Short communicationRgs4 mRNA expression is decreased in the brain of Fmr1 knockout mouse
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Acknowledgement
This work was supported by the Arvo and Lea Ylppö Foundation and Academy of Finland.
References (19)
- et al.
Immunocytochemical and biochemical characterization of FMRP, FXR1P, and FXR2P in the mouse
Exp. Cell Res.
(2000) - et al.
New insights into fragile X syndrome: from molecules to neurobehaviors
Trends Biochem. Sci.
(2003) - et al.
Symptoms of schizotypal personality disorder in Fragile X women
J. Am. Child Adolesc. Psych.
(1994) - et al.
The fragile X syndrome protein FMRP associates with BC1 RNA and regulates the translation of specific mRNAs at synapses
Cell
(2003) - et al.
Drosophila fragile X-related gene regulates the MAP1B homolog Futsch to control synaptic structure and function
Cell
(2001) - et al.
Knockout mouse model for Fxr2: a model for mental retardation
Hum. Mol. Genet.
(2002) - et al.
Fragile-X carrier females: evidence for a distinct psychopathological phenotype?
Am. J. Med. Genet.
(1996) - et al.
Cellular regulation of RGS proteins: modulators and integrators of G protein signaling
Pharmacol. Rev.
(2002) - et al.
Altered synaptic plasticity in a mouse model of fragile X mental retardation
Proc. Natl. Acad. Sci. U. S. A.
(2002)
Cited by (10)
Genetic deletion of regulator of G-protein signaling 4 (RGS4) rescues a subset of fragile X related phenotypes in the FMR1 knockout mouse
2011, Molecular and Cellular NeuroscienceCitation Excerpt :Although not statistically different, it is interesting to note that RGS4 mRNA levels were elevated in both brain regions at all time points examined. These findings differ from those of a previous report where in situ hybridization data indicated that RGS4 mRNA levels were decreased in hippocampal pyramidal neurons and in the retrosplenial cortex but not in the piriform cortex of 10 day old but not in adult FMR1 mice (Tervonen et al., 2005). The reason for this discrepancy may relate to subtle differences in the age of the animals used in the two studies, or to the lower degree of spatial resolution in real-time RT-PCR compared to in situ hybridization.
The fragile X mental retardation protein developmentally regulates the strength and fidelity of calcium signaling in Drosophila mushroom body neurons
2011, Neurobiology of DiseaseCitation Excerpt :If FMRP directly regulates calmodulin, then amplification of neuronal signaling could be envisioned whereby FMRP upregulates calmodulin to further facilitate its own activation, or other calmodulin-dependent processes. Both mammalian and Drosophila FMRP are able alter global and specific mRNA levels, though it is unclear whether the mRNA reductions identified here are direct or indirect effects of loss of dFMRP (D'Hulst et al., 2006; Epstein et al., 2009; Tervonen et al., 2005; Tessier and Broadie, 2008; Xu et al., 2004; Zalfa et al., 2007). It will therefore be necessary in the future to determine whether our findings are also apparent at the protein level, and whether spatial distributions of these proteins may be important for their function in the MB, as has been demonstrated in the visual system (Porter et al., 1993).
Whole genome microarray analysis of gene expression in subjects with fragile X syndrome
2007, Genetics in MedicineCitation Excerpt :The remaining genes either did not have sufficiently strong signals to be detected or did not have a significant difference in signal intensity. Several genes have recently been reported to have reduced expression in Fmr1 knockout mice including GABAA receptor Δ subunit (Gabrd), a ρ guanine exchange factor and a regulator of G-protein signaling (Rgs4).17,18 Unfortunately, none of these genes had a reliable detection signal on our microarrays.
Molecular and cellular aspects of mental retardation in the Fragile X syndrome: From gene mutation/s to spine dysmorphogenesis
2012, Advances in Experimental Medicine and BiologyVignettes: Models in absentia
2012, Results and Problems in Cell Differentiation