The prevalence of SMN gene deletion/duplication in spinal muscular atrophy families referred to neuro-genetic centers of Mashhad, Iran
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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1 Online-Ressource.
- Language
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Englisch
- Bibliographic citation
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The prevalence of SMN gene deletion/duplication in spinal muscular atrophy families referred to neuro-genetic centers of Mashhad, Iran ; volume:25 ; number:1 ; day:31 ; month:7 ; year:2024 ; pages:1-9 ; date:12.2024
The Egyptian journal of medical human genetics ; 25, Heft 1 (31.7.2024), 1-9, 12.2024
- Creator
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Shariati, Mohammad
Davoudi, Alireza
Boostani, Reza
Ashrafzadeh, Farah
Beiraghi Toosi, Mehran
Todarbary, Nafiseh
Akhondian, Javad
Hashemi, Narges
Sadr-Nabavi, Ariane
- Contributor
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SpringerLink (Online service)
- DOI
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10.1186/s43042-024-00551-0
- URN
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urn:nbn:de:101:1-2410250838238.694449999510
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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14.08.2025, 10:44 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Shariati, Mohammad
- Davoudi, Alireza
- Boostani, Reza
- Ashrafzadeh, Farah
- Beiraghi Toosi, Mehran
- Todarbary, Nafiseh
- Akhondian, Javad
- Hashemi, Narges
- Sadr-Nabavi, Ariane
- SpringerLink (Online service)
Other Objects (12)
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Posttranslational modifications of the Spinal Muscular Atrophy gene product SMN : Implications for therapy and pathophysiology
Recombinant SMN protein synergizes with spinal muscular atrophy therapy to counteract pathological motor neuron phenotypes
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Calpain Inhibition Increases SMN Protein in Spinal Cord Motoneurons and Ameliorates the Spinal Muscular Atrophy Phenotype in Mice
Enhancement of SMN protein levels in a mouse model of spinal muscular atrophy using novel drug‐like compounds
A small molecule antagonist of SMN disrupts the interaction between SMN and RNAP II
VPAC2 receptor agonist BAY 55-9837 increases SMN protein levels and moderates disease phenotype in severe spinal muscular atrophy mouse models
Small-molecule flunarizine increases SMN protein in nuclear Cajal bodies and motor function in a mouse model of spinal muscular atrophy
Weekly reports referred
SMN deficiency perturbs monoamine neurotransmitter metabolism in spinal muscular atrophy
SMN
Understanding how SMN protein regulates the autophagy-lysosome pathway in spinal muscular atrophy
Posttranslational modifications of the Spinal Muscular Atrophy gene product SMN : Implications for therapy and pathophysiology
Recombinant SMN protein synergizes with spinal muscular atrophy therapy to counteract pathological motor neuron phenotypes
Sonderdienst militärischer Nachrichten (SMN)
Calpain Inhibition Increases SMN Protein in Spinal Cord Motoneurons and Ameliorates the Spinal Muscular Atrophy Phenotype in Mice
Enhancement of SMN protein levels in a mouse model of spinal muscular atrophy using novel drug‐like compounds
A small molecule antagonist of SMN disrupts the interaction between SMN and RNAP II
VPAC2 receptor agonist BAY 55-9837 increases SMN protein levels and moderates disease phenotype in severe spinal muscular atrophy mouse models
Small-molecule flunarizine increases SMN protein in nuclear Cajal bodies and motor function in a mouse model of spinal muscular atrophy
Weekly reports referred
SMN deficiency perturbs monoamine neurotransmitter metabolism in spinal muscular atrophy
SMN
Understanding how SMN protein regulates the autophagy-lysosome pathway in spinal muscular atrophy
Posttranslational modifications of the Spinal Muscular Atrophy gene product SMN : Implications for therapy and pathophysiology
Recombinant SMN protein synergizes with spinal muscular atrophy therapy to counteract pathological motor neuron phenotypes
Sonderdienst militärischer Nachrichten (SMN)
Calpain Inhibition Increases SMN Protein in Spinal Cord Motoneurons and Ameliorates the Spinal Muscular Atrophy Phenotype in Mice
Enhancement of SMN protein levels in a mouse model of spinal muscular atrophy using novel drug‐like compounds
A small molecule antagonist of SMN disrupts the interaction between SMN and RNAP II
VPAC2 receptor agonist BAY 55-9837 increases SMN protein levels and moderates disease phenotype in severe spinal muscular atrophy mouse models
Small-molecule flunarizine increases SMN protein in nuclear Cajal bodies and motor function in a mouse model of spinal muscular atrophy