Spontaneous seizure and partial lethality of juvenile Shank3-overexpressing mice in C57BL/6 J background
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1756-6606
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Spontaneous seizure and partial lethality of juvenile Shank3-overexpressing mice in C57BL/6 J background ; volume:11 ; number:1 ; day:10 ; month:10 ; year:2018 ; pages:1-3 ; date:12.2018
Molecular brain ; 11, Heft 1 (10.10.2018), 1-3, 12.2018
- Creator
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Jin, Chunmei
- Contributor
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Zhang, Yinhua
Kim, Shinhyun
Kim, Yoonhee
Lee, Yeunkum
Han, Kihoon
SpringerLink (Online service)
- DOI
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10.1186/s13041-018-0403-6
- URN
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urn:nbn:de:101:1-2018111822013989671008
- 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
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Associated
- Jin, Chunmei
- Zhang, Yinhua
- Kim, Shinhyun
- Kim, Yoonhee
- Lee, Yeunkum
- Han, Kihoon
- SpringerLink (Online service)
Other Objects (12)
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Modeling synthetic lethality
Transcriptional and functional complexity of Shank3 provides a molecular framework to understand the phenotypic heterogeneity of SHANK3 causing autism and Shank3 mutant mice
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Microglia unravel immune-associated alterations in Shank3 deficiency
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Accuracy of seizure semiology obtained from first-time seizure witnesses
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Transcriptome analysis of Shank3-overexpressing mice reveals unique molecular changes in the hypothalamus
Increased ribosomal protein levels and protein synthesis in the striatal synaptosome of Shank3-overexpressing transgenic mice
Kainate and AMPA receptor binding in brains of seizure prone DBA/2J and seizure resistant C57BL/6J mice
Modeling synthetic lethality
Transcriptional and functional complexity of Shank3 provides a molecular framework to understand the phenotypic heterogeneity of SHANK3 causing autism and Shank3 mutant mice
The failure of two major formaldehyde catabolism enzymes (ADH5 and ALDH2) leads to partial synthetic lethality in C57BL/6 mice
SHANK3 deficiency leads to myelin dysregulation in a Shank3∆11(-/-) mouse model and human iPSC-derived cerebral organoids
Funktionelle Analyse von SHANK3-Mutationen assoziiert mit Synaptopathien
Microglia unravel immune-associated alterations in Shank3 deficiency
Epilepsy surgery: late seizure recurrence after initial complete seizure freedom
Accuracy of seizure semiology obtained from first-time seizure witnesses
The Lynx family : survivability, modularity, lethality, performance
Transcriptome analysis of Shank3-overexpressing mice reveals unique molecular changes in the hypothalamus
Increased ribosomal protein levels and protein synthesis in the striatal synaptosome of Shank3-overexpressing transgenic mice
Kainate and AMPA receptor binding in brains of seizure prone DBA/2J and seizure resistant C57BL/6J mice
Modeling synthetic lethality
Transcriptional and functional complexity of Shank3 provides a molecular framework to understand the phenotypic heterogeneity of SHANK3 causing autism and Shank3 mutant mice
The failure of two major formaldehyde catabolism enzymes (ADH5 and ALDH2) leads to partial synthetic lethality in C57BL/6 mice
SHANK3 deficiency leads to myelin dysregulation in a Shank3∆11(-/-) mouse model and human iPSC-derived cerebral organoids
Funktionelle Analyse von SHANK3-Mutationen assoziiert mit Synaptopathien
Microglia unravel immune-associated alterations in Shank3 deficiency
Epilepsy surgery: late seizure recurrence after initial complete seizure freedom
Accuracy of seizure semiology obtained from first-time seizure witnesses