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Your search keyword '"Rho guanine exchange factor 12"' showing total 3 results
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3 results on '"Rho guanine exchange factor 12"'

1. Expression profiling suggests underexpression of the GABAA receptor subunit δ in the fragile X knockout mouse model

Author

Ilse Gantois, Jo Vandesompele, Frank Speleman, Edwin Reyniers, Rudi D'Hooge, Lies-Anne Severijnen, Rob Willemsen, Flora Tassone, and R. Frank Kooy

Subjects
Fragile X syndrome, Fragile X knockout mouse, GABAA receptor subunit δ, Rho guanine exchange factor 12, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

It is still unclear why absence of the fragile X protein (FMRP) leads to mental retardation and specific behavioral problems. In neurons, the protein transports specific mRNAs towards the actively translating ribosomes near the synapses.To unravel the mechanism leading to the disorder, we performed global gene expression analysis by means of the differential display method using the fragile X mouse model. To verify differential expression, we used microarray technology and real-time PCR. Three differentially expressed cDNAs showed consistent underexpression in the fragile X knockout mouse, including a GABAA receptor subunit δ, a Rho guanine exchange factor 12 and an EST BU563433. In addition, we identified 5 genes that showed differential expression dependent on the sample of RNA analysis. We consider their differential expression as provisional. It is possible that these differentially expressed genes play an important role in the cognitive and behavioral problems observed in the fragile X syndrome.

Published
2006
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2. Expression profiling suggests underexpression of the GABAA receptor subunit δ in the fragile X knockout mouse model

Author

Gantois, Ilse, Vandesompele, Jo, Speleman, Frank, Reyniers, Edwin, D'Hooge, Rudi, Severijnen, Lies-Anne, Willemsen, Rob, Tassone, Flora, and Kooy, R. Frank

Subjects
*GABA, *FRAGILE X syndrome, *INTELLECTUAL disabilities, *MESSENGER RNA, *ANTISENSE DNA
Abstract

Abstract: It is still unclear why absence of the fragile X protein (FMRP) leads to mental retardation and specific behavioral problems. In neurons, the protein transports specific mRNAs towards the actively translating ribosomes near the synapses. To unravel the mechanism leading to the disorder, we performed global gene expression analysis by means of the differential display method using the fragile X mouse model. To verify differential expression, we used microarray technology and real-time PCR. Three differentially expressed cDNAs showed consistent underexpression in the fragile X knockout mouse, including a GABAA receptor subunit δ, a Rho guanine exchange factor 12 and an EST BU563433. In addition, we identified 5 genes that showed differential expression dependent on the sample of RNA analysis. We consider their differential expression as provisional. It is possible that these differentially expressed genes play an important role in the cognitive and behavioral problems observed in the fragile X syndrome. [Copyright &y& Elsevier]

Published
2006
Full Text
View/download PDF

3. Expression profiling suggests underexpression of the GABAA receptor subunit δ in the fragile X knockout mouse model

Author

Edwin Reyniers, Lies Anne Severijnen, R. Frank Kooy, Rob Willemsen, Jo Vandesompele, Flora Tassone, Ilse Gantois, Rudi D'Hooge, Frank Speleman, and Clinical Genetics

Subjects
Male, Rho guanine exchange factor 12, Protein subunit, Biology, GABAA receptor subunit δ, lcsh:RC321-571, Fragile X Mental Retardation Protein, Mice, Receptors, GABA, Sequence Homology, Nucleic Acid, Gene expression, medicine, Animals, Humans, Fragile X knockout mouse, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Gene, Oligonucleotide Array Sequence Analysis, Mice, Knockout, Differential display, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Brain, medicine.disease, Immunohistochemistry, Molecular biology, Fragile X syndrome, Gene expression profiling, Disease Models, Animal, Neurology, Fragile X Syndrome, Knockout mouse, Gene chip analysis
Abstract

It is still unclear why absence of the fragile X protein (FMRP) leads to mental retardation and specific behavioral problems. In neurons, the protein transports specific mRNAs towards the actively translating ribosomes near the synapses. To unravel the mechanism leading to the disorder, we performed global gene expression analysis by means of the differential display method using the fragile X mouse model. To verify differential expression, we used microarray technology and real-time PCR. Three differentially expressed cDNAs showed consistent underexpression in the fragile X knockout mouse, including a GABAA receptor subunit δ, a Rho guanine exchange factor 12 and an EST BU563433. In addition, we identified 5 genes that showed differential expression dependent on the sample of RNA analysis. We consider their differential expression as provisional. It is possible that these differentially expressed genes play an important role in the cognitive and behavioral problems observed in the fragile X syndrome.

Published
2006

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