ArticleBrain research2013
Correcting deregulated Fxyd1 expression ameliorates a behavioral impairment in a mouse model of Rett syndrome.
Article in Brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Insulin-Like Growth Factor-1 Down-Regulates the Phosphorylation of FXYD1 and Rescues Behavioral Deficits in a Mouse Model of Rett Syndrome.Frontiers in neuroscience · 2020Article
- Correcting deregulated Fxyd1 expression rescues deficits in neuronal arborization and potassium homeostasis in MeCP2 deficient male mice.Brain research · 2018Article
- Transcriptome level analysis in Rett syndrome using human samples from different tissues.Orphanet journal of rare diseases · 2018Review
- CD44 is required for spatial memory retention and sensorimotor functions.Behavioural brain research · 2014Article
- Hippocampal subregions exhibit both distinct and shared transcriptomic responses to aging and nonneurodegenerative cognitive decline.The journals of gerontology. Series A, Biological sciences and medical sciences · 2014Article
- Ontogeny of object versus location recognition in the rat: acquisition and retention effects.Developmental psychobiology · 2014Article
- Sodium-potassium ATPase emerges as a player in hippocampal phenotypes of Angelman syndrome mice.Journal of neurophysiology · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Rett syndrome (RTT) is an X-linked neurodevelopmental disorder caused by mutations in the MECP2. Several genes have been shown to be MECP2 targets. We previously identified FXYD1 (encoding phospholemman; a protein containing the motif phenylalanine-X-tyrosine-aspartate), a gene encoding a transmembrane modulator of the Na, K-ATPase (NKA) enzyme, as one of them. In the absence of MECP2, FXYD1 expression is increased in the frontal cortex (FC) of both RTT patients and Mecp2(Bird) null mice. Here, we show that Fxyd1 mRNA levels are also increased in the FC and hippocampus (HC) of male mice carrying a truncating mutation of the Mecp2 gene (Mecp2(308)). To test the hypothesis that some of the behavioral phenotypes seen in these Mecp2 mutants could be ameliorated by genetically preventing the Fxyd1 response to MECP2 deficiency, we crossed Fxyd1 null male mice with Mecp2(308) heterozygous females and behaviorally tested the adult male offspring. Mecp2(308) mice had impaired HC-dependent novel location recognition, and this impairment was rescued by deletion of both Fxyd1 alleles. No other behavioral or sensorimotor impairments were rescued. These results indicate that reducing FXYD1 levels improves a specific cognitive impairment in MECP2-deficient mice.
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