Mutations in NONO lead to syndromic intellectual disability and inhibitory synaptic defects

The NONO protein has been characterized as an important transcriptional regulator in diverse cellular contexts. Here we show that loss of NONO function is a likely cause of human intellectual disability and that NONO-deficient mice have cognitive and affective deficits. Correspondingly, we find spec...

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Gepubliceerd in:Nat Neurosci
Hoofdauteurs: Mircsof, Dennis, Langouët, Maéva, Rio, Marlène, Moutton, Sébastien, Siquier-Pernet, Karine, Bole-Feysot, Christine, Cagnard, Nicolas, Nitschke, Patrick, Gaspar, Ludmila, Žnidarič, Matej, Alibeu, Olivier, Fritz, Ann-Kristina, Wolfer, David P, Schröter, Aileen, Bosshard, Giovanna, Rudin, Markus, Koester, Christina, Crestani, Florence, Seebeck, Petra, Boddaert, Nathalie, Prescott, Katrina, Hines, Rochelle, Moss, Steven J, Fritschy, Jean-Marc, Munnich, Arnold, Amiel, Jeanne, Brown, Steven A, Tyagarajan, Shiva K, Colleaux, Laurence
Formaat: Artigo
Taal:Inglês
Gepubliceerd in: 2015
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Article
Online toegang:https://ncbi.nlm.nih.gov/pmc/articles/PMC5392243/
https://ncbi.nlm.nih.gov/pubmed/26571461
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/nn.4169
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