Regulation of the miR-212/132 locus by MSK1 and CREB in response to neurotrophins
Remenyi, J
Hunter, CJ
Cole, C
Ando, H
Impey, S
Monk, CE
Martin, KJ
Barton, GJ
Hutvagner, G
Arthur, JSC
- Publication Type:
- Journal Article
- Citation:
- Biochemical Journal, 2010, 428 (2), pp. 281 - 291
- Issue Date:
- 2010-06-01
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Remenyi, J | en_US |
dc.contributor.author | Hunter, CJ | en_US |
dc.contributor.author | Cole, C | en_US |
dc.contributor.author | Ando, H | en_US |
dc.contributor.author | Impey, S | en_US |
dc.contributor.author | Monk, CE | en_US |
dc.contributor.author | Martin, KJ | en_US |
dc.contributor.author | Barton, GJ | en_US |
dc.contributor.author |
Hutvagner, G https://orcid.org/0000-0002-7231-9446 |
en_US |
dc.contributor.author | Arthur, JSC | en_US |
dc.date.issued | 2010-06-01 | en_US |
dc.identifier.citation | Biochemical Journal, 2010, 428 (2), pp. 281 - 291 | en_US |
dc.identifier.issn | 0264-6021 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/15258 | |
dc.description.abstract | Neurotrophins are growth factors that are important in neuronal development and survival as well as synapse formation and plasticity. Many of the effects of neurotrophins are mediated by changes in protein expression as a result of altered transcription or translation. To determine whether neurotrophins regulate the production of microRNAs (miRNAs), small RNA species that modulate protein translation or mRNA stability, we used deep sequencing to identify BDNF (brain-derived neurotrophic factor)-induced miRNAs in cultured primary cortical mouse neurons. This revealed that the miR-212/132 cluster contained the miRNAs most responsive to BDNF treatment. This cluster was found to produce four miRNAs: miR-132, miR-132*, miR-212 and miR-212*. Using specific inhibitors, mouse models and promoter analysis we have shown that the regulation of the transcription of the miR-212/132 miRNA cluster and the miRNAs derived from it are regulated by the ERK1/2 (extracellular-signal-regulated kinase 1/2) pathway, via bothMSK (mitogen and stress-activated kinase)-dependent and -independent mechanisms. © The Authors. | en_US |
dc.relation.ispartof | Biochemical Journal | en_US |
dc.relation.isbasedon | 10.1042/BJ20100024 | en_US |
dc.subject.classification | Biochemistry & Molecular Biology | en_US |
dc.subject.mesh | Neurons | en_US |
dc.subject.mesh | Cells, Cultured | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Mice, Inbred C57BL | en_US |
dc.subject.mesh | Mice, Transgenic | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Benzamides | en_US |
dc.subject.mesh | Mitogen-Activated Protein Kinase 1 | en_US |
dc.subject.mesh | Mitogen-Activated Protein Kinase 3 | en_US |
dc.subject.mesh | Ribosomal Protein S6 Kinases, 90-kDa | en_US |
dc.subject.mesh | Brain-Derived Neurotrophic Factor | en_US |
dc.subject.mesh | MicroRNAs | en_US |
dc.subject.mesh | Blotting, Northern | en_US |
dc.subject.mesh | Nucleic Acid Amplification Techniques | en_US |
dc.subject.mesh | Polymerase Chain Reaction | en_US |
dc.subject.mesh | Base Sequence | en_US |
dc.subject.mesh | Sequence Homology, Nucleic Acid | en_US |
dc.subject.mesh | Phosphorylation | en_US |
dc.subject.mesh | Molecular Sequence Data | en_US |
dc.subject.mesh | Cyclic AMP Response Element-Binding Protein | en_US |
dc.title | Regulation of the miR-212/132 locus by MSK1 and CREB in response to neurotrophins | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 2 | en_US |
utslib.citation.volume | 428 | en_US |
utslib.for | 0903 Biomedical Engineering | en_US |
utslib.for | 0601 Biochemistry and Cell Biology | en_US |
utslib.for | 03 Chemical Sciences | en_US |
utslib.for | 06 Biological Sciences | en_US |
utslib.for | 11 Medical and Health Sciences | en_US |
dc.location.activity | ISI:000278528800014 | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Engineering and Information Technology | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering | |
pubs.organisational-group | /University of Technology Sydney/Strength - CHT - Health Technologies | |
utslib.copyright.status | open_access | |
pubs.issue | 2 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 428 | en_US |
Abstract:
Neurotrophins are growth factors that are important in neuronal development and survival as well as synapse formation and plasticity. Many of the effects of neurotrophins are mediated by changes in protein expression as a result of altered transcription or translation. To determine whether neurotrophins regulate the production of microRNAs (miRNAs), small RNA species that modulate protein translation or mRNA stability, we used deep sequencing to identify BDNF (brain-derived neurotrophic factor)-induced miRNAs in cultured primary cortical mouse neurons. This revealed that the miR-212/132 cluster contained the miRNAs most responsive to BDNF treatment. This cluster was found to produce four miRNAs: miR-132, miR-132*, miR-212 and miR-212*. Using specific inhibitors, mouse models and promoter analysis we have shown that the regulation of the transcription of the miR-212/132 miRNA cluster and the miRNAs derived from it are regulated by the ERK1/2 (extracellular-signal-regulated kinase 1/2) pathway, via bothMSK (mitogen and stress-activated kinase)-dependent and -independent mechanisms. © The Authors.
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