell types. Interestingly, SMA patients display a reduced number of gems. Little is known about the regulation of nuclear body formation and stabilization. We have previously shown that a nuclear isoform of the fibroblast growth factor-2 (FGF-2(23)) binds directly to SMN. In this study, we analyzed the consequences of FGF-2(23) binding to SMN with regard to nuclear body formation. On a molecular level, we showed that FGF-2(23) competed with Gemin2 (a component of the SMN complex that is necessary for gem stabilization) for binding to SMN. Down-regulation of Gemin2 by siRNA caused destabilization of SMN-positive nuclear bodies. This process is reflected in both cellular and in vivo systems by a negative regulatory function of FGF-2 in nuclear body formation: in HEK293 cells, FGF-2(23) decreased the number of SMN-positive nuclear bodies. The same effect could be observed in motoneurons of FGF-2 transgenic mice. This study demonstrates the functional role of a growth factor in the regulation of structural entities of the nucleus.
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