Author | Catanese, Alberto | dc.contributor.author |
Author | Rajkumar, Sandeep | dc.contributor.author |
Author | Sommer, Daniel | dc.contributor.author |
Author | Freisem, Dennis | dc.contributor.author |
Author | Wirth, Alexander | dc.contributor.author |
Author | Aly, Amr | dc.contributor.author |
Author | Massa‐López, David | dc.contributor.author |
Author | Olivieri, Andrea | dc.contributor.author |
Author | Torelli, Federica | dc.contributor.author |
Author | Ioannidis, Valentin | dc.contributor.author |
Author | Lipecka, Joanna | dc.contributor.author |
Author | Guerrera, Ida Chiara | dc.contributor.author |
Author | Zytnicki, Daniel | dc.contributor.author |
Author | Ludolph, Albert | dc.contributor.author |
Author | Kabashi, Edor | dc.contributor.author |
Author | Mulaw, Medhanie A | dc.contributor.author |
Author | Roselli, Francesco | dc.contributor.author |
Author | Böckers, Tobias M | dc.contributor.author |
Date of accession | 2021-11-29T08:51:45Z | dc.date.accessioned |
Available in OPARU since | 2021-11-29T08:51:45Z | dc.date.available |
Date of first publication | 2021-06-14 | dc.date.issued |
Abstract | Synopsis
image
The lack of an effective treatment for ALS is calling for the development of novel therapeutic strategies. By using hiPSC‐derived motoneurons and focusing on synapse‐related processes, we provide new molecular targets rescuing the degenerative processes and neuronal loss in ALS.
Human C9orf72‐mutant motoneurons are characterized by reduced expression of synaptic gene, progressive loss of CREB activity and synapse loss.
Similar alterations are observed also in motoneurons harboring TBK1 pathogenic mutations, and in primary neurons upon overexpression of poly(GA) aggregates.
The K+ channel blockers Apamin and XE991 revert the CREB‐dependent loss of synaptic contacts and rescue the degenerative phenotypes of ALS motoneurons. | dc.description.abstract |
Language | en | dc.language.iso |
Publisher | Universität Ulm | dc.publisher |
License | CC BY 4.0 International | dc.rights |
Link to license text | https://creativecommons.org/licenses/by/4.0/ | dc.rights.uri |
Keyword | ALS | dc.subject |
Keyword | CREB | dc.subject |
Keyword | hiPSC | dc.subject |
Dewey Decimal Group | DDC 610 / Medicine & health | dc.subject.ddc |
MeSH | Amyotrophic lateral sclerosis; Therapy | dc.subject.mesh |
MeSH | Motor neurons | dc.subject.mesh |
MeSH | Synapses | dc.subject.mesh |
Title | Synaptic disruption and CREB‐regulated transcription are restored by K+ channel blockers in ALS | dc.title |
Resource type | Wissenschaftlicher Artikel | dc.type |
SWORD Date | 2021-09-08T12:28:20Z | dc.date.updated |
Version | publishedVersion | dc.description.version |
DOI | http://dx.doi.org/10.18725/OPARU-40024 | dc.identifier.doi |
URN | http://nbn-resolving.de/urn:nbn:de:bsz:289-oparu-40100-4 | dc.identifier.urn |
GND | Myatrophische Lateralsklerose | dc.subject.gnd |
GND | Motoneuron | dc.subject.gnd |
GND | Synapse | dc.subject.gnd |
Faculty | Fakultät für Naturwissenschaften | uulm.affiliationGeneral |
Institution | Institut für Anatomie und Zellbiologie | uulm.affiliationSpecific |
Institution | UKU. Klinik für Innere Medizin I | uulm.affiliationSpecific |
Institution | UKU. Klinik für Neurologie | uulm.affiliationSpecific |
Peer review | ja | uulm.peerReview |
DCMI Type | Text | uulm.typeDCMI |
Category | Publikationen | uulm.category |
In cooperation with | Deutsches Zentrum für Neurodegenerative Erkrankungen | uulm.cooperation |
In cooperation with | Université de Paris | uulm.cooperation |
In cooperation with | Imagine Institute des maladies génétiques | uulm.cooperation |
DOI of original publication | 10.15252/emmm.202013131 | dc.relation1.doi |
Source - Title of source | EMBO Molecular Medicine | source.title |
Source - Place of publication | Wiley Open Access | source.publisher |
Source - Volume | 13 | source.volume |
Source - Issue | 7 | source.issue |
Source - Year | 2021 | source.year |
Source - Article number | e13131 | source.articleNumber |
Source - ISSN | 1757-4684 | source.identifier.issn |
Source - eISSN | 1757-4676 | source.identifier.eissn |
Bibliography | uulm | uulm.bibliographie |
Is Supplemented By | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE168831 | dc.relation.isSupplementedBy |
Is Supplemented By | http://www.ebi.ac.uk/pride/archive/projects/PXD020316 | dc.relation.isSupplementedBy |
Is Supplemented By | https://www.embopress.org/action/downloadSupplement?doi=10.15252%2Femmm.202013131&file=emmm202013131-sup-0001-Appendix.pdf | dc.relation.isSupplementedBy |
Is Supplemented By | https://www.embopress.org/action/downloadSupplement?doi=10.15252%2Femmm.202013131&file=emmm202013131-sup-0002-EVFigs.pdf | dc.relation.isSupplementedBy |
Is Supplemented By | https://www.embopress.org/action/downloadSupplement?doi=10.15252%2Femmm.202013131&file=emmm202013131-sup-0003-SDataEV.zip | dc.relation.isSupplementedBy |
DFG project uulm | SFB 1149 / Gefahrenantwort, Störfaktoren und regeneratives Potential nach akutem Trauma / DFG / 251293561 | uulm.projectDFG |
DFG project uulm | GRK 1789 / CEMMA / Zelluläre und molekulare Mechanismen der Alterung / DFG / 194266605 | uulm.projectDFG |