dc.contributor.author | Rakic, S | |
dc.contributor.author | Kanatani, S | |
dc.contributor.author | Hunt, D | |
dc.contributor.author | Faux, C | |
dc.contributor.author | Cariboni, C | |
dc.contributor.author | Chiara, F | |
dc.contributor.author | Khan, S | |
dc.contributor.author | Wansbury, O | |
dc.contributor.author | Howard, BA | |
dc.contributor.author | Nakajima, K | |
dc.contributor.author | Nikolic, M | |
dc.contributor.author | Parnavelas, JG | |
dc.date.accessioned | 2016-09-28T14:41:35Z | |
dc.identifier.citation | under review at Development | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/153 | |
dc.description.abstract | Interneuron dysfunction is often associated with neurological and psychiatric disorders, such
as epilepsy, schizophrenia and autism. Some of these disorders arise during brain formation, at the
time of interneuron specification, migration and synapse formation. Here, we showed that the
signalling molecule cyclin-dependent kinase 5 (Cdk5), and its activator p35, control the migration of
interneurons towards and within the cerebral cortex by modulating the motogenic
ErbB4/phosphatidylinositol (PI) 3-kinase signalling pathway. We first identified ErbB4 as a novel
p35/Cdk5 kinase substrate. We then demonstrated that Cdk5-dependent ErbB4/PI3-kinase signalling
cascade regulates interneuron leading process dynamics (morphology) and directionality. Finally, we
showed that lack of Cdk5 activity in p35 mutants leads to permanent reduction in the final number of a
subtype of interneurons that may affect formation of neuronal circuits, thus increasing the risk of
neurodevelopmental disorders. Together, these findings identify Cdk5 as a crucial signalling factor in
cortical interneuron development. | |
dc.language | eng | |
dc.language.iso | eng | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.title | Cdk5 phosphorylation of ErbB4 is crucial for cortical interneuron migration | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2013-08-01 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2013-08-01 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | under review at Development | |
pubs.notes | No embargo | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Endocrine control mechanisms | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Endocrine control mechanisms | |
pubs.publication-status | Submitted | |
pubs.embargo.terms | No embargo | |
icr.researchteam | Endocrine control mechanisms | |
dc.contributor.icrauthor | Howard, Beatrice | |